Paralytic Disorders - Clinical Tree

Poliomyelitis

Acute anterior poliomyelitis is a viral infection localized in the anterior horn cells of the spinal cord and certain brainstem motor nuclei. One of three types of poliomyelitis viruses is usually the cause of infection, but other members of the enteroviral group can cause a condition clinically and pathologically indistinguishable from poliomyelitis. Viral transmission is primarily fecal-oral, and initial invasion by the virus occurs through the gastrointestinal and respiratory tracts and spreads to the central nervous system through a hematogenous route. Although most individuals in an endemic area are infected with poliovirus, only 0.5% of infected individuals develop paralytic poliomyelitis.

Since the introduction and extensive use of the poliomyelitis vaccine, the incidence of acute anterior poliomyelitis has decreased dramatically. In 1988, there were an estimated 350,000 cases; in 2013, fewer than 400 cases were reported. In 2017, there were 22 reported cases and in 2018, 29 cases. Currently, it most often affects children younger than 5 years old in developing tropical and subtropical countries and unimmunized individuals. In 2014, only three countries (Afghanistan, Nigeria, and Pakistan) were classified as polio-endemic by the WHO. Isolated outbreaks of poliomyelitis occurred in North America and Europe in the 1990s.

Administration of three doses of the Sabin oral polio vaccine, containing all three types of attenuated virus, can prevent the disease. The use of the live attenuated virus vaccine remains controversial. Live oral poliovirus vaccine (OPV) may immunize contacts who have not been vaccinated; however, this carries a risk of developing vaccine-associated paralytic polio, which has been estimated at 1 case per 2.5 million doses. Outbreaks of paralytic poliomyelitis in the United States have been associated with the use of live poliovirus vaccine. The implementation of an all-inactive polio vaccine (IPV) schedule in the United States in 2000 has eliminated indigenous acquired vaccine-associated poliomyelitis. Despite the safety and efficacy of the IPV, OPV remains the vaccine of choice for global eradication in many parts of the world where logistical issues and the higher cost of IPV prohibit its use and in places where inadequate sanitation necessitates an optimal mucosal barrier to wild-type poliovirus circulation. Challenges to the complete eradication of polio include the transmission of wild-type viruses in endemic areas, outbreaks related to vaccine-related polioviruses, and excretion of vaccine-related viruses in vaccines with B-cell immunodeficiencies.

In August of 2018, the Centers for Disease Control and Prevention (CDC) noted an increased number of reports of patients having symptoms clinically compatible with acute flaccid myelitis, a polio-like condition characterized by rapid onset of flaccid weakness in one or more limbs and spinal cord gray matter lesions. First described in 2014, the disease appears to have established a biennial pattern of recurrence, usually in the summer and fall and often following a viral respiratory infection. Of 106 patients identified with acute flaccid myelitis in 2018, 80 were classified as confirmed, six as probable, and 20 as noncases, a threefold increase in confirmed cases compared with 2017. The pattern of spinal cord involvement, similar to poliomyelitis, is suggestive of a viral infection, but a definitive connection with a particular virus has yet to be established. The most frequently cited causative agent is enterovirus D68, but the absence of direct virus isolation from affected tissues, infrequent detection in cerebrospinal fluid, and the limited number of animal studies has left the causal nature of the relationship unproven. A number of treatments have been tried, including immunoglobulin, corticosteroids, plasma exchange, and antiviral therapy. To date, however, no systematic studies have identified an effective medical treatment of acute flaccid myelitis, and supportive care is the mainstay of treatment. Most patients have some residual weakness a year or more after onset.

Pathologic findings

When the poliomyelitis virus invades the body through the oropharyngeal route, it multiplies in the alimentary tract lymph nodes and spreads through the blood, acutely attacking the anterior horn ganglion cells of the spinal cord, especially in the lumbar and cervical enlargements. How the virus penetrates the blood-brain barrier and why the virus has a predilection for the anterior horn cell is under investigation. The incubation period is 6 to 20 days. The anterior horn motor cells may be damaged directly by viral multiplication or toxic by-products of the virus or indirectly by ischemia, edema, and hemorrhage in the glial tissues surrounding them. Destruction of the spinal cord occurs focally and randomly, and within 3 days, Wallerian degeneration is evident throughout the length of the individual nerve fiber. Macrophages and neutrophils surround and partially remove necrotic ganglion cells, and the inflammatory response gradually subsides. Within the muscle, axonal “sprouting” occurs when nerve cells from surviving motor units develop new axons, which innervate muscle cells that have lost their lower motor neuron, thus expanding the size of the motor unit. After 4 months, residual areas of gliosis and lymphocytic cells fill the area of destroyed motor cells in the spine. Reparative neuroglial cells proliferate. Continuous disease activity has been reported in spinal cord segments 20 years after disease onset.

The number of individual muscles affected by the resultant flaccid paralysis and the severity of paralysis vary; the clinical weakness is proportional to the number of lost motor units. Weakness is clinically detectable only when more than 60% of the nerve cells supplying the muscle have been destroyed. Muscles innervated by the cervical and lumbar spinal segments are most often affected, and paralysis occurs twice as often in the lower extremity muscles as in upper extremity muscles. In the lower extremity, the most commonly affected muscles are the quadriceps, glutei, anterior tibial, medial hamstrings, and hip flexors; in the upper extremity, the deltoid, triceps, and pectoralis major are most often affected.

The potential for recovery of muscle function depends on the recovery of damaged, but not destroyed, anterior horn cells. Most clinical recovery occurs during the first month after the acute illness and is almost complete within 6 months, although limited recovery may occur for about 2 years. A muscle paralyzed at 6 months remains paralyzed.

Clinical course and treatment

Approximately 95% of patients infected with poliovirus remain asymptomatic. Nonspecific findings such as fever and sore throat occur in 4% to 8% of people infected. Between 0.5% and 2% of patients will progress to poliomyelitis. The course of poliomyelitis can be divided into three stages: acute, convalescent, and chronic. General guidelines for treatment are described here. Specific indications and techniques for operative procedures are discussed in specific sections.

Acute stage

The acute stage generally lasts 7 to 10 days, and up to 95% of all anterior horn cells may be infected. Symptoms range from mild malaise to generalized encephalomyelitis with widespread paralysis. With upper spinal cord involvement, diaphragmatic dysfunction and respiratory compromise can be life threatening. A high index of suspicion of this is necessary, especially in patients with shoulder involvement, given the close proximity of their respective anterior horn cells. In younger children, systemic symptoms include listlessness, sore throat, and a slight temperature elevation; these may resolve, but recurrent symptoms, including hyperesthesia or paresthesia in the extremities, severe headache, sore throat, vomiting, nuchal rigidity, back pain, and limitation of straight-leg raising, culminate in characteristically asymmetric paralysis. In older children and adults, symptoms include slight temperature elevation, marked flushing of the skin, and apprehension; muscular pain is common. Muscles are tender even to gentle palpation. Superficial reflexes usually are absent first, and deep tendon reflexes disappear when the muscle group is paralyzed. Differential diagnoses include Guillain-Barré syndrome and other forms of encephalomyelitis. In rare cases, transverse myelitis can follow receipt of OPV.

Treatment of poliomyelitis in the acute stage generally consists of bed rest, analgesics, and anatomic positioning of the limbs to prevent contractures. Gentle, passive range-of-motion exercises of all joints should be performed several times daily.

Convalescent stage

The convalescent stage begins 2 days after the temperature returns to normal and continues for 2 years. It has been estimated that approximately half of the infected anterior horn cells survive the initial infection, and muscle power improves spontaneously during this stage, especially during the first 4 months and more gradually thereafter. Treatment during this stage is similar to that during the acute stage. Muscle strength should be assessed monthly for 6 months and then every 3 months. Physical therapy should emphasize muscle activity in normal patterns and development of maximal capability of individual muscles. Muscles with more than 80% return of strength recover spontaneously without specific therapy. According to Johnson, an individual muscle with less than 30% of normal strength at 3 months should be considered permanently paralyzed.

Vigorous passive stretching exercises and wedging casts can be used for mild or moderate contractures. Surgical release of tight fascia and muscle aponeuroses and lengthening of tendons may be necessary for contractures persisting longer than 6 months. Orthoses should be used until no further recovery is anticipated.

Chronic stage

The chronic stage of poliomyelitis usually begins 24 months after the acute illness. During this time, the orthopaedist attempts to help the patient achieve maximal functional activity by management of the long-term consequences of muscle imbalance. Goals of treatment include correcting any significant muscle imbalances and preventing or correcting soft-tissue or bony deformities. Static joint instability usually can be controlled indefinitely by orthoses. Dynamic joint instability eventually results in a fixed deformity that cannot be controlled with orthoses. Young children are more prone than adults to develop bony deformity because of their growth potential. Soft-tissue surgery, such as tendon transfers, should be done in young children before the development of any fixed bony changes; bony procedures for correcting a deformity usually can be delayed until skeletal growth is near completion.

Tendon transfers

Tendon transfers are indicated when dynamic muscle imbalance results in a deformity that interferes with ambulation or function of the upper extremities. Surgery should be delayed until the maximal return of expected muscle strength in the involved muscle has been achieved. The objectives of a tendon transfer are (1) to provide active motor power to replace function of a paralyzed muscle or muscles, (2) to eliminate the deforming effect of a muscle when its antagonist is paralyzed, and (3) to improve stability by improving muscle balance.

Tendon transfer shifts a tendinous insertion from its normal attachment to another location so that its muscle can be substituted for a paralyzed muscle in the same region. In selecting a tendon for transfer, the following factors must be carefully considered:

1.
Strength. The muscle to be transferred must be strong enough to accomplish what the paralyzed muscle did or to supplement the power of a partially paralyzed muscle. A muscle to be transferred should have a rating of good or better because a transferred muscle loses at least one grade in power after transfer.
2.
Efficiency. The transferred tendon should be attached as close to the insertion of the paralyzed tendon as possible and should be routed in as direct a line as possible between the muscle’s origin and its new insertion.
3.
Excursion. The tendon to be transferred should have a range of excursion similar to the one it is reinforcing or replacing. It should be retained in its own sheath or placed into the sheath of another tendon, or it should be passed through tissues, such as subcutaneous fat, that would allow it to glide. Routing a tendon through fascial or osseous tunnels can lead to scarring and decreased excursion.
4.
Neurovascular. The nerve and blood supply to the transferred muscle must not be impaired or traumatized in making the transfer.
5.
Articular. The joint on which the muscle is to act must be in a satisfactory position; any contractures must be released before the tendon transfer. A transferred muscle cannot be expected to correct a fixed deformity.
6.
Tension. The transferred tendon must be securely attached under tension slightly greater than normal. If tension is insufficient, excursion is used in removing slack in the musculotendinous unit, rather than in producing the desired function.

Muscle transfers, whenever possible, should occur between agonistic muscles that are phasic, or active at the same time in the gait cycle. The anterior muscles of the leg are predominantly swing-phase muscles, and the posterior muscles, or flexors, are stance-phase muscles; in the thigh, the quadriceps is characteristically a stance-phase muscle, and the hamstrings are swing-phase muscles. In general, phasic transfers retain their preoperative phasic activities and regain their preoperative duration of contraction and electrical intensity. In contrast, nonphasic muscle transfers often retain their preoperative phasic activity and fail to assume the action of the muscles for which they are substituted and are not recommended. Some nonphasic transfers are capable of phasic conversion; however, phasic conversion is somewhat unpredictable and requires extensive postoperative physical therapy. Phasic conversion is not related to the use of splints and/or braces or time between disease onset and muscle transfer.

The ideal muscle for tendon transfer would have the same phasic activity as the paralyzed muscle, would be of about the same size in cross section and of equal strength, and could be placed in proper relationship to the axis of the joint to allow maximal mechanical effectiveness. Not all of these criteria can be met in every instance.

Paralytic deformities from muscle paralysis can be dynamic or static, and often both types are present. The extent to which the paralytic deformity is dynamic or static should be determined because a static deformity can be controlled with a brace in a growing child or with arthrodesis in an adult. A dynamic deformity is more likely to be appropriate for tendon transfer in children and adults. In a growing child with dynamic deformity, recurrence is possible with arthrodesis alone; in a child with static deformity, however, recurrence after arthrodesis is rare. In a growing child with dynamic deformity, an appropriate tendon transfer with minimal external support redistributes muscle power, preventing permanent deformity until the patient is old enough for an arthrodesis.

Arthrodesis

A relaxed or flail joint is stabilized by restricting its range of motion. Although a properly constructed brace may control a flail joint, a reconstructive operation that would not only eliminate the need for a brace but also improve function may be more effective. Arthrodesis is the most efficient method of permanent stabilization of a joint. Tenodeses that use flexor or extensor tendons to stabilize joints of the fingers (see Chapter 66, Chapter 71 ) are notable exceptions, as are tenodeses of the peroneus longus or Achilles tendon in paralytic calcaneal deformity; results are satisfactory here because the pull of gravity and body weight usually are not enough to overstretch the tendons.

Because the lower extremities are designed primarily to support the weight of the body, it is important that their joints are stable and their muscles have sufficient power. When the control of one or more joints of the foot and ankle is lost because of paralysis, stabilization may be required. In the upper extremity, reach, grasp, pinch, and release require more mobility than stability and more dexterity than power. An operation to limit or obliterate motion in a joint of an upper extremity should be performed only after careful study of its advantages and disadvantages and of its general effect on the patient, especially in normal daily activity. Because of the high prevalence of lower extremity weakness in patients with poliomyelitis and because many patients use ambulatory assistive devices, any surgical treatment that affects the upper extremity can have a dramatic impact on ambulation as well. Arthrodesis of the shoulder is useful for some patients but has certain cosmetic and functional disadvantages that must be weighed. Arthrodesis of the elbow is rarely indicated in poliomyelitis. Arthrodesis of the wrist, although useful for some patients, may increase the disability of other patients. A patient who must use a wheelchair or crutches and has a wrist that is fused in the “optimal” position (for grasp and pinch) may be unable to rise from a chair or to manipulate crutches because he or she cannot shift the body weight to the palm of the hand with the wrist extended.

Foot and ankle

Because the foot and ankle are the most dependent parts of the body and are subjected to significant amounts of stress, they are especially susceptible to deformity from paralysis. The most common deformities of the foot and ankle include claw toes, cavovarus foot, dorsal bunion, talipes equinus, talipes equinovarus, talipes cavovarus, talipes equinovalgus, and talipes calcaneus. When the paralysis is of short duration, these dynamic deformities are not fixed and may be evident only on contraction of unopposed muscles or on weight bearing; later, as a result of muscle imbalance, habitual posturing, growth, and abnormal weight-bearing alignment, a permanent deformity can occur from contracture of the soft tissues and eventual osseous changes.

Ambulation requires a stable plantigrade foot with even weight distribution between the heel and forefoot and no significant fixed deformity. In the foot, muscle transfer is performed to prevent contracture formation, balance the muscles responsible for dorsiflexion and plantarflexion and for inversion and eversion, and reestablish as normal a gait as possible. Arthrodesis to correct deformity or stabilize the joints usually should be delayed until about age 10 to 12 years to allow for adequate growth of the foot.

Tendon transfers

Tendon transfers around the foot and ankle after 10 years of age can be supplemented by arthrodesis to correct fixed deformities, to establish enough lateral stability for weight bearing, and to compensate in part for the loss of function in the evertor and invertor muscles of the foot. When tendon transfers and arthrodesis are combined in the same operation, the arthrodesis should be performed first.

Transfer of a tendon usually is preferable to excision, not only to preserve function but also to prevent further atrophy of the leg. When the paralysis is severe enough to require arthrodesis, there usually is some weakness of the dorsiflexor or plantar flexor muscles. In this case, the invertor or evertor muscles can be transferred to the midline of the foot anteriorly or posteriorly into the calcaneus and Achilles tendon. In the rare instance when a muscle function is discarded, 7 to 10 cm of its tendon should be excised to prevent scarring of the tendon ends by fibrous tissue. In addition to arthrodesis and tendon transfers, any deformities of the leg, such as excessive tibial torsion, genu varum, or genu valgum (bowlegs), should be corrected because otherwise they might cause recurrence of the foot deformity.

Paralysis of Specific Muscles

Isolated muscles may be paralyzed in patients with poliomyelitis, but more often combinations of muscles are affected. The specific muscle or muscles involved and the resulting muscle imbalance should be determined before treatment is started. Common deformities caused by muscle imbalance in the foot and ankle are described, according to the muscles involved. The exact pattern of muscle paralysis and the specific deformity that occurs must be carefully determined before any surgical intervention is undertaken.

Anterior Tibial Muscle

Severe weakness or paralysis of the anterior tibial muscle results in loss of dorsiflexion and inversion power and produces a slowly progressive deformity (equinus and cavus or varying degrees of planovalgus) that is first evident in the swing phase of gait. The extensors of the long toe, which usually assist dorsiflexion, become overactive in an attempt to replace the paralyzed anterior tibial muscle, causing hyperextension of the proximal phalanges and depression of the metatarsal heads. A cavovarus deformity occasionally results from unopposed activity of the peroneus longus combined with an active posterior tibial muscle.

Passive stretching and serial casting can be tried before surgery to correct the equinus contracture. Posterior ankle capsulotomy and Achilles tendon lengthening occasionally are required and are combined with anterior transfer of the peroneus longus to the base of the second metatarsal. The peroneus brevis is sutured to the stump of the peroneus longus to prevent a dorsal bunion. As an alternative, the extensor digitorum longus can be recessed to the dorsum of the midfoot to supply active dorsiflexion. Claw toe deformity is managed by transfer of the long toe extensors into the metatarsal necks (see Chapter 87 ).

Plantar fasciotomy and release of intrinsic muscles may be necessary before tendon surgery for a fixed cavovarus deformity. In this situation, the peroneus longus is transferred to the base of the second metatarsal and the extensor hallucis longus is transferred to the neck of the first metatarsal. The claw toe deformity frequently recurs because of reattachment of the extensor hallucis longus; this can be prevented by suturing its distal stump to the extensor hallucis brevis.

Anterior and Posterior Tibial Muscles

If the anterior tibial and the posterior tibial muscles are paralyzed, development of hindfoot and forefoot equinovalgus is more rapid and the deformity becomes fixed as the Achilles tendon and peroneal muscles shorten. This deformity may be similar to congenital vertical talus on a standing lateral radiograph, but the apparent vertical talus is not confirmed when a plantarflexion lateral view is obtained. Serial casting is used before surgery to stretch the tight Achilles tendon and to avoid weakening the gastrocnemius-soleus. If the peroneal muscles are normal, and both tibial muscles are paralyzed, one of the peroneal muscles must be transferred. Because of its greater excursion, the peroneus longus is transferred to the base of the second metatarsal to replace the anterior tibial and one of the long toe flexors replaces the posterior tibial. The peroneus brevis is sutured to the distal stump of the peroneus longus tendon.

Posterior Tibial Muscle

Isolated paralysis of the posterior tibial muscle is rare but can result in hindfoot and forefoot eversion. The flexor hallucis longus and the flexor digitorum longus have been used for tendon transfers in this situation. Through a posteromedial incision, the intrinsic plantar muscles are dissected sharply from their calcaneal origin, and one of the long toe flexors is exposed and divided. If the flexor digitorum longus is used, it is dissected from its tendon sheath posterior and proximal to the medial malleolus, rerouted through the posterior tibial sheath, and attached to the navicular. In rare cases, as an alternative, the extensor hallucis longus can be transferred posteriorly through the interosseous membrane and then through the posterior tibial tunnel.

For children 3 to 6 years old, Axer recommended bringing the conjoined extensor digitorum longus and peroneus tertius tendons through a transverse tunnel in the talar neck and suturing the tendon back onto itself. For fixed equinus deformity, lengthening of the Achilles tendon may be required before tendon transfer. For severe valgus, Axer recommended transfer of the peroneus longus into the medial side of the talar neck and transfer of the peroneus brevis into the lateral side. Isolated transfer of the peroneus brevis should not be done because it can cause a forefoot inversion deformity. After surgery, cast immobilization is continued for 6 weeks, followed by 6 months of orthosis wear.

Anterior Tibial, Toe Extensor, and Peroneal Muscles

Progressively severe equinovarus deformity develops when the posterior tibial and gastrocnemius-soleus are unopposed. The posterior tibial muscle increases forefoot equinus and cavus deformity by depressing the metatarsal head and shortening the medial arch of the foot. Further equinus and varus deformity result from contracture of the gastrocnemius-soleus, which acts as a fixed point toward which the plantar intrinsic muscles pull and increase forefoot adduction.

Stretching by serial casting may be attempted, but lengthening of the Achilles tendon usually is required. Radical soft-tissue release of the forefoot cavus deformity also may be necessary. Anterior transfer of the posterior tibial to the base of the third metatarsal or middle cuneiform can be supplemented by anterior transfer of the long toe flexors. Arthrodesis usually is not required; the deformity can be controlled by physical therapy and orthoses. A bony tunnel can be made through the base of the third metatarsal or the middle cuneiform, with suture of the transfer to a button over a felt pad placed on the non–weight bearing area of the plantar surface of the foot.

Peroneal Muscles

Isolated paralysis of the peroneal muscles is rare in patients with poliomyelitis but can cause severe hindfoot varus deformity because of the unopposed activity of the posterior tibial muscle. The calcaneus becomes inverted, the forefoot is adducted, and the varus deformity is increased by the action of the invertor muscles during gait. The unopposed anterior tibial activity can cause a dorsal bunion. In this situation, the anterior tibial muscle can be transferred laterally to the base of the second metatarsal; however, isolated transfer of the anterior tibial muscle can result in overactivity of the extensor hallucis longus, causing hyperextension of the hallux and development of a painful callus under the first metatarsal head. In children younger than 5 years of age, lengthening of the extensor hallucis longus tendon may be required. In children older than 5 years, the extensor hallucis longus should be transferred to the first metatarsal neck before the bony deformity becomes fixed.

Peroneal and Long Toe Extensor Muscles

Paralysis of the peroneal muscles and long toe extensors causes a less severe equinovarus deformity that can be treated by transfer of the anterior tibial tendon to the base of the third metatarsal or the middle cuneiform.

Gastrocnemius-Soleus Muscles

The gastrocnemius-soleus is a strong muscle group in the body, lifting the entire body weight with each step. Paralysis of the gastrocnemius-soleus, leaving the dorsiflexors unopposed, causes a rapidly progressive calcaneal deformity. Adequate tension of the Achilles tendon is important to the normal function of the long toe flexors and extensors and to the intrinsic foot muscles. If the gastrocnemius-soleus is weak, the posterior tibial, the peroneal muscles, and the long toe flexors cannot effectively plantarflex the hindfoot; however, they can depress the metatarsal heads and cause an equinus deformity. Shortening of the intrinsics and plantar fascia draws the metatarsal heads and the calcaneus together, similar to a bowstring. The long axes of the tibia and the calcaneus coincide, negating any residual power in the gastrocnemius-soleus.

Keeping the foot in slight equinus during the acute stage of poliomyelitis helps prevent overstretching of the gastrocnemius-soleus, and the position is maintained in the convalescent stage. If the gastrocnemius-soleus is weak, early walking is discouraged. Serial standing radiographs should be obtained frequently, especially in children younger than 5 years old, because of the rapid development of the deformity.

Surgical correction is indicated to prevent development of calcaneal deformity and to restore hindfoot plantarflexion. In the acute stage, the only absolute indication for tendon transfer in children younger than 5 years old is a progressive calcaneal deformity.

The combination of muscles transferred posteriorly depends on the residual strength of the gastrocnemius-soleus and the pattern of remaining muscle function. If the motor strength of the gastrocnemius-soleus is fair, posterior transfer of two or three muscles may be sufficient for normal gait. If the gastrocnemius-soleus is completely paralyzed, as many muscles as are available should be transferred. Plantar fasciotomy and intrinsic muscle release are required before tendon transfer in fixed forefoot cavus deformity.

The anterior tibial muscle can be transferred posteriorly 18 months after the acute stage of poliomyelitis. This can be done as an isolated procedure if the lateral stabilizers are balanced and the strong toe extensors can be used for dorsiflexion. In more severe deformity, transfer of the toe extensors to the metatarsal heads and fusion of the interphalangeal joints may be required to prevent claw toe deformity.

Posterior Transfer of Anterior Tibial Tendon

Technique 34.1

(DRENNAN)

▪
Take care to obtain maximal length of the anterior tibial tendon, which may have shortened because of the calcaneal deformity of the interosseous membrane.
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Split the insertion of the Achilles tendon longitudinally and develop osteoperiosteal flaps on the calcaneal tuberosity.
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Place the foot in maximal plantarflexion to ensure that the transfer is attached under appropriate tension. If necessary to obtain adequate plantarflexion, release other dorsal soft structures, including the ankle joint capsule, or lengthen the long toe extensors. If the attenuated Achilles tendon requires shortening, use a Z-plasty technique, resecting the redundant tendon from the proximal part.
▪
Attach the transferred anterior tibial tendon to the tuberosity of the calcaneus and to the distal stump of the Achilles tendon, which has retained its normal attachment to the calcaneal tuberosity.
▪
Close the wound in normal fashion and apply a long leg cast with the foot in the plantarflexed position. The cast is worn for 5 weeks, and a brace is worn for an additional 4 months.

If the invertors and evertors are balanced, a pure calcaneocavus deformity develops. Posterior transfer of only one set of these muscles causes instability and deformity. If the gastrocnemius-soleus strength is fair, transfer of the peroneus brevis and posterior tibial to the heel is sufficient to control the calcaneal deformity and allow normal gait. Lateral imbalance requires transposition of the acting invertor or evertor to the heel. Both peroneals are transferred to the heel for calcaneovalgus deformity, and the posterior tibial and flexor hallucis longus can be transferred for cavovarus deformity.

Westin and Defiore recommended tenodesis of the Achilles tendon to the fibula for paralytic calcaneovalgus deformity ( Fig. 34.1 ). They used a T-shaped incision in the periosteum instead of a drill hole, with imbrication of the distal segment of the sectioned tendon below the periosteum. For mobile calcaneal deformities, Makin recommended transfer of the peroneus longus into a groove cut in the posterior calcaneus, without disturbance of the origin or insertion of the tendon. The tendon is freed proximal to the lateral malleolus and at the cuboid groove, and the foot is maximally plantarflexed, allowing the peroneus longus to displace posteriorly into the calcaneal groove, where it eventually unites with the bone. Extraarticular subtalar arthrodesis may be required as a second procedure.

FIGURE 34.1, Anterior (A) and lateral (B) views of tenodesis of Achilles tendon to fibula.

In rare cases, if no invertors or evertors are present for transfer, the hamstrings can be used to replace the gastrocnemius-soleus. Prerequisites for this procedure include complete paralysis of the gastrocnemius-soleus, strong medial hamstrings or biceps femoris muscles, and strong ankle dorsiflexors and quadriceps muscles. The insertions of the semitendinosus and gracilis and occasionally the semimembranosus are mobilized, passed subcutaneously, and attached to the sagittally incised Achilles tendon. A mattress suture at the proximal end of the Achilles tendon prevents this incision from extending proximally. The tendons are sutured with the knee flexed to 25 degrees and the foot in plantarflexion.

Flail Foot

When all muscles distal to the knee are paralyzed, equinus deformity results because of passive plantarflexion. The intrinsic muscles may retain some function, leading to forefoot equinus or cavoequinus deformity. Radical plantar release, sometimes combined with plantar neurectomy, usually controls this deformity. Midfoot wedge resection may be required for the forefoot equinus deformity in older patients.

Dorsal Bunion

In a dorsal bunion deformity, the shaft of the first metatarsal is dorsiflexed and the great toe is plantarflexed; it usually results from muscle imbalance, although occasionally there may be other causes. In its early stages, the deformity is not fixed but is present only on weight bearing, especially walking. If the muscle imbalance is not corrected, the deformity becomes fixed, although it remains more pronounced on weight bearing.

Usually, only the metatarsophalangeal joint of the great toe is flexed, and on weight bearing the first metatarsal head is displaced upward; the longitudinal axis of the metatarsal shaft can be horizontal, or its distal end can even be directed slightly upward. The first cuneiform also can be tilted upward. A small exostosis can form on the dorsum of the metatarsal head. When flexion of the great toe is severe enough, the metatarsophalangeal joint can subluxate and the dorsal part of the cartilage of the metatarsal head eventually can degenerate. The plantar part of the joint capsule and the flexor hallucis brevis muscle can become contracted.

Two types of muscle imbalance can cause a dorsal bunion. The more common dorsiflexes the first metatarsal, and the plantarflexion of the great toe is secondary. The less common plantarflexes the great toe, and dorsiflexion of the first metatarsal is secondary.

The most common imbalance is between the anterior tibial and peroneus longus muscles; normally, the anterior tibial muscle raises the first cuneiform and the base of the first metatarsal, and the peroneus longus opposes this action. When the peroneus longus is weak or paralyzed or has been transferred elsewhere, the first metatarsal can be dorsiflexed by a strong anterior tibial muscle or by a muscle substituting for it. When the first metatarsal is dorsiflexed, the great toe becomes actively plantarflexed to establish a weight-bearing point for the medial side of the forefoot and to assist push-off in walking. Weakness of the dorsiflexor muscles of the great toe also may favor the development of this position of the toe. Many dorsal bunions develop after ill-advised tendon transfers for residual poliomyelitis. In such patients, the opposing actions of the peroneus longus and anterior tibial muscles on the first metatarsal were considered in the transfers. Before any transfer of the peroneus longus tendon, the effect of its loss on the first metatarsal must be carefully considered. When the anterior tibial is paralyzed and tendon transfer is feasible, the peroneus longus tendon or the tendons of the peroneus longus and peroneus brevis should be transferred to the third cuneiform, rather than to the insertion of the anterior tibial; as an alternative, the peroneus brevis tendon can be transferred to the insertion of the anterior tibial, leaving the peroneus longus tendon undisturbed. We believe that when the peroneus longus tendon is transferred, the proximal end of its distal segment should be securely fixed to bone at the level of division. When the gastrocnemius-soleus group is weak or paralyzed, and the anterior tibial and peroneus longus muscles are strong, the peroneus longus should not be transferred to the calcaneus unless the anterior tibial is transferred to the midline of the foot. A dorsal bunion does not always follow ill-advised tendon transfers, however, because the muscle imbalance may not be severe enough to cause it. When the deformity is progressive, surgery may simply consist of transferring the anterior tibial (or the previously transferred peroneus longus) to the third cuneiform; correcting the deformity itself may be unnecessary. When the deformity is fixed, however, surgery must correct not only the muscle imbalance but also the deformity.

The second and less common muscle imbalance that can cause a dorsal bunion results from paralysis of all muscles controlling the foot except the gastrocnemius-soleus group, which may be of variable strength, and the long toe flexors, which are strong. These strong toe flexors help steady the foot in weight bearing and sustain the push-off in walking. The flexor hallucis longus assumes a large share of this added function and with active use, the great toe may be almost constantly plantarflexed; the first metatarsal head is displaced upward to accommodate it. A strong flexor hallucis brevis muscle also may help produce the deformity.

There are other, less common causes for the deformity. It can develop in conjunction with a hallux rigidus in which dorsiflexion of the first metatarsophalangeal joint is painful. The articular surfaces become irregular, and the plantar part of the joint capsule gradually contracts; proliferation of bone on the dorsum of the first metatarsal head often becomes pronounced and blocks dorsiflexion of the joint. When walking, the patient may unconsciously supinate the foot and plantarflex the great toe to protect the weight-bearing pad of the great toe. A dorsal bunion also is sometimes seen in a severe congenital flatfoot with a rocker-bottom deformity (see Chapter 29 ). Transfer of the flexor hallucis longus to the neck of the first metatarsal, combined with bony correction by plantar closing wedge osteotomy of the first metatarsal when necessary, currently is our preferred technique for correction of dorsal bunions ( Chapter 29 , Technique 29.19). A strong unopposed anterior tibial tendon that contributes to forefoot supination is an indication for addition of a split anterior tibial tendon transfer.

Bony procedures (Osteotomy and Arthrodesis)

The object of arthrodesis in patients with poliomyelitis is to reduce the number of joints the weakened or paralyzed muscles must control. The structural bony deformity must be corrected before a tendon transfer is performed. Stabilizing procedures for the foot and ankle are traditionally of five types: (1) calcaneal osteotomy, (2) extraarticular subtalar arthrodesis, (3) triple arthrodesis, (4) ankle arthrodesis, and (5) bone blocks to limit motion at the ankle joint. These procedures can be performed singly or in combination with other procedures. The choice of operations depends on the age of the patient and the particular deformity that must be corrected.

Calcaneal Osteotomy

Calcaneal osteotomy can be performed for correction of hindfoot varus or valgus deformity in growing children. For cavovarus deformity, it can be combined with release of the intrinsic muscles and the plantar fascia, and for calcaneovarus deformity, with posterior displacement calcaneal osteotomy. Fixed valgus deformity may require medial displacement osteotomy in a plane parallel to the peroneal tendons.

Dillwyn Evans Osteotomy

The Dillwyn Evans osteotomy can be used for talipes calcaneovalgus deformity as an alternative to triple arthrodesis in children 8 to 12 years old. This osteotomy, the reverse of the original technique used in clubfeet, lengthens the calcaneus by a transverse osteotomy of the calcaneus and the insertion of a bone graft to open a wedge and lengthen the lateral border of the foot ( Fig. 34.2 ).

Subtalar Arthrodesis

Paralytic equinovalgus deformity results from paralysis of the anterior tibial and posterior tibial and the unopposed action of the peroneals and gastrocnemius-soleus. The calcaneus is everted and displaced laterally and posteriorly. The sustentaculum tali no longer functions as the calcaneal buttress for the talar head, which shifts medially and into equinus. Hindfoot and forefoot equinovalgus deformities develop rapidly and, with growth, become fixed and require bony correction.

Grice and Green developed an extraarticular subtalar fusion to restore the height of the medial longitudinal arch in patients 3 to 8 years old. Ideally, this procedure is performed when the valgus deformity is localized to the subtalar joint and when the calcaneus can be manipulated into its normal position beneath the talus. Careful clinical and radiographic examinations should determine whether the valgus deformity is located primarily in the subtalar joint or the ankle joint. If the forefoot is not mobile enough to be made plantigrade when the hindfoot is corrected, the procedure is contraindicated. The most common complications of the Grice and Green arthrodesis are varus deformity and increased ankle joint valgus because of overcorrection. Bone infection, pseudarthrosis, graft resorption, and degenerative arthritis of the metatarsal joints also have been reported.

Dennyson and Fulford described a technique for subtalar arthrodesis in which a screw is inserted across the subtalar joint for internal fixation and an iliac crest graft is placed in the sinus tarsi. Because the screw provides internal fixation, maintenance of the correct position does not depend on the bone graft.

Subtalar Arthrodesis

Technique 34.2

(GRICE AND GREEN)

▪
Make a short curvilinear incision on the lateral aspect of the foot directly over the subtalar joint.
▪
Carry the incision down through the soft tissues to expose the cruciate ligament overlying the joint. Split this ligament in the direction of its fibers, and dissect the fatty and ligamentous tissues from the sinus tarsi.
▪
Dissect the short toe extensors from the calcaneus, and reflect them distally. The relationship of the calcaneus to the talus now can be determined, and the mechanism of the deformity can be demonstrated.
▪
Place the foot in equinus, and then invert it to position the calcaneus beneath the talus. A severe, long-standing deformity may require division of the posterior subtalar joint capsule or removal of a small piece of bone laterally from beneath the anterosuperior calcaneal articular surface.
▪
Insert an osteotome or broad periosteal elevator into the sinus tarsi, and block the subtalar joint to evaluate the stability of the graft and its proper size and position.
▪
Prepare the graft beds by removing a thin layer of cortical bone from the inferior surface of the talus and the superior surface of the calcaneus ( Fig. 34.3 ).
▪
Now make a linear incision over the anteromedial surface of the proximal tibial metaphysis, incise the periosteum, and take a block of bone large enough for two grafts (usually 3.5 to 4.5 cm long and 1.5 cm wide). As alternatives to tibial bone, take a short segment of the distal fibula or a circular segment of the iliac crest.
▪
Cut the grafts to fit the prepared beds. Use a rongeur to shape the grafts so that they can be countersunk into the cancellous bone to prevent lateral displacement.
▪
With the foot held in a slightly overcorrected position, place the grafts in the sinus tarsi. Evert the foot to lock the grafts in place.
▪
If a segment of the fibula or iliac crest is used, a smooth Kirschner wire can be used to hold the graft in place for 12 weeks. A screw can be inserted anteriorly from the talar neck into the calcaneus for rigid fixation.
▪
Apply a long leg cast with the knee flexed, the ankle in maximal dorsiflexion, and the foot in the corrected position.

Postoperative Care

After 12 weeks of non–weight bearing, the long leg cast is removed and a short leg walking cast is applied and worn for an additional 4 weeks.

Subtalar Arthrodesis

Technique 34.3

(DENNYSON AND FULFORD)

▪
Make an oblique incision in the line of the skin creases, centered over the sinus tarsi and extending from the middle of the front of the ankle proximally and laterally to the peroneal tendons ( Fig. 34.4A ).
▪
Raise the origin of the extensor digitorum brevis, along with a pad of subcutaneous fat, proximally and reflect it distally to expose the sinus tarsi.
▪
Remove the fat from the sinus tarsi by sharp dissection close to the bone and, with a narrow gouge, remove cortical bone from the apex of the sinus tarsi to expose cancellous bone on the undersurface of the talar neck and on the nonarticular area in the upper calcaneal surface ( Fig. 34.4B ). Do not remove cortical bone from the outer part of the sinus tarsi in the area through which the screw will pass.
▪
Expose the depression on the superior surface of the talar neck by blunt dissection between the tendon of the extensor digitorum longus and the neurovascular bundle.
▪
Hold the calcaneus in its correct position, and pass a bone awl from this depression through the neck of the talus and across the sinus tarsi to enter the upper surface of the calcaneus toward the lateral side until it pierces the cortex of the calcaneus at its inferolateral border ( Fig. 34.4C ). The awl must pass through cortical bone on both the superior and inferior surfaces of the talar neck and on the superior and inferolateral surfaces of the calcaneus.
▪
Determine the length of the awl that is within the bones, and insert a minifragment cancellous screw of the same length. Tighten the screw until its head is seated into the superior surface of the talus.
▪
Pack chips of cancellous bone from the iliac crest into the apex of the sinus tarsi ( Fig. 34.4D ).
▪
Replace the extensor digitorum brevis, and close the wound.
▪
Apply a long leg, non–weight bearing cast.

Postoperative Care

The long leg cast is removed at 6 to 8 weeks, and a short leg walking cast is applied and worn for an additional 4 to 6 weeks.

Triple Arthrodesis

The most effective stabilizing procedure in the foot is triple arthrodesis ( Fig. 34.5 ): fusion of the subtalar, calcaneocuboid, and talonavicular joints. Triple arthrodesis limits motion of the foot and ankle to plantarflexion and dorsiflexion. It is indicated when most of the weakness and deformity are at the subtalar and midtarsal joints. Triple arthrodesis is performed (1) to obtain stable and static realignment of the foot, (2) to remove deforming forces, (3) to arrest progression of deformity, (4) to eliminate pain, (5) to eliminate the use of a short leg brace or to provide sufficient correction to allow fitting of a long leg brace to control the knee joint, and (6) to obtain a more normal-appearing foot. Generally, triple arthrodesis is reserved for severe deformity in children 12 years old and older; occasionally, it may be required in children 8 to 12 years old with progressive, uncontrollable deformity.

The exact technique of triple arthrodesis depends on the type of deformity, and this should be determined before surgery. A paper tracing can be made from a lateral radiograph of the ankle, and the components of the subtalar joint are divided into three sections: the tibiotalar and calcaneal components and another component comprising all the bones of the foot distal to the midtarsal joint. These are reassembled with the foot in the corrected position so that the size and shape of the wedges to be removed can be measured accurately.

In talipes equinovalgus, the medial longitudinal arch of the foot is depressed, the talar head is enlarged and plantarflexed, and the forefoot is abducted. Raising the talar head and shifting the sustentaculum tali medially beneath the talar head and neck restores the arch. A medially based wedge consisting of a portion of the talar head and neck is excised ( Fig. 34.5C ). When the hindfoot valgus deformity is corrected, the forefoot tends to supinate; this is controlled by midtarsal joint resection with a medially based wedge. An additional medial incision may be required for resection of the talonavicular joint.

In talipes equinovarus, the enlarged talar head lies lateral to the midline axis of the foot and blocks dorsiflexion. A laterally based subtalar wedge, combined with midtarsal joint resection, places the talar head slightly medial to the midline axis of the foot ( Fig. 34.5D ).

In talipes calcaneocavus, the arthrodesis should allow posterior displacement of the foot at the subtalar joint. After stripping of the plantar fascia, a wedge-shaped or cuneiform section of bone is removed to allow correction of the cavus deformity, and a wedge of bone is removed from the subtalar joint to correct the rotation of the calcaneus ( Fig. 34.5D ).

The muscle balance of the foot and ankle determines how much the foot should be displaced posteriorly. Posterior displacement of the foot transfers its fulcrum (the ankle) anteriorly to a position near its center and lengthens its posterior lever arm; this is especially important when the gastrocnemius-soleus group is weak.

Triple Arthrodesis

Technique 34.4

▪
Make an oblique incision centered over the sinus tarsi in line with the skin creases on the lateral side of the foot, beginning dorsolaterally at the lateral border of the tendons of the long toe extensors at the level of the talonavicular joint ( Fig. 34.5A ). Continue the incision posteriorly, angling plantarward and ending at the level of the peroneal tendons. Carefully protect the extensor and peroneal tendons, and carry the incision sharply down through the sinus tarsi to the extensor digitorum brevis muscle.
▪
Reflect the origin of this muscle distally along with the fat in the sinus tarsi.
▪
Clean the remainder of the sinus tarsi of all tissue to expose the subtalar and calcaneocuboid joints and the lateral portion of the talonavicular joint.
▪
Incise the capsules of the talonavicular, calcaneocuboid, and subtalar joints circumferentially to obtain as much mobility as possible. If this release allows the foot to be placed in a normal position, removal of large bony wedges is not required. If correction is impossible after soft-tissue release, appropriate bone wedges are removed ( Fig. 34.5C and D ).
▪
Identify the anterior articular process of the calcaneus and excise it at the level of the floor of the sinus tarsi for better exposure of all joints.
▪
To make this osteotomy, use an osteotome placed parallel to the plantar surface of the foot; preserve the bone for grafting.
▪
With an osteotome, remove the articular surfaces of the calcaneocuboid joint to expose cancellous bone.
▪
Remove an equal amount from both bones unless wedge correction of a bone deformity is required ( Fig. 34.5B ).
▪
Remove the distal portion of the head of the talus with ¼-inch and ½-inch straight and curved osteotomes. Remove only enough bone to expose the cancellous bone of the talar head unless a medial wedge is required to correct a fixed deformity. A small lamina spreader can be inserted for better exposure. A second medial incision may be necessary to expose the most medial portion of the talonavicular joint.
▪
Remove the proximal articular surface and subchondral bone of the navicular and shape and roughen the surfaces for a snug fit with the talus.
▪
Excise the articular surfaces of the sustentaculum tali and the anterior facet of the subtalar joint.
▪
Approach the subtalar joint and completely remove its articular surfaces. For better exposure of the posterior portion, use the small lamina spreader to expose the subtalar joint. Remove appropriate wedges from this joint if necessary; otherwise, make the joint resections parallel to the articular surfaces.
▪
Cut the removed bone into small pieces to be used for bone grafting. Place most of the bone graft around the talonavicular joint and in the depth of the sinus tarsi.
▪
Correction is maintained with internal fixation, usually smooth Steinmann pins or Kirschner wires.
▪
Close the muscle pedicle of the extensor digitorum brevis over the sinus tarsi to reduce the dead space.
▪
Close the wound over a suction drain and apply a well-padded, short leg cast.

Postoperative Care

Considerable bleeding from the drain and through the wound itself can be expected. The foot should be elevated to minimize swelling. The drain is removed at 24 to 48 hours. Walking with crutches or a walker, with touch-down weight bearing on the operated foot, is allowed as tolerated. The cast and pins or wires are removed at 6 to 8 weeks, and a short leg walking cast is applied and worn until union is complete, usually 4 weeks more.

Correction of Cavus Deformity

Technique 34.5

▪
Perform a medial radical plantar release to correct the contracted soft tissues bridging the longitudinal arch. Then forcibly correct the cavus deformity as much as possible.
▪
Expose the calcaneocuboid, talonavicular, and subtalar joints through the incision described earlier.
▪
With an osteotome, remove from the talonavicular and calcaneocuboid joints a wedge-shaped or cuneiform section of bone with its base anterior and large enough to correct the cavus deformity that remains after the plantar fascial stripping.
▪
Dorsiflex the forefoot and appose the raw surfaces to see if the cavus is corrected; if so, expose the subtalar joint and remove from it a wedge of bone with its base posterior to correct the deformity or rotation of the calcaneus (see Fig. 34.5D ). Be sure that all bone surfaces fit together well and that the foot is in satisfactory position before closing the wound.

Postoperative Care

Correction usually is maintained with Steinmann pins or Kirschner wires. A cast is applied, and firm pressure is exerted on the sole of the foot while the plaster is setting to stretch the plantar structures as much as possible. When internal fixation is not used, the cast and sutures are removed at 10 to 14 days, the foot is inspected, and radiographs are made. If the position is not satisfactory, the foot is manipulated with the patient under general anesthesia. A new cast, snug but properly padded, is then applied and is molded to the contour of the foot; this cast is removed at 12 weeks.

Complications of Triple Arthrodesis

The most common complication of triple arthrodesis is pseudarthrosis, especially of the talonavicular joint. The additional stress on the ankle joint caused by loss of mobility of the hindfoot can lead to the development of degenerative arthritis. Excessive resection of the talus can cause osteonecrosis, especially in adolescents; this usually is evident on radiographs 8 to 12 weeks after triple arthrodesis. Ligamentous laxity around the ankle joint may require ankle fusion. Muscle imbalance after hindfoot stabilization can lead to forefoot deformity; unopposed function of the anterior tibial or peroneal muscles is the most common cause of this complication and should be corrected by tendon transfer. Residual deformity usually is caused by insufficient correction at surgery, inadequate immobilization, pseudarthrosis, or muscle imbalance.

Talectomy

Talectomy provides stability and posterior displacement of the foot and generally is recommended for children 5 to 12 years old when the deformity is not correctable by arthrodesis. Talectomy limits motion of the ankle joint, especially dorsiflexion, and creates a tibiotarsal ankylosis. Posterior displacement of the foot places the distal tibia over the center of the weight-bearing area, producing even weight distribution and good lateral stability. Appearance usually is satisfactory, pain is relieved, and special shoes or orthoses are not required.

The most common cause of failure of talectomy is muscle imbalance, usually the presence of a strong anterior or posterior tibial muscle. Intrinsic muscle activity can cause contracture of the plantar fascia, resulting in a forefoot equinus deformity. In children younger than 5 years old, recurrence of the deformity is frequent, and pain is common in individuals older than 15 years, especially with inadequate excision of the entire talus. Tibiocalcaneal arthrodesis can be performed for failed talectomy and most commonly is indicated because of persistent pain. The technique of talectomy is described in Chapter 29 .

Lambrinudi Arthrodesis

The Lambrinudi arthrodesis is recommended for correction of isolated fixed equinus deformity in patients older than 10 years. Retained activity in the gastrocnemius-soleus, combined with inactive dorsiflexors and peroneals, causes the footdrop deformity. The posterior talus abuts the undersurface of the tibia, and the posterior ankle joint capsule contracts to create a fixed equinus deformity. In the Lambrinudi procedure, a wedge of bone is removed from the plantar distal part of the talus so that the talus remains in complete equinus at the ankle joint while the remainder of the foot is repositioned to the desired degree of plantarflexion. Tendon resection or transfer may be necessary to prevent varus or valgus deformity if active muscle power remains. The Lambrinudi arthrodesis is not recommended for a flail foot or when hip or knee instability requires a brace. A good result depends on the strength of the dorsal ankle ligaments. If anterior subluxation of the talus is noted on a weight-bearing lateral radiograph, a two-stage pantalar arthrodesis is recommended. Complications of the Lambrinudi arthrodesis include ankle instability, residual varus or valgus deformities caused by muscle imbalance, and pseudarthrosis of the talonavicular joint.

Technique 34.6

(LAMBRINUDI)

▪
With the foot and ankle in extreme plantarflexion, make a lateral radiograph and trace the film. Cut the tracing into three pieces along the outlines of the subtalar and midtarsal joints; from these pieces the exact amount of bone to be removed from the talus can be determined with accuracy before surgery. In the tracing, the line representing the articulation of the talus with the tibia is left undisturbed but that corresponding to its plantar and distal parts is to be cut so that when the navicular and the calcaneocuboid joint are later fitted to it, the foot will be in 5 to 10 degrees of equinus relative to the tibia ( Fig. 34.6 ) unless the extremity has shortened; more equinus may then be desirable.
▪
Expose the sinus tarsi through a long, lateral curved incision.
▪
Section the peroneal tendons by a Z-shaped cut, open the talonavicular and calcaneocuboid joints, and divide the interosseous and lateral collateral ligaments of the ankle to permit complete medial dislocation of the tarsus at the subtalar joint.
▪
With a small power saw (more accurate than a chisel or osteotome), remove the predetermined wedge of bone from the plantar and distal parts of the neck and body of the talus. Remove the cartilage and bone from the superior surface of the calcaneus to form a plane parallel with the longitudinal axis of the foot.
▪
Next make a V-shaped trough transversely in the inferior part of the proximal navicular and denude the calcaneocuboid joint of enough bone to correct any lateral deformity.
▪
Firmly wedge the sharp distal margin of the remaining part of the talus into the prepared trough in the navicular and appose the calcaneus and talus. Take care to place the distal margin of the talus well medially in the trough; otherwise, the position of the foot will not be satisfactory. The talus is now locked in the ankle joint in complete equinus, and the foot cannot be further plantarflexed.
▪
Insert smooth Kirschner wires for fixation of the talonavicular and calcaneocuboid joints.
▪
Suture the peroneal tendons, close the wound in the routine manner, and apply a cast with the ankle in neutral or slight dorsiflexion.

Postoperative Care

The cast and sutures are removed at 10 to 14 days, and the position of the foot is evaluated by radiographs. If the position is satisfactory, a short leg cast is applied, but weight bearing is not allowed for another 6 weeks, after which a short leg walking cast is applied and is worn until fusion is complete, usually at 3 months.

Ankle Arthrodesis

Ankle fusion may be indicated for a flail foot or for recurrence of deformity after triple arthrodesis. Compression arthrodesis (see Chapter 11 ) generally is recommended for older children and adolescents. Subcutaneous plantar fasciotomy and lengthening of the Achilles tendon can be performed initially, followed by ankle arthrodesis.

Pantalar Arthrodesis

Pantalar arthrodesis is fusion of the tibiotalar, talonavicular, subtalar, and calcaneocuboid joints. For flail feet with paralyzed quadriceps, pantalar arthrodesis may be indicated to eliminate the need for long leg braces. The ideal patient for this operation is one with a flail foot and ankle and normal muscles around the hip and knee. Absolute prerequisites for this procedure include a strong gluteus maximus to initiate toe-off during gait and a normally aligned knee with full extension or a few degrees of hyperextension.

The ankle should be fused in 5 to 10 degrees of plantarflexion to produce the backward thrust on the knee joint necessary for stable weight bearing. Excessive plantarflexion of the ankle results in pain and increased pressure under the metatarsal heads; acceptable plantarflexion should be confirmed with a lateral radiograph during surgery. Pantalar arthrodesis can be done in two stages: the first in the foot and the second in the ankle because it is difficult to achieve and maintain proper position of the foot and the ankle at the same time. Provelengios et al. described one-stage pantalar arthrodesis in 24 patients (average age, 20 years) with a Steinmann pin used to stabilize the ankle and subtalar joints. At an average follow-up of 37 years, 22 of the 24 patients were satisfied with their outcomes. The position of the fused ankle did not correlate with the development of ipsilateral knee pain. More recently, the authors modified their technique by using a circular external fixator to stabilize all four joints. Complications of pantalar arthrodesis include pseudarthrosis, painful plantar callosities caused by unequal weight distribution, and excessive heel equinus, which causes increased pressure on the forefoot. Provelengios et al. reported a complication rate of 46%, but all were minor wound or skin problems.

Tendon transfer techniques

Talipes Equinovarus

Talipes equinovarus caused by poliomyelitis is characterized by equinus deformity of the ankle, inversion of the heel, and, at the midtarsal joints, adduction and supination of the forefoot. When the deformity is of long duration there also is a cavus deformity of the foot; clawing of the toes may develop secondary to substitution of motor patterns. In paralytic talipes equinovarus, the peroneal muscles are paralyzed or severely weakened but the posterior tibial muscle usually is normal; the anterior tibial may be weakened or normal. The gastrocnemius-soleus is comparatively strong but becomes contracted by a combination of motor imbalance, growth, gravity, and posture. Treatment depends on the age of the patient, the forces causing the deformity, the severity of the deformity, and its rate of increase.

Anterior transfer of the posterior tibial tendon removes a dynamic deforming force and aids active dorsiflexion of the foot; however, transfer alone rarely restores active dorsiflexion. Rerouting of the tendon anterior to the medial malleolus diminishes its plantarflexion power and lengthens the posterior tibial muscle; the deformity may not be corrected, however, because the muscle retains its varus pull. The entire tendon can be transferred through the interosseous membrane to the middle cuneiform, or the tendon can be split, with the lateral half transferred to the cuboid.

Anterior Transfer of Posterior Tibial Tendon

Technique 34.7

(BARR)

▪
Make a skin incision on the medial side of the ankle, beginning distally at the insertion of the posterior tibial tendon and extending proximally over the tendon just posterior to the malleolus and from there proximally along the medial border of the tibia for 5.0 to 7.5 cm.
▪
Free the tendon from its insertion, preserving as much of its length as possible.
▪
Split its sheath, and free it in a proximal direction until the distal 5.0 cm of the muscle has been mobilized. Carefully preserve the nerves and vessels supplying the muscle.
▪
Make a second skin incision anteriorly; begin it distally at the level of the ankle joint and extend it proximally for 7.5 cm just lateral to the anterior tibial tendon. Carry the dissection deep between the tendons of the anterior tibial muscle and the extensor hallucis longus, carefully preserving the dorsalis pedis artery; expose the interosseous membrane just proximal to the malleoli.
▪
Cut a generous window in the interosseous membrane but avoid stripping the periosteum from the tibia or fibula.
▪
Pass the posterior tibial tendon through the window between the bones, taking care that it is not kinked, twisted, or constricted and that the vessels and nerves to the muscle are not damaged. Pass the tendon beneath the cruciate ligament, which can be divided if necessary to relieve pressure on the tendon.
▪
Expose the third cuneiform or the base of the third metatarsal through a transverse incision 2.5 cm long.
▪
Retract the extensor tendons, sharply incise the periosteum over the bone in a cruciate fashion, and fold back osteoperiosteal flaps.
▪
Drill a hole through the bone in line with the tendon and large enough to receive it; anchor it in the bone with a pull-out wire. Be sure that the button on the plantar surface of the foot is well padded.
▪
Suture the osteoperiosteal flaps to the tendon with two figure-of-eight nonabsorbable sutures.
▪
Close the incision and apply a plaster cast to hold the foot in calcaneovalgus position.

Instead of the long medial incision used by Barr, we make a short longitudinal one to free the posterior tibial tendon at its insertion and withdraw it through another incision 5 cm long at the musculotendinous junction just posterior to the subcutaneous border of the tibia ( Fig. 34.7 ). The tendon also can be anchored to bone by passing it through a hole drilled in the bone, looping it back, and suturing it to itself with nonabsorbable sutures.

FIGURE 34.7, Ober anterior transfer of posterior tibial tendon. A, Insertion of posterior tibial tendon has been exposed. Note line of skin incision over muscle. B, Tendon has been freed from its insertion, and muscle has been dissected from tibia. C, Tendon and muscle have been passed through anterior tibial compartment to dorsum of foot, and tendon has been anchored in third metatarsal. SEE TECHNIQUES 34.7 AND 34.8 .

Postoperative Care

The cast is removed at 3 weeks, the wounds are inspected, the sutures are removed, and a short leg walking cast is applied with the foot in the neutral position and the ankle in slight dorsiflexion. Six weeks after surgery the cast is removed, and a program of rehabilitative exercises is started that is continued under supervision until a full range of active resisted function is obtained. The transfer is protected for 6 months by a double-bar foot-drop brace with an outside T-strap.

Anterior Transfer of Posterior Tibial Tendon

Technique 34.8

(OBER)

▪
Through a medial longitudinal incision 7.5 cm long, free the posterior tibial tendon from its attachment to the navicular ( Fig. 34.7A ).
▪
Make a second longitudinal medial incision 10 cm long centered over the musculotendinous junction of the posterior tibial tendon and muscle.
▪
Withdraw the tendon from the proximal wound and free the muscle belly well up on the tibia ( Fig. 34.7B ).
▪
Strip the periosteum obliquely on the medial surface of the tibia so that when the tendon is moved into the anterior tibial compartment only the belly of the muscle will come in contact with denuded bone. The tendon must not be in contact with the tibia.
▪
Make a third incision over the base of the third metatarsal, draw the posterior tibial tendon from the second into the third incision, and anchor its distal end in the base of the third metatarsal ( Fig. 34.7C ).

Postoperative Care

Postoperative care is the same as after Technique 34.7.

Split Transfer of Anterior Tibial Tendon

Technique 34.9

▪
Make a 2- to 3-cm longitudinal incision dorsomedially over the medial cuneiform ( Fig. 34.8A ).
▪
Identify the anterior tibial tendon and split it longitudinally in the midportion. Detach the lateral half of the tendon from its insertion, preserving as much length as possible, and continue the split proximally to the extent of the incision.
▪
Make a second 2- to 3-cm incision anteriorly over the distal tibia, identify the tibialis anterior tendon sheath, and split it longitudinally.
▪
Continue the split in the anterior tibial tendon proximally into this incision and up to the musculotendinous junction. Umbilical tape can be used to continue the split in the tendon. Place the tape into the split and bring its two ends into the proximal incision. Before the lateral half of the tendon is detached, continue the split to the musculotendinous junction by pulling on the tape.
▪
Once the split in the tendon is complete, detach the lateral half and bring it into the proximal wound.
▪
Make a third 2- to 3-cm longitudinal incision over the cuboid on the dorsolateral aspect of the foot.
▪
Drill two holes in the cuboid, placing them as far away from each other as possible so that they meet well within the body of the cuboid ( Fig. 34.8B ). Enlarge the holes with a curet if necessary, but be certain to leave a bridge of bone between the two holes.
▪
Pass the split lateral portion of the anterior tibial tendon distally through the subcutaneous tunnel from the proximal incision to the dorsolateral incision over the cuboid.
▪
Attach a nonabsorbable suture to the end of the tendon, and pass it into one hole in the cuboid and out the other ( Fig. 34.8C ).
▪
Hold the foot in dorsiflexion, pull the tendon tight, and suture the free end to the proximal portion of the tendon under moderate tension ( Fig. 34.8D ).
▪
As an alternative, drill a hole in the cuneiform through the plantar cortex, pass the tendon through this hole, and anchor it on the plantar aspect of the foot with a suture over felt and a button.

Postoperative Care

A short leg cast is worn for 6 weeks. An ankle-foot orthosis may be needed for 6 months.

Split Transfer of the Posterior Tibial Tendon

The split transfer of the posterior tibial tendon technique is used more often for patients with cerebral palsy and is described in Chapter 33 .

Talipes Cavovarus

Paralytic talipes cavovarus can be caused by an imbalance of the extrinsic muscles or by persistent function of the short toe flexors and other intrinsic muscles when the foot is otherwise flail. Treatment of the cavus foot is discussed in Chapter 87 .

Talipes Equinovalgus

Talipes equinovalgus usually develops when the anterior and posterior tibial muscles are weak, the peroneus longus and peroneus brevis are strong, and the gastrocnemius-soleus is strong and contracted. The gastrocnemius-soleus pulls the foot into equinus and the peroneals into valgus position; when the extensor digitorum longus and the peroneus tertius muscles are also strong, they help to pull the foot into valgus position on walking. Structural changes in the bones and ligaments follow the muscle imbalance; eventually, the plantar calcaneonavicular ligament becomes stretched and attenuated, the weight-bearing thrust shifts to the medial border of the foot, the forefoot abducts and pronates, and the head and neck of the talus become depressed and prominent on the medial side of the foot.

Treatment of this deformity in a skeletally immature foot is difficult. Subtalar arthrodesis and anterior transfer of the peroneus longus and brevis tendons usually suffice until skeletal maturity is reached; if necessary, a triple arthrodesis can then be done. Failure to transfer the tendons is the usual cause of recurrence.

Paralysis of the anterior tibial muscle alone usually causes only a moderate valgus deformity that is more pronounced during dorsiflexion of the ankle and may disappear during plantarflexion. Treatment of this deformity may require transfer of the peroneus longus to the first cuneiform, transfer of the extensor digitorum longus, or the Jones procedure (see Chapter 87 ). Paralysis of the posterior tibial alone can cause a planovalgus deformity. Normally, this muscle inverts the foot during plantarflexion; when it is paralyzed, a valgus deformity develops. Because most of the functions of the foot are performed during plantarflexion, loss of the posterior tibial is a severe impairment. Treatment of this deformity may involve transfer of the peroneus longus tendon, the flexor digitorum longus, the flexor hallucis longus, or the extensor hallucis longus. Paralysis of the anterior tibial and the posterior tibial muscles results in an extreme deformity similar to rocker-bottom flatfoot. For this deformity, a transfer to replace the posterior tibial is necessary, followed by another to replace the anterior tibial if necessary. Extraarticular subtalar arthrodesis may be indicated for equinovalgus deformity in children 4 to 10 years old. The equinus must be corrected by Achilles tendon lengthening at surgery to allow the calcaneus to be brought far enough distally beneath the talus to correct the deformity. The technique of Grice and Green (see Technique 34.2) or preferably of Dennyson and Fulford (see Technique 34.3) can be used. Talipes equinovalgus in skeletally mature patients usually requires triple arthrodesis (see Technique 34.4) and lengthening of the Achilles tendon, followed in 4 to 6 weeks by appropriate tendon transfers.

Peroneal Tendon Transfer

Technique 34.10

▪
Expose the tendons of the peroneus longus and peroneus brevis through an oblique incision paralleling the skin creases at a point midway between the distal tip of the lateral malleolus and the base of the fifth metatarsal.
▪
Divide the tendons as far distally as possible, securely suture the distal end of the peroneus longus to its sheath to prevent the development of a dorsal bunion, and free the tendons proximally to the posterior border of the lateral malleolus. (When they are to be transferred at the time of arthrodesis, they can be divided through a short extension of the routine incision, as shown in Fig. 34.5 .)
▪
Make a second incision 5 cm long at the junction of the middle and distal thirds of the leg overlying the tendons. Gently withdraw the tendons from their sheaths, taking care not to disrupt the origin of the peroneus brevis muscle.
▪
The new site of insertion of the peroneal tendons is determined by the severity of the deformity and the existing muscle power. When the extensor hallucis longus is functioning and is to be transferred to the neck of the first metatarsal, the peroneal tendons should be transferred to the lateral cuneiform; when no other functioning dorsiflexor is available, they should be transferred to the middle cuneiform anteriorly.
▪
Expose the new site of insertion of the tendons through a short longitudinal incision.
▪
Retract the tendons of the extensor digitorum longus, and make a cruciate or H-shaped cut in the periosteum of the recipient bone.
▪
Raise and fold back osteoperiosteal flaps and drill a hole in the bone large enough to receive the tendons. Then bring the tendons out beneath the cruciate crural ligament into this incision and anchor them side by side and under equal tension through a hole drilled in the bone, either by suturing them back on themselves or by securely fixing them to bone using a platform staple.
▪
As an alternative, drill a hole through the middle cuneiform and pull the tendons through the hole and then through a button on the plantar aspect of the foot.
▪
When there is significant clawing of the great toe, the extensor hallucis longus tendon should be transferred to the neck of the first metatarsal and then the interphalangeal joint is fused (Jones procedure, see Chapter 87 ).
▪
Residual clawing of the lateral four toes usually is of little or no significance after transfer of the peroneal and extensor hallucis longus tendons.

Peroneus Longus, Flexor Digitorum Longus, or Flexor or Extensor Hallucis Longus Tendon Transfer

Technique 34.11

(FRIED AND HENDEL)

▪
In this operation the tendon of the peroneus longus, flexor digitorum longus, flexor hallucis longus, or extensor hallucis longus can be transferred to replace a paralyzed posterior tibial muscle.
▪
When the peroneus longus tendon is to be transferred, make a longitudinal incision 5 to 8 cm long laterally over the shaft of the fibula.
▪
After incising the fascia of the peroneal muscles, inspect them; if their color does not confirm their preoperative grading, the transfer will fail.
▪
Now make a second incision along the lateral border of the foot over the cuboid and the peroneus longus tendon.
▪
Free the tendon, divide it as far distally in the sole of the foot as possible, suture its distal end in its sheath, and withdraw the tendon through the first incision.
▪
By blunt dissection create a space between the gastrocnemius-soleus and the deep layer of leg muscles; from here make a wide tunnel posterior to the fibula and to the deep muscles and directed to a point proximal and posterior to the medial malleolus.
▪
Now make a small incision at this point, and draw the peroneus longus tendon through the tunnel; it now emerges where the posterior tibial tendon enters its sheath.
▪
Make a fourth incision 5 cm long over the middle of the medial side of the foot centered below the tuberosity of the navicular.
▪
Free and retract plantarward the anterior border of the abductor hallucis muscle, and expose the tuberosity of the navicular and the insertion of the posterior tibial tendon; proximal to the medial malleolus, open the sheath of this tendon, and into it introduce and advance a curved probe until it emerges with the tendon at the sole of the foot.
▪
Using the probe, pull the peroneus longus tendon through the same sheath, which is large enough to contain this second tendon.
▪
Drill a narrow tunnel through the navicular, beginning on its plantar surface lateral to the tuberosity and emerging through its anterior surface.
▪
Pull the peroneus longus tendon through the tunnel in an anterior direction and anchor it with a Bunnell pull-out suture. Also, suture it to the posterior tibial tendon close to its insertion.
▪
Close the wounds, and apply a short leg cast with the foot in slight equinus and varus position.
▪
When the flexor digitorum longus tendon is to be transferred, make the incision near the medial malleolus as just described but extend it for about 7 cm.
▪
Free the three deep muscles and observe their color; if it is satisfactory, make the incision on the medial side of the foot as just described.
▪
Free and retract the short plantar muscles and expose the flexor digitorum longus tendon as it emerges from behind the medial malleolus.
▪
Free the tendon as far distally as possible, divide it, and withdraw it through the first incision; now pass it through the sheath of the posterior tibial tendon and anchor it in the navicular as just described.
▪
When the flexor hallucis longus tendon is to be transferred, use the same procedure as described for the flexor digitorum longus.
▪
When the extensor hallucis longus tendon is to be transferred, cut it near the metatarsophalangeal joint of the great toe.
▪
Suture its distal end to the long extensor tendon of the second toe.
▪
Withdraw the proximal end through an anterolateral longitudinal incision over the distal part of the leg.
▪
Open the interosseous membrane widely, make the incision near the medial malleolus as previously described, and with a broad probe draw the tendon through the interosseous space and through the sheath of the posterior tibial tendon to the insertion of that tendon.
▪
Then continue with the operation as described for transfer of the peroneus longus tendon.

Postoperative Care

A short leg walking cast is applied. At 6 weeks the walking cast is removed, a splint is used at night, and muscle reeducation is started.

Talipes Calcaneus

Talipes calcaneus is a rapidly progressive paralytic deformity that results when the gastrocnemius-soleus is paralyzed and the other extrinsic foot muscles, especially the muscles that dorsiflex the ankle, remain functional. Mild deformity in skeletally immature patients should be treated conservatively with braces or orthoses until the rate of progression of the deformity can be determined. For rapidly progressing deformities, especially in young children, early tendon transfers are recommended. The goal of surgery in the skeletally immature foot is to stop progression of the deformity or to correct severe deformity without damaging skeletal growth; arthrodesis may be necessary after skeletal maturity. If muscles of adequate power are available, tendons should be transferred early to improve function and avoid progressive deformity. If adequate muscles are unavailable, tenodesis of the Achilles tendon to the fibula may be appropriate.

The calcaneotibial angle ( Fig. 34.9 ) is formed by the intersection of the axis of the tibia with a line drawn along the plantar aspect of the calcaneus. Normally, this angle measures between 70 and 80 degrees; in equinus deformity it is greater than 80 degrees, and in calcaneal deformity it is less than 70 degrees. When the tenodesis is fixed at 70 degrees or more at the time of surgery, a tendency to develop a progressive equinus deformity with growth has been noted. Progressive equinus also is directly related to the patient’s age at surgery: the younger the patient, the greater the calcaneotibial angle and the more likely the development of progressive equinus deformity with subsequent growth.

FIGURE 34.9, Measurement of calcaneotibial angle (see text).

In skeletally mature feet, initial surgery for talipes calcaneus consists of plantar fasciotomy and triple arthrodesis that corrects the calcaneus and the cavus deformities; the arthrodesis should displace the foot as far posteriorly as possible to lengthen its posterior lever arm (the calcaneus) and reduce the muscle power required to lift the heel. Six weeks after arthrodesis, the tendons of the peroneus longus and peroneus brevis and the posterior tibial tendon are transferred to the calcaneus; and when the extensor digitorum longus is functional, it can be transferred to a cuneiform and then the anterior tibial tendon can be transferred to the calcaneus.

Tenodesis of The Achilles Tendon

Technique 34.12

(WESTIN)

▪
With the patient supine and tilted toward the nonoperative side, apply and inflate a pneumatic tourniquet.
▪
Make a posterolateral longitudinal incision just behind the posterior border of the fibula beginning 7 to 10 cm above the tip of the lateral malleolus and extending distally to the insertion of the Achilles tendon on the calcaneus.
▪
Expose the tendon and section it transversely at the musculotendinous junction, usually 6 cm from its insertion. Stevens advised that the tendon be split eccentrically, leaving the lateral one fifth to prevent retraction. Transect the medial four fifths proximally.
▪
Expose the peroneus brevis and longus tendons, and if they are completely paralyzed or spastic, excise them. Expose the distal fibula, taking care not to damage the distal fibular physis.
▪
About 4 cm proximal to the distal physis, use a fine drill bit to make a transverse hole in an anteroposterior direction. Make the hole large enough for the Achilles tendon to pass through it easily ( Fig. 34.10A ).
▪
If the tendon is too large, trim it longitudinally for about 2.5 cm. Bring the tendon through the hole, and suture it to itself under enough tension to limit ankle dorsiflexion to 0 degrees ( Fig. 34.10B ). Do not suture the tendon with the foot in too much equinus because of the possibility of causing a fixed equinus deformity.
▪
In patients with active anterior tibial tendons, simultaneous transfer of this tendon through the interosseous membrane to the calcaneus is indicated to avoid stretching of the Achilles tendon after surgery ( Fig. 34.10C ).

Postoperative Care

Weight bearing is allowed in a short leg cast with the ankle in 5 to 10 degrees of equinus. The cast is removed at 6 weeks, and an ankle-foot orthosis is fitted with the ankle in neutral position. Any residual cavus deformity is corrected by plantar release 3 to 6 months after tenodesis.

In skeletally mature feet, initial surgery for talipes calcaneus consists of plantar fasciotomy and triple arthrodesis that corrects both the calcaneus and cavus deformities; the arthrodesis should displace the foot as far posteriorly as possible to lengthen its posterior lever arm (the calcaneus) and reduce the muscle power required to lift the heel. Six weeks after arthrodesis, the tendons of the peroneus longus and peroneus brevis and the posterior tibial muscles are transferred to the calcaneus, and when the extensor digitorum longus is functional, it can be transferred to a cuneiform and then the anterior tibial muscle can be transferred to the calcaneus.

Posterior Transfer of Peroneus Longus, Peroneus Brevis, and Posterior Tibial Tendons

Technique 34.13

▪
Expose the peroneus longus and peroneus brevis tendons through an oblique incision 2.5 cm long midway between the tip of the lateral malleolus and the base of the fifth metatarsal.
▪
Divide the tendons as far distally as possible and securely suture the distal end of the peroneus longus tendon to its sheath.
▪
Bring the tendons out through a second incision overlying the peroneal sheath at the junction of the middle and distal thirds of the leg.
▪
If desired, suture the peroneus brevis at its musculotendinous junction to the peroneus longus tendon and discard the distal end of the peroneus brevis tendon.
▪
Expose the posterior tibial tendon through a short incision over its insertion; free its distal end, and gently bring it out through a second incision 2.5 cm long at its musculotendinous junction 5 cm proximal to the medial malleolus.
▪
Reroute all three tendons subcutaneously to and out of a separate incision lateral and anterior to the insertion of the Achilles tendon.
▪
Drill a hole in the superior surface of the posterior part of the calcaneus just lateral to the midline of the bone and enlarge it enough to receive the tendons; anchor the tendons in the hole with a large pull-out suture while holding the foot in equinus and the heel in the corrected position. An axial pin also can be inserted into the calcaneus and left in place for 6 weeks.
▪
With interrupted figure-of-eight sutures, fix the tendons to the Achilles tendon near its insertion; then close the wounds.

Postoperative Care

The foot is immobilized in a long leg cast with the ankle in plantarflexion and the knee at 20 degrees. The pull-out sutures and cast (and axial pin, if used) are removed at 6 weeks, and physical therapy is started. Weight bearing is not allowed until active plantar flexion is possible and dorsiflexion to the neutral position has been regained. The foot is protected for at least 6 more months by a reverse 90-degree ankle stop brace and an appropriate heel elevation.

Posterior Transfer of Posterior Tibial, Peroneus Longus, and Flexor Hallucis Longus Tendons

Technique 34.14

(GREEN AND GRICE)

▪
Place the patient prone for easier access to the heel.
▪
First, expose the posterior tibial tendon through an oblique incision 3 or 4 cm long from just inferior to the medial malleolus to the plantar aspect of the talonavicular joint; open its sheath, and divide it as close to bone as possible for maximal length.
▪
Remove the epitenon from its distal 3 or 4 cm, scarify it, and insert a 1-0 or 2-0 braided nonabsorbable suture into its distal end.
▪
When the flexor hallucis longus tendon also is to be transferred, expose it through this same incision where it lies posterior and lateral to the flexor digitorum longus tendon.
▪
At the proper level for the desired tendon length, place two braided nonabsorbable sutures in the flexor hallucis longus tendon and divide it between them; suture the distal end of this tendon to the flexor digitorum longus tendon.
▪
Second, make a longitudinal medial incision, usually about 10 cm long, over the posterior tibial muscle, extending distally from the junction of the middle and distal thirds of the leg.
▪
Open the medial compartment of the leg, and identify the posterior tibial and flexor hallucis longus muscle bellies.
▪
Using moist sponges, deliver the tendons of these two muscles into this wound.
▪
Third, make an incision parallel to the bottom of the foot from about a fingerbreadth distal to the lateral malleolus to the base of the fifth metatarsal.
▪
Expose the peroneus longus and peroneus brevis tendons throughout the length of the incision and divide that of the peroneus longus between sutures as far distally as possible in the sole of the foot and free its proximal end to behind the lateral malleolus.
▪
Place a suture in the peroneus brevis tendon, detach it from its insertion on the fifth metatarsal, and suture it to the distal end of the peroneus longus tendon.
▪
Make a lateral longitudinal incision over the posterior aspect of the fibula at the same level as the medial incision and deliver the peroneus longus tendon into it.
▪
Make a posterolateral transverse incision 6 cm long over the calcaneus in the part of the heel that neither strikes the ground nor presses against the shoe. Deepen the incision, reflect the skin flaps subcutaneously, and expose the Achilles tendon and calcaneus.
▪
Beginning laterally, partially divide the Achilles tendon at its insertion and reflect it medially, exposing the calcaneal apophysis.
▪
With a 9/64-inch (3.57-mm) drill bit, make a hole through the calcaneus beginning in the center of its apophysis and emerging through its plantar aspect near its lateral border. Enlarge the hole enough to receive the three tendons and ream its posterior end to make a shallow facet for their easier insertion.
▪
Next, through the medial wound on the leg (the second incision), incise widely the intermuscular septum between the medial and posterior compartments; insert a tendon passer through the wound and along the anterior side of the Achilles tendon to the transverse incision over the calcaneus. Thread the sutures in the ends of the posterior tibial and flexor hallucis longus tendons through the tendon passer and deliver the tendons at the heel.
▪
Through the lateral wound on the leg (the fourth incision), open widely the intermuscular septum between the medial and posterior compartments in this area and pass the peroneus longus tendon to the heel.
▪
Pass all tendons through smooth tissues in a straight line from as far proximally as possible to avoid angulation.
▪
With a twisted wire probe, bring the tendons through the hole in the calcaneus; suture them to the periosteum and ligamentous attachments where they emerge.
▪
When the dorsiflexors are weak, suture them under enough tension to hold the foot in 10 to 15 degrees of equinus, and when they are strong, suture them in about 30 degrees of equinus. Also, suture the tendons to the apophysis at the proximal end of the tunnel and to each other with 2-0 or 3-0 sutures.
▪
Replace the Achilles tendon posterior to the transferred tendons and suture it in its original position.
▪
Close the wounds, and apply a long leg cast with the foot in equinus.

Postoperative Care

At 3 weeks, the cast is bivalved and exercises are started with the leg in the anterior half of the cast; the bivalved cast is reapplied between exercise periods. At first, dorsiflexion exercises are not permitted, but, later, guided reciprocal motion is allowed. The exercises are gradually increased, and at 6 weeks the patient is allowed to stand but not to bear full weight on the foot. The periods of partial weight bearing on crutches are increased, depending on the effectiveness of the transfer, the cooperation of the patient, and the ability to control his or her motions. Usually at 6 to 8 weeks a single step is allowed, using crutches and an elevated heel; later more steps are allowed, using crutches and a plantarflexion spring brace with an elastic strap posteriorly. Crutches are used for 6 to 12 months.

Knee

The disabilities caused by paralysis of the muscles acting across the knee joint include (1) flexion contracture of the knee, (2) quadriceps paralysis, (3) genu recurvatum, and (4) flail knee.

Flexion contracture of the knee

Flexion contracture of the knee can be caused by a contracture of the iliotibial band; contracture of this band can cause not only flexion contracture but also genu valgum and an external rotation deformity of the tibia on the femur. Flexion contracture also can be caused by paralysis of the quadriceps muscle when the hamstrings are normal or only partially paralyzed. When the biceps femoris is stronger than the medial hamstrings, there may be genu valgum and an external rotation deformity of the tibia on the femur; often the tibia subluxates posteriorly on the femur.

Contractures of 15 to 20 degrees or less in young children can be treated with posterior hamstring lengthening and capsulotomy. More severe contractures usually require a supracondylar extension osteotomy of the femur ( Fig. 34.11 ).

FIGURE 34.11, Supracondylar extension osteotomy of femur for fixed knee flexion deformity in older child.

Flexion contractures of more than 70 degrees result in deformity of the articular surfaces of the knee. In a growing child with poliomyelitis, a decrease in pressure and a tendency toward posterior subluxation cause increased growth on the anterior surface of the proximal tibia and distal femur. The quadriceps expansion adheres to the femoral condyles, and the collateral ligaments are unable to glide easily. Severe knee flexion contractures in growing children can be treated by division of the iliotibial band and hamstring tendons, combined with posterior capsulotomy. Skeletal traction after surgery is maintained through a pin in the distal tibia; a second pin in the proximal tibia pulls anteriorly to avoid posterior subluxation of the tibia. Long-term use of a long leg brace may be required to allow the joint to remodel. Supracondylar osteotomy may be required as a second-stage procedure in older patients near skeletal maturity.

Quadriceps paralysis

Disability from paralysis of the quadriceps muscle is severe because the knee may be extremely unstable, especially if there is even a mild fixed flexion contracture. When there is slight recurvatum, the knee may be stable if the gastrocnemius-soleus is active.

Tendons usually are transferred around the knee joint to reinforce a weak or paralyzed quadriceps muscle; transfers are unnecessary for paralysis of the hamstring muscles because, in walking, gravity flexes the knee as the hip is flexed. Several muscles are available for transfer to the quadriceps tendon and patella: the biceps femoris, semitendinosus, sartorius, and tensor fasciae latae. When the power of certain other muscles is satisfactory, transfer of the biceps femoris has been the most successful. Transfer of one or more of the hamstring tendons is contraindicated unless one other flexor in the thigh and the gastrocnemius-soleus, which also acts as a knee flexor, are functioning. If a satisfactory result is to be expected after hamstring transfer, the power not only of the hamstrings but also of the hip flexors, the gluteus maximus, and the gastrocnemius-soleus must be fair or better; when the power of the hip flexor muscles are less than fair, clearing the extremity from the floor may be difficult after surgery. Transfer of the tensor fasciae latae and sartorius muscles, although theoretically more satisfactory, is insufficient because these muscles are not strong enough to replace the quadriceps.

Ease in ascending or descending steps depends on the strength of the hip flexors and extensors. Strong hamstrings are necessary for active extension of the knee against gravity after the transfer; however, a weak medial hamstring can be transferred to serve as a checkrein on the patella to prevent it from dislocating laterally. A normal gastrocnemius-soleus is desirable because it aids in preventing genu recurvatum and remains as an active knee flexor after surgery; it may not always prevent genu recurvatum, however, which can result from other factors. Recurvatum after hamstring transfers can be kept to a minimum if (1) strength in the gastrocnemius-soleus is fair or better; (2) the knee is not immobilized in hyperextension after surgery; (3) talipes equinus, when present, is corrected before weight bearing is resumed; (4) postoperative bracing is used to prevent knee hyperextension; and (5) physical therapy is begun to promote active knee extension.

Transfer of Biceps Femoris and Semitendinosus Tendons

Technique 34.15

▪
Make an incision along the anteromedial aspect of the knee to conform to the medial border of the quadriceps tendon, the patella, and the patellar tendon.
▪
Retract the lateral edge of the incision, and expose the patella and the quadriceps tendon.
▪
Incise longitudinally the lateral side of the thigh and leg from a point 7.5 cm distal to the head of the fibula to the junction of the proximal and middle thirds of the thigh.
▪
Isolate and retract the common peroneal nerve, which is near the medial side of the biceps tendon.
▪
With an osteotome, free the biceps tendon, along with a thin piece of bone, from the head of the fibula. Do not divide the lateral collateral ligament, which lies firmly adherent to the biceps tendon at its point of insertion.
▪
Free the tendon and its muscle belly proximally as far as the incision will permit; free the origin of the short head of the biceps proximally to where its nerve and blood supplies enter so that the new line of pull of the muscle may be as oblique as possible.
▪
Create a subcutaneous tunnel from the first incision to the lateral thigh incision, and make it wide enough for the transferred muscle belly to glide freely.
▪
To further increase the obliquity of pull of the transferred muscle, divide the iliotibial band, the fascia of the vastus lateralis, and the lateral intermuscular septum at a point distal to where the muscle will pass.
▪
Beginning distally over the insertion of the medial hamstring tendons into the tibia, make a third incision longitudinally along the posteromedial aspect of the knee and extend it to the middle of the thigh.
▪
Locate the semitendinosus tendon; it inserts on the medial side of the tibia as far anteriorly as its crest and lies posterior to the tendon of the sartorius and distal to that of the gracilis. Divide the insertion of the semitendinosus tendon and free the muscle to the middle third of the thigh.
▪
Reroute this muscle and tendon subcutaneously to emerge in the first incision over the knee.
▪
Make an I-shaped incision through the fascia, quadriceps tendon, and periosteum over the anterior surface of the patella, and strip these tissues medially and laterally. With an 11⁄64-inch (4.36-mm) drill bit, make a hole transversely through the patella at the junction of its middle and proximal thirds; if necessary, enlarge the tunnel with a small curet.
▪
Place the biceps tendon in line with and anterior to the quadriceps tendon, the patella, and the patellar tendon.
▪
Suture the biceps tendon to the patella with the knee in extension or hyperextension.
▪
When only the biceps tendon is transferred, close the soft tissues over the anterior aspect of the patella and the transferred tendon. With interrupted sutures, fix the biceps tendon to the medial side of the quadriceps tendon.
▪
When the semitendinosus also is transferred, place it over the biceps and suture the two together with interrupted sutures; place additional sutures proximally and distally through the semitendinosus, quadriceps, and patellar tendons.
▪
Alternatively, detach the insertion of the semitendinosus from the tibia through an incision 2.5 cm long and bring it out through a posteromedial incision 7.5 cm long over its musculotendinous junction ( Fig. 34.12 ). Incise the enveloping fascia to prevent acute angulation of the muscle, and pass the tendon subcutaneously in a straight line to the patellar incision.

Postoperative Care

With the knee in the neutral position, a long leg cast is applied. To prevent swelling, the extremity is elevated by raising the foot of the bed rather than by using pillows; otherwise, flexion of the hip may put too much tension on the transferred tendons. At 3 weeks, physical therapy and active and passive exercises are started. Knee flexion is gradually developed, and the hamstring muscles are reeducated. At 8 weeks, weight bearing is started, with the extremity supported by a controlled dial knee brace locked in extension. Knee motion is gradually allowed in the brace when the muscles of the transferred tendons are strong enough to extend the knee actively against considerable force. To prevent overstretching or strain of the muscles, a night splint is worn for at least 6 weeks and the brace for at least 12 weeks.

Genu recurvatum

In genu recurvatum the deformity is the opposite of that in a flexion contracture and the knee is hyperextended. Mild genu recurvatum can cause some disability, but when the quadriceps is severely weakened or paralyzed, such a deformity is desirable because it stabilizes the knee in walking. Severe genu recurvatum is significantly disabling, however.

Genu recurvatum from poliomyelitis is of two types: that caused by structural articular and bone changes stemming from lack of power in the quadriceps and that caused by relaxation of the soft tissues around the posterior aspect of the knee. In the first type, the quadriceps lacks the power to lock the knee in extension; the hamstrings and gastrocnemius-soleus usually are normal. The pressures of weight bearing and gravity cause changes in the tibial condyles and in the proximal third of the tibial shaft. The condyles become elongated posteriorly; their anterior margins are depressed compared with their posterior margins; and the angle of their articular surfaces to the long axis of the tibia, which is normally 90 degrees, becomes more acute. The proximal third of the tibial shaft usually bows posteriorly, and partial subluxation of the tibia may gradually occur. In the second type, the hamstrings and the gastrocnemius-soleus muscles are weak. Hyperextension of the knee results from stretching of these muscles, often followed by stretching of the posterior capsular ligament.

The prognosis after correction of the first type of recurvatum is excellent. The skeletal deformity is corrected first, and then one or more hamstrings can be transferred to the patella. Irwin described an osteotomy of the proximal tibia to correct the first type of genu recurvatum caused by structural bone changes. Storen modified the Campbell osteotomy by immobilizing the fragments of the tibia with a Charnley clamp.

Osteotomy of the Tibia for Genu Recurvatum

Technique 34.16

(IRWIN)

▪
Through a short longitudinal incision, remove a section of the shaft of the fibula about 2.5 cm long from just distal to the neck.
▪
Pack the defect with chips from the sectioned piece of bone.
▪
Close the periosteum and overlying soft tissues.
▪
Through an anteromedial incision, expose and, without entering the joint, osteotomize the proximal fourth of the tibia as follows: With a thin osteotome or a power saw, outline a tongue of bone but leave it attached to the anterior cortex of the distal fragment. At a right angle to the longitudinal axis of the knee joint and parallel to its lateral plane, pass a Kirschner wire through the distal end of the proposed proximal fragment before the tibial shaft is divided. Complete the osteotomy with a Gigli saw, an osteotome, or a power saw.
▪
Lift the proximal end of the distal fragment from its periosteal bed, and remove from it a wedge of bone of predetermined size, its base being the posterior cortex.
▪
Replace the tongue of bone in its recess in the proximal fragment, and push the fragments firmly together.
▪
Suture the periosteum, which is quite thick in this area, firmly over the tongue of bone; this is enough fixation to keep the fragments in position until a cast can be applied.

The osteotomy can be fixed with percutaneous Kirschner wires, an external fixator, or, in adults, rigid plate fixation. Figure 34.13 shows correction of genu recurvatum by the Campbell technique.

FIGURE 34.13, Closing wedge osteotomy for genu recurvatum. A, Wedge of bone removed from tibia. B, Recurvatum secondary to anterior tilt of tibial plateau. C, Five months after operation. SEE TECHNIQUE 34.16.

Soft-Tissue Operations for Genu Recurvatum

Another type of genu recurvatum results from stretching of the posterior soft tissues. The prognosis is less certain after correction of this type of deformity; no muscles are available for transfer, the underlying cause cannot be corrected, and the deformity can recur. An operation on the soft tissues, triple tenodesis of the knee, has been described for correcting paralytic genu recurvatum. If the deformity is 30 degrees or less, prolonged bracing of the knee in flexion usually prevents an increase in deformity. When the deformity is severe, however, bracing is ineffective, the knee becomes unstable and weak, the gait is inefficient, and, in adults, pain is marked. The three following principles must be considered if operations on the soft tissues for genu recurvatum are to be successful:

1.
The fibrous tissue mass used for tenodesis must be sufficient to withstand the stretching forces generated by walking; all available tendons must be used.
2.
Healing tissues must be protected until they are fully mature. The operation should not be undertaken unless the surgeon is sure that the patient will conscientiously use a brace that limits extension to 15 degrees of flexion for 1 year.
3.
The alignment and stability of the ankle must meet the basic requirements of gait. Any equinus deformity must be corrected to at least neutral. If the strength of the soleus is less than good on the standing test, this defect must be corrected by tendon transfer, tenodesis, or arthrodesis of the ankle in the neutral position.

Triple Tenodesis for Genu Recurvatum

The operation for triple tenodesis for genu recurvatum consists of three parts: proximal advancement of the posterior capsule of the knee with the joint flexed 20 degrees, construction of a checkrein in the midline posteriorly using the tendons of the semitendinosus and gracilis, and creation of two diagonal straps posteriorly using the biceps tendon and the anterior half of the iliotibial band.

Technique 34.17

(PERRY, O’BRIEN, AND HODGSON)

▪
Place the patient prone, apply a tourniquet high on the thigh, and place a large sandbag beneath the ankle to flex the knee about 20 degrees.
▪
Make an S-shaped incision beginning laterally parallel to and 1 cm anterior to the biceps tendon; extend it distally 4 cm to the transverse flexion crease of the knee, carry it medially across the popliteal fossa, and extend it distally for 4 or 5 cm overlying or just medial to the semitendinosus tendon.
▪
Identify the sural nerve and retract it laterally. Then identify the tibial nerve and the popliteal artery and vein, and protect them with a soft rubber tape. Next, identify and free the peroneal nerve and protect it in a similar manner. Retract the neurovascular bundle laterally and identify the posterior part of the joint capsule.
▪
Detach the medial head of the gastrocnemius muscle in a step-cut fashion, preserving a long, strong proximal strap of the Z to be used in the tenodesis ( Fig. 34.14A ).
▪
Next, use a knife to detach the joint capsule from its attachment to the femur just proximal to the condyles and the intercondylar notch.
▪
Detach the tendons of the gracilis and semitendinosus at their musculotendinous junctions, and suture their proximal ends to the sartorius. Be sure to divide these tendons as far proximally as possible because all available length will be needed.
▪
Next, drill a hole in the tibia, beginning at a point in the midline posteriorly inferior to the physis and emerging near the insertion of the pes anserinus; take care to avoid the physis.
▪
Drill a hole in the femur, beginning in the midline posteriorly proximal to the femoral physis and emerging on the lateral aspect of the distal femur ( Fig. 34.14B ).
▪
Draw the tendons of the gracilis and semitendinosus through the hole in the tibia, pass them posterior to the detached part of the capsule, and pull them through the hole in the femur to emerge on the lateral aspect of the distal femur; suture the tendons to the periosteum here under moderate tension with heavy nonabsorbable sutures with the knee flexed 20 degrees.
▪
Advance the free edge of the joint capsule proximally on the femur until all slack has disappeared and suture it to the periosteum in its new position using nonabsorbable sutures.
▪
Detach the biceps tendon from its muscle, rotate it on its fibular insertion, pass it across the posterior aspect of the joint deep to the neurovascular structures, and anchor it to the femoral origin of the medial head of the gastrocnemius under moderate tension ( Fig. 34.14C ).
▪
Detach the anterior half of the iliotibial band from its insertion on the tibia, pass it deep to the intact part of the band, the biceps tendon, and the neurovascular structures, and suture it to the semimembranosus insertion on the tibia under moderate tension.
▪
If one of the tendons being used is of an active muscle, split that tendon and use only half of it in the tenodesis, leaving the other half attached at its insertion.
▪
Close the wound in layers, and use suction drainage for 48 hours. Apply a well-padded cast from groin to toes with the knee flexed 30 degrees to prevent tension on the sutures.

Postoperative Care

The cast is removed at 6 weeks, and a long leg brace that was fitted before surgery is applied. The brace is designed to limit extension of the knee to 15 degrees of flexion. Full weight bearing is allowed in the brace, and at night a plaster shell is used to hold the knee flexed 15 degrees. Twelve months after surgery the patient is readmitted to the hospital and the flexion contracture of the knee is corrected gradually to neutral by serial plaster casts; unprotected weight bearing is then permitted. It is important that the soft tissues are completely healed before being subjected to excessive stretching caused by unprotected weight bearing or by wedging plaster casts.

Flail knee

When the knee is unstable in all directions, and muscle power sufficient to overcome this instability is unavailable for tendon transfer, either a long leg brace with a locking knee joint must be worn or the knee must be fused. Fusion of the knee in a good position not only permits a satisfactory gait but also improves it by eliminating the weight of the brace; fusion of the knee causes inconvenience while sitting. One option is to defer fusion until the patient is old enough to weigh its advantages and disadvantages before a final decision is made. For patients who are heavy laborers and would have trouble maintaining a brace, the advantages of being free of a brace outweigh the advantages of being able to sit with the knee flexed in a brace; in these patients, an arthrodesis is indicated. Others who sit much of the time may prefer to use a brace permanently. When both legs are badly paralyzed, one knee can be fused and the other stabilized with a brace.

Before an arthrodesis is performed, a cylinder cast can be applied on a trial basis, immobilizing the knee in the position in which it would be fused; this allows the patient to make an informed decision concerning the advantages and disadvantages of arthrodesis of the knee. The techniques of knee fusion are described in Chapter 8 .

Tibia and femur

Angular and torsional deformities of the tibia and femur are more often caused by conditions other than poliomyelitis, such as congenital abnormalities, metabolic disorders, or trauma, and the various osteotomies used for their treatment are discussed in Chapter 29, Chapter 36 .

Hip

Paralysis of the muscles around the hip can cause severe impairment. This impairment may include flexion and abduction contractures of the hip, hip instability and limping caused by paralysis of the gluteus maximus and medius muscles, and paralytic hip dislocation.

Flexion and abduction contractures of the hip

An abduction contracture is the most common deformity associated with paralysis of the muscles around the hip; it usually occurs in conjunction with flexion and external rotation contractures of varying degrees. Less often, a contracture of the hip may occur that consists of adduction with flexion and internal rotation. When contractures of the hip are severe and bilateral, locomotion is possible only as a quadruped; the upright position is possible after the contractures have been released.

Spasm of the hamstrings, hip flexors, tensor fasciae latae, and hip abductors is common during the acute and convalescent stages of poliomyelitis. Straight-leg raising usually is limited. The patient assumes the frog position, with the knees and hips flexed and the extremities completely externally rotated. When this position is maintained for even a few weeks, secondary soft-tissue contractures occur; a permanent deformity develops, especially when the gluteal muscles have been weakened. The deformity puts the gluteus maximus at a disadvantage and prevents its return to normal strength. If the faulty position is not corrected, growth of the contracted soft tissues would fail to keep pace with bone growth and the deformity would progressively increase. If positioning in bed is correct while muscle spasm is present, and if the joints are carried through a full range of motion at regular intervals after the muscle spasm disappears, contractures can be prevented and soft tissues can be kept sufficiently long and elastic to meet normal functional demands.

The large expanse of the tensor fasciae latae must be recognized before the deforming possibilities of the iliotibial band can be appreciated. Proximally, the fascia lata arises from the coccyx, the sacrum, the crest of the ilium, the inguinal ligament, and the pubic arch and invests the muscles of the thigh and buttock. Either the superficial or the deep layer is attached to most of the gluteus maximus muscle and to all of the tensor fasciae latae muscle. All of the attachments of the fascia converge to form the iliotibial band on the lateral side of the thigh.

Contracture of the iliotibial band can contribute to the following deformities:

1.
Flexion, abduction, and external rotation contracture of the hip. The iliotibial band lies lateral and anterior to the hip joint, and its contracture can cause flexion and abduction deformity. The hip is externally rotated for comfort and, if not corrected, the external rotators of the hip contract and contribute to a fixed deformity.
2.
Genu valgum and flexion contracture of the knee. With growth, the contracted iliotibial band acts as a taut bowstring across the knee joint and gradually abducts and flexes the tibia.
3.
Limb-length discrepancy. Although the exact mechanism has not been clearly defined and may be related more to the loss of neurologic and muscle function, a contracted iliotibial band on one side may be associated with considerable shortening of that extremity after years of growth.
4.
External tibial torsion, with or without knee joint subluxation. Because of its lateral attachment distally, the iliotibial band gradually rotates the tibia and fibula externally on the femur; this rotation may be increased if the short head of the biceps is strong. When the deformity becomes extreme, the lateral tibial condyle subluxates on the lateral femoral condyle and the head of the fibula lies in the popliteal space.
5.
Secondary ankle and foot deformities. With external torsion of the tibia, the axes of the ankle and knee joints are malaligned, causing structural changes that may require surgical correction.
6.
Pelvic obliquity. When the iliotibial band is contracted, and the patient is supine with the hip in abduction and flexion, the pelvis may remain at a right angle to the long axis of the spine (see Fig. 34.18 ). When the patient stands, however, and the affected extremity is brought into the weight-bearing position (parallel to the vertical axis of the trunk), the pelvis assumes an oblique position: The iliac crest is low on the contracted side and high on the opposite side. The lateral thrust forces the pelvis toward the unaffected side. The trunk muscles on the affected side lengthen, and the muscles on the opposite side contract. An associated lumbar scoliosis can develop. If not corrected, the two contralateral contractures (i.e., the band on the affected side and the trunk muscles on the unaffected side) hold the pelvis in this oblique position until skeletal changes fix the deformity (see Fig. 34.19 ).
7.
Increased lumbar lordosis. Bilateral flexion contractures of the hip pull the proximal part of the pelvis anteriorly; for the trunk to assume an upright position, a compensatory increase in lumbar lordosis must develop.

A flexion and abduction contracture of the hip can be minimized or prevented in the early convalescent stage of poliomyelitis. The patient should be placed in bed with the hips in neutral rotation, slight abduction, and no flexion. All joints must be carried through a full range of passive motion several times daily; the hips must be stretched in extension, adduction, and internal rotation. To prevent rotation, a bar similar to a Denis Browne splint is useful, especially when a knee roll is used to prevent a genu recurvatum deformity; the bar is clamped to the shoe soles to hold the feet in slight internal rotation. The contracture is carefully watched for in the acute and early convalescent stages; if found, it must be corrected before ambulation is allowed.

Secondary adaptive changes occur soon after the iliotibial band contracts, and the resulting deformity, regardless of its duration or of the patient’s age, cannot be corrected by conservative measures; on the contrary, attempts at correction with traction only increase the obliquity and hyperextension of the pelvis and cannot exert any helpful corrective force on the deformity.

Simple fasciotomies around the hip and knee may correct a minor contracture, but recurrence is common; they do not correct a severe contracture. For abduction and external rotation contractures, a complete release of the hip muscles (Ober-Yount procedure) is indicated. For severe deformities, complete release of all muscles from the iliac wing with transfer of the crest of the ilium (Campbell technique) is indicated.

Complete Release of Hip Flexion, Abduction, and External Rotation Contracture

Technique 34.18

(OBER; YOUNT)

▪
With the patient in a lateral position, make a transverse incision medial and distal to the anterior superior iliac spine, extending it laterally above the greater trochanter.
▪
Divide the iliopsoas tendon distally, and excise 1 cm of it.
▪
Detach the sartorius from its origin in the anterior superior iliac spine, detach the rectus from the anterior inferior iliac spine, and divide the tensor fasciae latae from its anterior border completely posteriorly ( Fig. 34.15 ).
▪
Detach the gluteus medius and minimus and the short external rotators from their insertions on the trochanter.
▪
Retract the sciatic nerve posteriorly and then open the hip capsule from anterior to posterior, parallel with the acetabular labrum.
▪
Close the wound over a suction drain, and apply a hip spica cast with the hip in full extension, 10 degrees of abduction, and, if possible, internal rotation.
▪
For the Yount procedure, expose the fascia lata through a lateral longitudinal incision just proximal to the femoral condyle.
▪
Divide the iliotibial band and fascia lata posteriorly to the biceps tendon and anteriorly to the midline of the thigh at a level 2.5 cm proximal to the patella.
▪
At this level, excise a segment of the iliotibial band and lateral intermuscular septum 5 to 8 cm long.
▪
Before closing the wound, determine by palpation that all tight bands have been divided.

Postoperative Care

The cast is removed at 2 weeks, and a long leg brace with a pelvic band is fitted with the hip in the same position.

Complete Release of Muscles from Iliac Wing and Transfer of Crest of Ilium

Technique 34.19

(CAMPBELL)

▪
Incise the skin along the anterior one half or two thirds of the iliac crest to the anterior superior spine and then distally for 5 to 10 cm on the anterior surface of the thigh.
▪
Divide the superficial and deep fasciae to the crest of the ilium.
▪
Strip the origins of the tensor fasciae latae and gluteus medius and minimus muscles subperiosteally from the wing of the ilium down to the acetabulum ( Fig. 34.16A ).
▪
Free the proximal part of the sartorius from the tensor fasciae latae.
▪
With an osteotome, resect the anterior superior iliac spine along with the origin of the sartorius muscle and allow both to retract distally and posteriorly.
▪
Denude the anterior border of the ilium down to the anterior inferior iliac spine. Free subperiosteally the attachments of the abdominal muscles from the iliac crest (or resect a narrow strip of bone with the attachments). Strip the iliacus muscle subperiosteally from the inner table.
▪
Free the straight tendon of the rectus femoris muscle from the anterior inferior iliac spine and the reflected tendon from the anterior margin of the acetabulum, or simply divide the conjoined tendon of the muscle. Releasing these contracted structures often will allow the hip to be hyperextended without increasing the lumbar lordosis; this is a most important point because, in this situation, correction may be more apparent than real.
▪
If the hip cannot be hyperextended, other contracted structures must be divided. If necessary, divide the capsule of the hip obliquely from proximally to distally and, as a last resort, free the iliopsoas muscle from the lesser trochanter by tenotomy.
▪
After the deformity has been completely corrected, resect the redundant part of the denuded ilium with an osteotome ( Fig. 34.16B ).
▪
Suture the abdominal muscles to the edge of the gluteal muscles and tensor fasciae latae over the remaining rim of the ilium with interrupted sutures. Suture the superficial fascia on the medial side of the incision to the deep fascia on the lateral side to bring the skin incision 2.5 cm posterior to the rim of the ilium.
▪
To preserve the iliac physis in a young child, modify the procedure as follows. Free the muscles subperiosteally from the lateral surface of the ilium.
▪
Detach the sartorius and rectus femoris as just described and, if necessary, release the capsule and iliopsoas muscle. Stripping the muscles from the medial surface of the ilium is unnecessary.
▪
Now with an osteotome, remove a wedge of bone from the crest of the ilium distal to the physis from anterior to posterior; its apex should be as far posterior as the end of the incision and its base anterior and 2.5 cm or more in width, as necessary to correct the deformity.
▪
Then displace the crest of the ilium distally to contact the main part of the ilium, and fix it in place with sutures through the soft tissues.

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