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Poliomyelitis
The original language of this chapter by Dr. Tachdjian has been left unaltered as much as possible because we currently have no direct experience with acute poliomyelitis.
Poliomyelitis is an acute infectious disease caused by a group of neurotropic viruses that initially invade the gastrointestinal and respiratory tracts and subsequently spread to the central nervous system (CNS) through the hematogenous route. The poliomyelitis virus has a special affinity for the anterior horn cells of the spinal cord and for certain motor nuclei of the brainstem. These cells undergo necrosis, which results in loss of innervation of the motor units that they supply.
The first description of paralytic poliomyelitis was given by Underwood in 1789.
Infection may be caused by type I, II, or III poliomyelitis virus. No cross-immunity exists among the various types of poliovirus; thus infection may recur in the same individual. , Poliovirus is a member of the enterovirus group, which includes coxsackievirus and the echoviruses. Paralytic disease that is clinically and pathologically indistinguishable from poliomyelitis can be produced by various other enteroviruses. These viruses may be isolated by tissue culture.
In the past, poliomyelitis was an epidemic disease in the summer and fall months, with sporadic cases occurring throughout winter and spring. The development and widespread use of a prophylactic vaccine greatly reduced the incidence of poliomyelitis; however, sporadic cases still do occur, and continued rehabilitation of patients who have had the disease remains a concern of the orthopaedic surgeon. , , , ,
More recently, attention has focused on cases of poliomyelitis caused by oral vaccine, so-called vaccine-associated paralytic poliomyelitis. The risk of contracting poliomyelitis from the vaccine remains extremely low, with a rate of 1 case per 2.5 million doses. Between 1980 and 1989, 80 such cases were reported in the United States. During the same period, no cases resulted from wild virus, and five cases of imported disease were reported. People at risk for contracting vaccine-associated disease were infants receiving their first dose, persons in contact with vaccine recipients who were not vaccinated, and immunologically compromised people. Because of this rare but devastating occurrence, the Centers for Disease Control and Prevention (CDC) recommended that children be inoculated first with inactivated vaccine, followed by oral attenuated vaccine. In 2006 the CDC reported that vaccine-associated paralytic polio cases had been eliminated in the United States after this change in vaccine administration; the last such case was reported in 1999. It is important to differentiate vaccine-related polio from Guillain-Barré syndrome. The latter has been reported to occur more frequently during oral polio vaccination campaigns.
Worldwide Eradication Efforts
The effort to eliminate poliomyelitis worldwide continues. Great credit goes to several organizations for their work, including Rotary International, the Bill and Melinda Gates Foundation, the United Nations Children’s Fund, and the World Health Organization. a
a References , , , , , , .
A number of recent steps have been made toward world eradication, the first being introduction of at least one dose of inactivated polio vaccine into the routine immunization programs. Within a 25-year period, 105 of 126 countries were able to add this vaccine as a protection against live vaccine induced polio. A second important step noted in 2017 is the worldwide eradication of type 2 poliovirus. In addition, this report notes the absence of detection of type 3 poliovirus worldwide since November of 2012. The remaining challenge to total eradication is reaching isolated subpopulations, often in dangerous locations where polio virus still exists, most recently Nigeria, Pakistan, and Afganistan. Continuing efforts have been making progress by focusing upon the “the dynamics of human and social behavior change.” Specific methods including building trust in vaccinators, providing facts about transmission, overcoming key rumors, and strengthening community support for vaccination. , Planning for full global withdrawal of oral polio vaccine after eradication has already begun with the global switching from trivalent vaccine to bivalent vaccine. Although the eradication of the type 2 virus is only the second worldwide eradication of a virus (after smallpox), the elusive goal of total polio eradication remains a high priority for global health.
Postpolio Syndrome
Another manifestation of poliomyelitis that has received considerable attention is the occurrence of postpolio syndrome. This syndrome is characterized by increasing muscle weakness, fatigue, pain, and loss of function in individuals who contracted poliomyelitis 20 or more years earlier. Perry and associates showed that this condition represents a chronic overuse syndrome, with overstressed muscles “wearing out.” Another theory of the origin of this phenomenon is the failure of axonal sprouts that formed during the healing process after poliomyelitis. , The prevalence is higher in women than in men, and the syndrome is more likely in those who contracted polio at an early age. However, a discussion of the management of this problem is beyond the scope of a text on pediatric orthopaedics.
This chapter deals with general principles of the management of paralytic deformities of the musculoskeletal system that result from poliomyelitis. These principles are applicable not only to the treatment of poliomyelitis but also to the management of similar problems of flaccid paralysis secondary to other causes. For a detailed account of the disease and its medical aspects of management, the reader is referred to the voluminous literature on the subject.
Pathology
Poliovirus has a definite predilection for the anterior horn cells of the spinal cord and for certain motor nuclei in the brainstem. The lumbar and cervical enlargements of the spinal cord are the most commonly affected. The damaging action on the motoneurons may be direct, occurring through the toxic effects of the virus, or indirect, occurring through ischemia, edema, and hemorrhage in the neurons’ supportive glial tissue.
The motoneurons swell and the Nissl substance in their cytoplasm undergoes chromatolysis. An inflammatory reaction ensues, with infiltration of polymorphonuclear and mononuclear cells into the gray matter, particularly the perivascular areas. The necrotic bodies are subsequently replaced by scar tissue.
Involvement of the anterior horn cells varies from minimal injury, with temporary inhibition of metabolic activity and rapid recovery, to complete and irrevocable destruction.
Paralysis is of the flaccid type, with the individual motor units following the “all-or-none” law, because the virus affects the anterior horn cells rather than the muscle. The percentage of motor units destroyed varies, and the resultant muscle weakness is proportionate to the number of motor units that are lost. For example, a muscle with “poor” muscle strength will have 20% of its motor units functioning, whereas a muscle with “good” motor strength will have 80% of its motor units functioning. These remaining functional motor units are called guiding neuromuscular units and are of particular importance in retaining patterns of motion of the individual muscles or muscle groups during the recovery stage. The recovery of muscle power primarily depends on restitution of the anterior horn cells of the spinal cord that have been damaged but not destroyed.
Course and Prognosis
The course of the disease is subdivided into acute, convalescent, and chronic phases. The acute phase, which lasts from 5 to 10 days, is the period of acute illness when paralysis may occur. It is further subdivided into the preparalytic phase and the paralytic phase. The acute phase is ordinarily thought to end when the patient has had no fever for 48 hours.
The convalescent phase encompasses the 16-month period after the acute phase. During this time a varying degree of spontaneous recovery in muscle power takes place. This phase is also further subdivided into the sensitive phase (lasting from 2 weeks to several months), characterized by hypersensitivity of muscles, which are tender and “in spasm,” and the insensitive phase, in which the muscles are no longer sensitive but are still in the period of recovery.
The chronic or residual phase is the final stage of the disease after recovery of muscle power has taken place. It encompasses the rest of the patient’s life after termination of the convalescent period.
Immediately after onset it is difficult to make an accurate prognosis regarding the rate and extent of spontaneous recovery. It is best to assume that the involved muscles will recover until the subsequent course of the disease demonstrates otherwise. Muscle recovery is most marked in the first 3 to 6 months, and the potential for recovery ceases approximately 16 to 18 months after onset.
The two primary factors to consider in the prognosis are the severity of the initial paralysis and the diffuseness of its regional distribution. If total paralysis of a muscle persists beyond the second month, severe motor cell destruction is indicated, and the likelihood of any significant return of function is poor. If the initial paralysis is partial, the prognosis is better.
The condition of the neighboring muscles is another consideration. A weakened muscle surrounded by completely paralyzed muscles has less chance of recovery than does a muscle of corresponding power that is surrounded by strong muscles. Muscle spasm, contracture of antagonist muscle groups, deformity, and inadequate early treatment are other factors that may interfere with recovery of muscle function.
Treatment Overview
Management of poliomyelitis varies with the stage of the disease and the severity and extent of paralysis. , Treatment in the acute febrile stage is primarily the domain of the pediatrician or internist, and patients are admitted to infectious disease hospitals or to isolation units of general hospitals. However, care of the musculoskeletal system is important from the first day of the disease. It is imperative that the orthopaedic surgeon be consulted to examine a patient with a suspected case of poliomyelitis before lumbar puncture is performed. The surgeon should be responsible for all orders concerning management of the musculoskeletal system. The pediatrician is responsible for general care of the patient, especially any problems of respiratory system and bulbar involvement, should they develop. Once afebrile for 18 hours (i.e., after termination of the acute stage), the patient should be transferred to the service of the orthopaedic surgeon, who assumes the dominant role. Such delineation in addition to continuity of supervision is mandatory because it stimulates early attention to deforming tendencies and prevents their development.
Acute Phase
During the initial, febrile phase of the disease, the primary concerns of the orthopaedic surgeon are the comfort of the patient and the prevention of deformity. It is best to place the patient on complete bed rest and restrict physical activities to a minimum. The patient is irritable and apprehensive. It is important to reassure the patient and allay fears.
General medical measures consist of the administration of a varied diet with relatively high fluid intake, attention to urinary retention and bladder paralysis, prevention of constipation and fecal impaction, and provision of analgesia for pain. Opiates and other medications that have a depressing action on the CNS should not be given in the presence of impending paralysis of the muscles of respiration.
A detailed determination of the severity and extent of muscle paralysis is not warranted during this febrile period. However, by gentle handling of the limbs and trunk, the clinician can make an approximate assessment of the degree and distribution of the motor weakness without much distress to the patient. This initial muscle examination has diagnostic and therapeutic implications. It also provides the necessary information to prevent the development of potential deformities consequent to paralysis.
Ordinarily, paralysis develops 2 or 3 days after the onset of fever and increases in severity for several days. Progressive involvement ceases only after the elevated temperature returns to normal. Characteristically, the paralysis in poliomyelitis is asymmetric. In the presence of symmetric paralysis of the limbs and trunk, a paralytic disease other than poliomyelitis should be considered. In a large epidemic the care of patients will be much simplified if those with paralysis are separated from those without paralysis.
Management of Respiratory Involvement
Patients with bulbar and respiratory involvement require specialized intensive care. An early appraisal of the distribution and extent of paralysis will help detect muscle weakness in certain areas that should alert the clinician to the possible development of such distressing complications. For example, a patient who cannot lift his or her head because of paralysis of the anterior neck muscles or one who has a nasal intonation of the voice, difficulty swallowing, and weakness of the facial muscles should be watched carefully for bulbar involvement. Prompt diagnosis and treatment are essential to keep the patient’s airways open because the condition may be fatal. Aspiration of unswallowed secretions is a definite danger. The foot of the bed is elevated, and the patient is placed in a prone or lateral position. Frequent suction or postural drainage is usually required. Occasionally, intubation or tracheostomy may be necessary.
Another anatomic area that should be observed for muscle weakness is the shoulder girdle. The nerve supply to the deltoid muscle is provided by the fifth cervical root; it is adjacent to the fourth cervical root, which innervates the diaphragm. Consequently, progressive paralysis of the deltoid muscle is usually followed by paralysis of the intercostal muscles and the diaphragm. An increased rate of breathing, use of accessory muscles of respiration, and restlessness, anxiety, and disorientation are signs that should alert the physician to the possible need for a mechanical respirator. Paralysis of the diaphragm is easily detected on fluoroscopy. Abdominal muscle weakness is determined by asking the patient to lift the head and shoulder or the lower limbs. Asymmetry of power is indicated by the Beevor sign, which is a shift of the umbilicus toward the stronger muscles.
Prevention of Deformity
Patient positioning should provide correct anatomic alignment of the limbs and proper posture of the trunk. The aim is to prevent the development of deformities. The bed should give adequate support and should not sag. A firm foam rubber mattress is preferable. Bed boards should be placed beneath the mattress and should be hinged to permit sitting in the later convalescent period. A padded footboard is used to maintain the ankles and feet in neutral position when the patient is lying supine or prone. Pulling the end of the mattress approximately 10 cm away from the footboard provides an interspace in which the heels are allowed to fall. Periods in the supine position should be alternated with periods in the prone position. The prone position is important for maintenance of good muscle tone of the gluteus maximus and erector spinae muscles.
When the patient is lying supine, the knees should be held in slight flexion with padded rolls under them and behind the proximal ends of the tibiae to prevent genu recurvatum and posterior subluxation of the tibiae. A slightly flexed position of the knees relaxes the sensitive hamstrings. However, excessive flexion of the knees should be avoided. Sandbags or rolled pads are placed on the lateral sides of the thighs and legs to prevent external rotation deformity of the lower limbs. Intermittent use of rolls between the scapulae will prevent forward hunching of the shoulders.
The limbs should not be maintained in rigidly fixed positions. Several times a day the joints are carried passively through their range of motion; this will help relieve muscle pain. However, overstretching of the muscles should be avoided. The patient should be handled as gently as possible. Passive motion of the joints of a limb is imperative to prevent stiffness and myostatic contractures. At times, during severe spasm of the hip flexors, hamstrings, and gastrocnemius, the sensitivity and pain of muscles are so great that anatomic alignment cannot be assumed without excessive discomfort.
Management of Muscle Spasm
“Muscle spasm,” a principal manifestation of poliomyelitis in its early stages, is characterized by protective contraction of the muscles to prevent a potentially painful movement. “Muscle resistance to stretch” is more descriptive of this reflex guarding action of the muscles, which resembles the muscle spasm associated with painful phenomena such as hamstring spasm in synovitis of the knee. True spasticity and signs of upper motoneuron involvement are absent. The exact cause of the muscle pain and sensitivity is unknown. Most probably these manifestations are the result of inflammatory changes in the posterior ganglia and meninges. Other possible causes are lesions in the reticular substance and lesions of the internuncial neurons in which inhibitory fibers to the anterior horn cells are affected.
The degree of muscle pain and sensitivity varies considerably. Some muscle discomfort is usually present in the preparalytic period. Nerve traction tests, such as those of Lasègue and Kernig, increase muscle spasm and pain. Spontaneous severe pain is rare but occasionally seen in adult patients. The important consideration is that the painful strong muscles tend to shorten during the sensitive phase; if these muscles are maintained in their shortened position, myostatic contracture and fixed deformity will develop.
In the acute and sensitive phase of convalescence, application of moist heat relieves the sensitivity of the muscles and alleviates discomfort. Physiologically, heat increases local temperature and enhances blood flow to the muscle. It has no specific therapeutic effect on the course of the paralysis and actual recovery of involved nerve cells. Heat is more beneficial if it is applied intermittently for short periods. (The moist heat methods are those introduced in the 1950s by Sister Kenny. , )
In the acute phase, to minimize handling of the patient, a lay-on wool pack is used. It consists of three layers, one of wool blanket material (wrung out of boiling water by passing it twice through a wringer) and one of waterproof material, which in turn is covered by an outer layer of wool blanket. The number of these packs and the duration of their use are individualized according to the intensity of pain and spasm. In general, two moist heat packs are applied during a 20-minute period. Continuous and overzealous use of heat should be avoided because it can be tiring and harmful to the patient. Moist heat is best used before physical therapy in the acute phase to assist in developing greater range of joint motion and to facilitate the performance of active exercises. Warm tub baths are substituted for the lay-on packs within a few days after the patient’s temperature has returned to normal and when the patient’s general condition permits. The buoyant effect of water makes it easier for the weakened muscles to move. Active exercises in water in the acute phase should be closely supervised so that the patient does not substitute stronger muscles for the weaker ones. Again, the patient’s comfort is the primary consideration. The temperature of the tub baths should be approximately 100°F, and the total period of immersion in the tub should not exceed 20 minutes. In cases of extensive paralysis, overhead cranes may be used to lower the patient directly into the tub from the stretcher.
Convalescent Phase
The objectives of treatment during the convalescent stage are (1) attainment of maximum recovery in individual muscles, (2) restoration and maintenance of normal range of joint motion, (3) prevention of deformities and correction of deformities if they occur, and (4) achievement of the best possible physiologic status of the neuromusculoskeletal system.
Management of Muscle Spasm and Prevention of Deformity
In the early part of the convalescent stage, because muscle sensitivity and spasm are still present, the use of hot packs is continued for the comfort of the patient. Passive exercises are performed four to six times a day to prevent the development of contractural deformity. When joint motion is limited, gentle passive stretching exercises are added to the therapy program. This exercise regimen should not cause the patient discomfort; however, the threshold of pain may be very low in an apprehensive, sensitive person. A firm but sympathetic attitude by the therapist is important, and the patient should be encouraged more each time to gain a greater degree of motion. Tendencies toward deformity should be observed, such as external rotation and abduction of the hips, plantar flexion of the feet, or adduction of the shoulders. Passive stretching exercises should be directed toward preventing and correcting deformity.
Muscle Examination
Several days after onset of the convalescent stage, a complete muscle examination should be performed. Ordinarily, it is done in stages to avoid fatiguing or disturbing the patient. This initial motor assessment provides a basis for comparison with subsequent examinations, and it also serves as a guide to the therapy regimen that is to be instituted. The rate and extent of muscle recovery are determined by repeating these muscle tests periodically—monthly during the first 4 months, bimonthly during the following 8 months, and then quarterly during the second year of the disease. The prognostic value of the serial muscle tests is evident: when a muscle exhibits little or no improvement in power during a 3-month period, it is unlikely that it will recover or gain strength of functional significance. In such a case the patient should be fitted with appropriate orthotic support and allowed greater activity. In contrast, a muscle that shows steady improvement has a good possibility of recovering to a functional level; hence it is unwise to apply an above-knee orthosis to this weak limb and permit the patient to walk.
Preserving and Restoring Neuromuscular Function
In management of the convalescent stage of poliomyelitis, the following aspects of neuromuscular function must be considered.
Patterns of Motor Activity
Limb motions are complex and are not the result of isolated contraction of a single muscle. The functions of many muscles are integrated and coordinated in the execution of a movement and are controlled by the automatic reflexes of the CNS. In dorsiflexion of the ankle, for example, the anterior tibial muscle, the toe extensors, and the peroneus tertius are the prime movers that execute the desired movement, whereas the triceps surae and the toe flexors are the antagonist muscles that become relaxed because of the reciprocal innervation of the agonist and antagonist muscles. The synergist and fixation muscles also contract while the prime mover acts.
In the presence of muscle weakness, the tendency is to use a strong group of muscles that can perform the action more easily and readily, thus excluding the weaker muscles from the pattern of motor activity. A muscle that has been temporarily paralyzed will be left out of the pattern of motion permanently if other muscles substitute for its action during the period of its recovery. In the convalescent stage, these muscular substitutions and abnormal patterns of motor activity should be avoided.
Some neuromuscular units often remain intact in the paralyzed muscles; they act as “guiding contractile units,” and in the performance of active exercises, these functioning neuromuscular units should be used to guide the body part in execution of normal motion.
For example, in reeducation of a poor anterior tibial muscle, the ankle joint is first passively dorsiflexed through its full arc of motion to stretch any contracture of the triceps surae muscle. The limb is then placed in a side-lying position to eliminate the force of gravity, and the ankle joint is again passively dorsiflexed in some inversion through its full range. The therapist assists the patient to localize the action of the anterior tibial muscle and emphasizes that substitution by the toe extensors and peroneus tertius muscle should be avoided.
Next the patient is asked to produce an active, sustained contraction of the anterior tibial throughout its full arc of motion, first with and then without assistance. As the muscle becomes stronger, the limb is placed in the supine position to make the muscle work against gravity, and gradually increasing manual resistance is applied. The active exercises are graduated on the basis of performance. Muscles that are overworked lose strength.
In poliomyelitis, reciprocal innervation between agonist and antagonist muscles is often disturbed, with resultant loss of synergistic muscular action and the normal pattern of motor activity.
Fatigue
A paralyzed muscle is easily fatigued. This is readily shown by its rapid loss of power and inability to function after several effective contractions. Forcing a weak muscle beyond its point of maximal action does not increase its strength; on the contrary, it inhibits recovery of the paralyzed muscle. It is important to observe the level of functional activity of a weak muscle so that it is not forced to exceed its capability.
Contractural Deformity and Progressive Loss of Function
Flaccid paralysis is the chief cause of functional loss. Muscular action is also inhibited by pain, sensitivity, and spasm. When a muscle is maintained in a shortened position for a prolonged period, myostatic contracture develops. Muscle imbalance and increased stress secondary to abnormal patterns of activity are other factors producing deformity. Growth is an important consideration in the management of poliomyelitis in children. The contour of bony structures is influenced by paralysis and dynamic muscle imbalance. For example, when the triceps surae muscle is weak and the ankle dorsiflexors are of normal motor strength, a progressive calcaneus deformity of the hindfoot results. If the child is permitted to walk without support and protection, the loss of power of the triceps surae muscle will be greater because the muscle is working against gravity. Fig. 33.1 shows the vicious cycle of factors causing progressive loss of function in poliomyelitis.
In the asensitive stage, proper alignment of the limbs and full range of joint motion must be restored and maintained. Passive stretching exercises are performed vigorously. In the presence of muscle imbalance and a tendency to develop contracture, bivalved casts should be used at night to maintain the part in correct position. When a deformity is fixed, wedging casts or traction may be applied.
Active exercises are performed to integrate recovering motor units into the normal pattern of motion; their primary objective is not to produce hypertrophy of muscles that are already functioning normally. Hydrotherapy and active exercises in a pool are prescribed for patients with extensive paralysis. Motion of the hips, shoulders, and trunk is greatly facilitated in the pool because the buoyant effect of the water facilitates coordinated motion of the parts. However, strict supervision by the therapist is mandatory to prevent substitution of strong muscles for those that are weak. Excessive exercises and overwork should be avoided. Patients with extensive paralysis are initially instructed to ambulate in the pool; when adequate control of the trunk and lower limbs is achieved, this is no longer necessary. Standing balance should be developed first, followed by walking with the help of crutches. The gait pattern should be a reciprocal four-point gait, with the amount of body weight borne depending on the degree of paralysis. The physical therapist assists in locomotion so that abnormal mechanisms do not develop. During the convalescent period, use of an orthosis should be kept to a minimum because it increases the workload on the paralytic levels and tends to produce abnormal gait patterns. However, in severe paralysis of the lower limbs and trunk, locomotion may be impossible without the support of an adequate orthosis. General activities of the patient are gradually increased. During the first few minutes of locomotion the gait may be effective, but with fatigue it may become poor. Random, purposeless activity should be discouraged.
Chronic Phase
The goals of treatment in the residual stage are to enable the patient to attain maximal function and to obtain the greatest amount of productive activity despite residual weakness. With continued growth and use of the limb, progressive deformities that will ultimately cause loss of function may develop. Hence an equally important task during the chronic stage is to prevent deformities and to correct them, should they develop. The residual stage is a dynamic, not a static, period. Much can be done to improve the functional capacity of the patient.
Physical Therapy
In the residual stage the physical therapy regimen is directed toward (1) increasing the motor strength of muscles by active hypertrophy exercises, (2) preventing or correcting deformity by passive stretching exercises, and (3) achieving maximum functional activity.
Active Hypertrophy Exercises
Active hypertrophy exercises are performed primarily for the benefit of marginal muscles, to elevate or maintain their functional level. (There is little to be gained by exercising zero or “trace” muscles that remain unchanged after 18 months, and the same is true of muscles that have a “good” or “normal” rating.) For example, when the anterior tibial and toe extensor muscles are “fair” in motor strength and the triceps surae muscles are “normal,” active exercises of the ankle dorsiflexors should be performed to maintain them at the antigravity functional level. Progressive resistance exercises entail the use of activity graded in proportion to the strength of the involved muscles. These exercises are recommended in the residual stage of poliomyelitis to increase the strength and improve the endurance of such individual muscles or groups of muscles as a “fair” quadriceps or triceps surae or a “fair plus” hip abductor muscle to maximum capacity. Whether progressive resistive exercises are of any permanent value when the motor strength of a muscle is less than “fair minus” is doubtful; a “poor” quadriceps muscle cannot, through hypertrophy exercises, be improved to “fair” strength so that it can lift the leg against gravity. However, correction of flexion deformity of the knee may provide added strength by eliminating the need for the quadriceps muscle to work against deformity.
Passive Stretching Exercises
Prevention of contractural deformity is much simpler than correction of such deformity. When a limb is continuously maintained in one position, contracture and fixed deformity develop as a result of the effects of gravity and dynamic imbalance of muscles. An ankle joint held in plantar flexion because of weak dorsiflexors and a strong triceps surae is susceptible to the development of progressive equinus deformity if the ankle is not passively stretched into dorsiflexion every day. The calf muscles should also be passively stretched to prevent the development of equinus deformity; this is implemented by the use of a solid ankle orthosis to hold the foot out of equinus and in neutral position. Passive stretching exercises should be performed gently several times a day. However, in the presence of muscle imbalance, these exercises are not adequate to prevent deformity, and other measures should be undertaken, such as the use of an ankle foot orthosis at night to hold the foot in neutral position and wearing of an ankle foot orthosis with an active dorsiflexion-assist during the day.
Functional Training
The purpose of a functional training program is to enable the patient to overcome the handicaps imposed by the physical disability. The residual deficit in function varies, depending on the extent and severity of paralysis. The needs of a growing child progressively change. In the residual stage the patient is taught how to use all available muscles to accomplish a task successfully. This is in contrast to the convalescent stage, when the patient is not allowed to substitute stronger muscles for weaker ones. For example, when the anterior tibial is “poor” in motor strength in the convalescent stage, the child is not permitted to use the toe extensors to dorsiflex the foot when active exercises are performed with the anterior tibial. However, in the chronic stage, if anterior tibial function is still “poor,” the child is taught how to dorsiflex the foot by using the toe extensors and peroneal muscles.
At times the activity of stronger muscles is suppressed to prevent the development of deformity. For example, an individual with “normal” sartorius, biceps femoris, and peroneal muscles but “poor” iliopsoas, medial hamstring, and anterior tibial muscles walks with a marked external rotation deformity of the foot and leg. It is important to supervise such a patient’s gait and teach the patient to suppress the eversion power of the peroneals and the externally rotating power of the biceps femoris and the sartorius to prevent the development of an external rotation deformity of the lower limb.
To teach a child merely to walk with crutches and orthoses is not satisfactory. The child should be instructed in activities of daily living, such as how to get in and out of chairs, open doors, and enter an automobile.
Orthoses and Other Apparatus
Use of an apparatus may be necessary during the asensitive period of the convalescent stage and the residual stage of poliomyelitis. The primary objectives of the orthosis are to (1) support the patient and enable the patient to walk and increase functional activity, (2) protect a weak muscle from overstretching, (3) augment the action of weak muscles or substitute for muscles completely lost, (4) prevent deformity and malposition, and (5) correct deformity by stretching certain groups of muscles that have been contracted. The support, substitution, and corrective mechanisms may be combined in a single apparatus. In general, dynamic splinting is more desirable than static splinting.
General Principles
Certain general principles should be followed regarding the use of an orthosis in patients with poliomyelitis. Whenever satisfactory recovery of function is expected, an orthosis should be used with caution on the lower limbs because it is likely to produce an abnormal gait pattern. Thus during the early convalescent period, use of an orthosis should be deferred until after maximum recovery of muscle function has taken place. Locomotion without an orthosis but with the support of crutches should be attempted to stimulate active muscular function through the exercise of walking. However, use of an orthosis should not be postponed if deformities appear likely to develop from the stress of weight bearing. The needs of each patient are different, and the use of a lower limb orthosis depends on the severity of the muscle weakness and the degree of dynamic imbalance of the muscles. If the patient has extensive paralysis of the lower limbs, use of an orthosis may be the only means of achieving stance and locomotion.
In general, use of an orthosis should be as minimal as the condition permits. For example, if a patient with paralysis of both lower limbs were to be fitted with two knee-ankle orthoses, he or she would also need to use two crutches to walk. If the patient were to use two crutches, he or she could do as well with a knee ankle orthosis on one leg only because only minimal motor strength is required of the other leg to walk without an orthosis. During the stance phase on the leg without the orthotic support, the tripod base is completed by the two crutches; the knee is stabilized by being locked in hyperextension. “Fair” motor strength in the ankle dorsiflexors and hip flexor muscles allows clearance of the lower limb in the swing phase.
It is imperative to explain to the patient the reasons for using an orthosis. The patient should understand clearly that wearing the orthosis will help in the early convalescent stage of the disease and that the orthosis may be discarded later, after training or reconstructive surgery. For example, the use of a dorsiflexion-assist below-knee orthosis may be unnecessary after a successful anterior transfer of the peroneal tendons, or an opponens splint may be discarded after a satisfactory opponens tendon transfer. In addition, when the child becomes an adult, he or she may no longer need an above-knee orthosis to prevent genu recurvatum.
The continued use of an orthosis should be reevaluated regularly. Before advising that use of an orthosis be discontinued, the clinician should be certain that no possibility for the development of progressive deformities exists and that the level and quality of functional performance will not deteriorate.
Specific Applications
Lower Extremity
When the toe extensor and anterior tibial muscles are paralyzed and the triceps surae muscle is normal, a dorsiflexion-assist spring orthosis (which acts as an active substitute for the weak ankle dorsiflexors) is preferable to a below-knee caliper orthosis with a posterior stop that prevents plantar flexion of the ankle beyond neutral position. In paralysis of the gastrocnemius and soleus muscles, a plantar flexion–assist spring below-knee orthosis with a dorsiflexion stop at neutral position is prescribed ( Fig. 33.2 ). In the presence of a flail ankle and foot, a double-action ankle joint (both plantar flexion–assist and dorsiflexion-assist) is provided, and a varus or valgus T-strap is added to the shoe as necessary. In addition, inside or outside wedges are prescribed for the shoe depending on the deformity of the foot.
When the muscles controlling the knee are paralyzed, an above-knee orthosis with a drop-lock knee joint is prescribed. This type of orthosis provides knee stability for walking and can be unlocked during sitting. If genu recurvatum results from paralysis of the triceps surae in the presence of some strength of the quadriceps femoris, it can be controlled by an above-knee orthosis with a free knee joint constructed so that complete extension of the orthosis at the knee is prevented. Proper positioning of the thigh and calf bands also checks genu recurvatum. Genu varum or knock-knee pads are added as necessary. When flexion deformity of the knee is present as a result of dynamic imbalance between the hamstrings and quadriceps femoris muscles, a well-padded anterior knee component is prescribed. An Engen extension knee orthosis is worn at night to correct flexion deformity of the knee.
Hip
If the muscles controlling the hip are weak, stability of the hip joint can be provided by an ischial weight-bearing thigh socket; crutches are used if necessary. Rotational alignment of the lower limbs is obtained by the addition of rotation straps or twisters. Ordinarily the patient walks better without a pelvic band and drop-lock hips; however, in a young child with gluteus maximus paralysis, these devices may be used temporarily for balance. Frequently the spine also requires support. When upright posture is resumed, the abdominal muscles overstretch, and severe lumbar lordosis and paralytic scoliosis develop. Any asymmetric involvement of the abdominal and trunk musculature should always be carefully noted. An abdominal corset support with metal stays often serves to control abdominal muscle paralysis. If the trunk extensors are weak, a spinal orthosis with an abdominal corset is provided. If the spine is unstable and collapsing, it may be supported by a molded plastic body jacket constructed from a plaster-of-Paris cast made while the patient is standing, with traction provided by a head sling. In paralytic scoliosis, usually a Milwaukee brace is worn, provided that lower limb paralysis is not extensive and wearing such an appliance does not prevent ambulation. In these instances the Milwaukee brace is used intermittently during periods of recumbency or sitting, or both.
Upper Extremity
In the upper limb the paralyzed shoulder muscles, particularly the deltoid, are best protected from the effects of gravity with a sling, which allows functional use of the forearm and hand. During the initial period of 6 to 8 weeks an abduction shoulder splint may be worn at night and during part of the day to prevent overstretching of the deltoid muscle, particularly when the patient has associated paralytic subluxation or dislocation of the shoulder joint. A cock-up wrist splint is used when the wrist extensors are paralyzed, and an opponens splint is used when the opponens of the thumb is weak. When the intrinsic muscles of the hand are paralyzed, hyperextension of the metacarpophalangeal joints is prevented by a knuckle-bender dynamic splint.
Surgical Treatment
A multitude of operative procedures can be performed both for the correction of paralytic deformities and for the total physical rehabilitation of a child with poliomyelitis. These procedures may include fasciotomy, capsulotomy, tendon transfers, osteotomy, and arthrodesis. Leg length inequality commonly occurs in poliomyelitis as a result of shortening in the paralyzed leg.
Principles of Tendon Transfer
Tendon transfer entails shifting the insertion of a muscle from its normal attachment to another site to replace the active muscular action that was lost by paralysis and to restore dynamic muscle balance. The procedure was originally described by Nicoladoni in 1882. Many surgeons have devised various types of tendon transfers and established their usefulness. Lange, Velpeau, Vulpius, Codivilla, Mayer, Biesalski, Goldthwait, Ober, Steindler, Bunnell, and Green are some who may be mentioned. b
b References , , , , , , , , , , , .
The term tendon transplantation should not be used interchangeably with tendon transfer because the two are not synonymous. Tendon transplantation refers to the excision of a tendon and its use as a free graft. In muscle transplantation, both the origin and the insertion of a muscle are detached, and the entire muscle with its intact neurovascular supply is transplanted to a completely new site.
The basic principles of tendon transfers have been outlined by Green and are listed here.
- 1.
The muscle to be transferred must have adequate motor strength to carry out the new function. As a rule, the motor rating of the muscle should be good or normal to warrant transfer. The function that the transferred muscle is intended to perform is another consideration. In the lower limb, for example, in the presence of footdrop, anterior transfer of the peroneus longus is adequate to produce effective ankle dorsiflexion, whereas in calcaneus limp, posterior transfer of the peroneus longus alone to the os calcis is not sufficient to substitute for action of the gastrocnemius-soleus, and the additional action of two or three motors such as the flexor digitorum communis and the anterior tibial muscles is required. Ordinarily, one grade of motor power is lost after a muscle is transferred.
- 2.
The range of motion of muscles on contraction is an important consideration. This range must be similar to that of the muscles for which they are being substituted; furthermore, whenever muscles are transferred in combination, their range of contraction should not differ significantly. The transfer of antagonistic muscles is not ordinarily as effective as the transfer of muscles having similar function or corollary activity. However, with meticulous postoperative care, antagonistic muscles may be transferred effectively with good results. Posterior transfer of the anterior tibial to the os calcis and transfer of the hamstring muscles to the patella are common examples of such antagonistic transfers.
- 3.
In choosing the muscles for transfer, the surgeon must weigh the loss of original function that will result from the tendon transfer against the gains to be obtained. For example, in the presence of hip flexor weakness, the hamstring muscles should not be transferred to the patella for quadriceps paralysis because loss of active knee flexion added to the lack of hip flexion will be a greater disability. Whenever possible, muscle balance must be restored. Ideally, a deforming muscle force must be shifted so that it substitutes for an essential weakness. For example, in the foot and ankle, the muscles of inversion and eversion and those of plantar flexion and dorsiflexion should be balanced. A common pitfall is transfer of the peroneus longus muscle posteriorly to the os calcis in the presence of a strong anterior tibial muscle. Normally, the anterior tibial muscle dorsiflexes the first metatarsal and the peroneus longus opposes this action. With posterior transfer of the peroneus longus, the unopposed anterior tibial gradually causes the first metatarsal to ride up and produces a dorsal bunion. Thus the peroneus longus should not be transferred to the os calcis unless the anterior tibial is shifted from its insertion on the first metatarsal to the midline of the foot.
- 4.
The joints on which the transferred muscle is to act should have functional range of motion. All contractural deformity should be corrected by wedging casts or soft tissue release before tendon transfer. For example, an anterior transfer for footdrop should not be performed in the presence of equinus deformity of the ankle.
- 5.
A smooth gliding channel with adequate space must be provided for excursion of the tendon in its new location. The paratenon and synovial sheath are preserved over the tendon surface during dissection. It is preferable to pass the tendon beneath the deep fascia through tissues that permit free gliding rather than subcutaneously. A wide portion of the intermuscular septum is excised whenever muscles are passed from one muscle compartment to another. Sufficient space should be provided for the tendon so that adhesions will not form. An Ober tendon passer of appropriate size should be used to redirect the tendon to its new insertion; the tendon passer spreads the tissues and prevents binding.
- 6.
The neurovascular supply of the transferred muscle must not be damaged while transferring the tendon. The surgeon must be careful to avoid denervating the muscle while freeing it for redirection. When the tendon is pulled up from the distal wound into the proximal incision, traction should not be applied to the origin of the muscle. Stretching of the motor nerve can be prevented by using a double-hand technique: the proximal segment of the tendon is held steady with a moist sponge while traction is applied on its distal segment with another sponge. Acute angulation or torsion of the neurovascular bundle is another cause of injury. Gentle handling is imperative to preserve innervation and function of the transferred muscle.
- 7.
In rerouting of the tendon, a straight line of contraction must be provided between the origin of the muscle and its new insertion. Angular courses and passages over pulley systems should be avoided. To allow adequate freeing of the muscle toward its origin, the incision over the belly of the muscle must be long and proximally located.
- 8.
The tendon should be reattached to its new site under sufficient tension so that the transferred muscle will have a maximal range of contraction. The transferred muscle should be tested during the operation to ensure that it will hold the part in optimal position. In the lower limb, where weight-bearing forces are involved, the tendon is ordinarily attached to bone, whereas in the upper limb it is sutured to the tendon. An important technical detail is scarification of the distal segment of the tendon that is to be anchored to a bone or tendon; this is achieved by excising the sheath and paratenon and “roughening” the tendon by scraping and crosshatching it with a knife. To diminish any tension on the tendon while it is healing, the position of immobilization in a cast should allow the transferred tendon to be in a relaxed attitude. For example, when the flexor carpi ulnaris is transferred to the extensor carpi radialis longus, the tension on the tendon should be sufficient to hold the wrist in 30 degrees of dorsiflexion. However, when the cast is applied, the wrist is immobilized in the overcorrected position of 45 to 50 degrees of dorsiflexion.
Postoperative Care and Training
Postoperative care and training are fundamental to achieving a good result. The following principles, given by Green, should be followed meticulously.
The age of the patient at the time of tendon transfer is an important preoperative consideration. The child should be old enough, preferably older than 4 years, to cooperate in training of the transfer. A delay in tendon transfer in the presence of muscle imbalance leads to progressive deformity. Usually, conservative measures should be undertaken to control deforming factors, but early surgery may be indicated when a delay in tendon transfer would result in increasing structural deformity. A common example is the rapid development of progressive calcaneus deformity of the foot with paralysis of the gastrocnemius-soleus muscles and strong ankle dorsiflexors. An early posterior transfer prevents the development of a deformed foot.
Support of the part in an overcorrected position should be continued until the muscle has assumed full function and there is no tendency for the deformity to recur. A bivalved cast or an orthosis holds the transferred tendon in a relaxed position.
It is best to teach the patient preoperatively to localize active contraction in the muscle to be transferred. Active exercises are continued postoperatively as soon as the reaction to surgery and pain have subsided. The surgeon should assist the physical therapist during the initial exercises. When tendon transfer is combined with arthrodesis, muscle reeducation is delayed until adequate bony union has taken place.
The patient is instructed to contract the transferred muscle voluntarily by moving the part through the arc of motion that was the original normal action of the muscle while the therapist manually guides the part to move in the direction that is intended to be provided by the transfer. For example, when the peroneus longus muscle is transferred anteriorly to the base of the second metatarsal, the active motion called for is eversion in combination with guided dorsiflexion, or if the anterior tibial muscle has been transferred posteriorly to the os calcis, active inversion is combined with guided plantar flexion of the ankle. In anterior transfer of the hamstrings to the patella for quadriceps femoris paralysis, the patient is placed in a side-lying position and asked to extend the hip actively (using the hamstrings) as the knee is guided into extension. If the flexor carpi ulnaris has been transferred to the extensor carpi radialis longus, the wrist is gently guided into extension as the patient turns it in the ulnar direction. With one hand the therapist should palpate the belly and tendon of the transferred muscle to ensure its contraction. In the beginning the exercises are performed in the bivalved cast. Motion of the concerned joint is executed slowly, steadily, and smoothly through as full a range as possible. Soon the limb is taken out of the cast and is properly positioned, and measures are taken to prevent stretching of the tendon out of its resting position.
Occasionally the patient is unable to contract the transferred muscle actively and has difficulty “finding” it. To enable the patient to use the transfer actively and to help in acquiring the feeling desired, the therapist may exert gentle mild tension on the transferred tendon, have the patient shift positions during attempts at active contraction, or advise the patient in the use of corollary motions. If difficulty finding the transfer persists after 2 weeks, electrical stimulation may be used to initiate contraction as the patient attempts to use the muscle. After a few sessions the patient begins to feel the transfer and to contract it voluntarily.
As soon as the patient is able to contract the transferred muscle actively, exercises in the direction of the original action of the muscle are discontinued and only motions in the new function provided by the transfer are performed.
When poor motor strength develops in the transferred muscle (i.e., it can carry the part through the full range of motion with gravity eliminated), the physical therapist instructs one of the parents to perform the exercises with the child. The exercise regimen is supervised by the physical therapist and the surgeon, who check it at weekly or biweekly intervals.
Initially the limb should be retained in the bivalved cast for support, except during the exercise periods. As soon as the motor strength of the transfer becomes “fair,” use of a bivalved cast during the day is gradually discontinued. Controlled activities are permitted to develop function. These activities are permitted sooner in the upper than in the lower limb. The age and dependability of the patient are other considerations. Resistive exercises to develop power are begun whenever the transfer has a normal range of action and is “fair” in strength. It is also important to exercise the antagonistic muscles to prevent disuse atrophy.
The next stage of training is incorporation of the transfer into the new functional pattern. This is particularly important in the lower limb, in which the muscles are concerned with gait. For example, the action of a peroneus transfer may be good in that it can dorsiflex the ankle through a full range and take moderate resistance, yet during locomotion, voluntary control over the transfer may be lost and the patient may walk with a footdrop gait. The transition to walking requires diligent supervision. Of particular importance is the use of crutches, which protect the limb from undue strain and at the same time allow the patient to be taught to use the transfer and to become accustomed to it. First, the patient is asked to take a single step, and the therapist ensures that the muscle contracts and dorsiflexes the ankle. As soon as the transfer functions throughout all the phases of a single step, the walking periods are gradually increased until the normal gait pattern becomes a conditioned reflex.
Orthoses should be used in the postoperative period judiciously and for specific reasons. Orthotic support protects the part and allows early activity. This is indicated particularly when paralysis is extensive, as in myelomeningocele. In a posterior transfer to the os calcis, for example, a plantar flexion–assist orthosis with a dorsiflexion stop at right angles and crutches may be used to assist in developing function in the transfers and prevent stretching. However, standing and walking exercises are also performed without the brace to stimulate function in the transfer. Prolonged use of a bivalved night cast is important to prevent the development of a contractural deformity that would oppose the action of the transfer (e.g., equinus deformity of the ankle in the setting of anterior transfer for dorsiflexion).
From the beginning, daily stretching exercises should be a part of the exercise regimen. Stretching and night support are continued over a long period until full strength has developed in the muscle and balanced function is observed between agonistic and antagonistic muscles with no tendency for recurrence of the original deformity. In fact, the use of stretching and active exercises should be a simple rule of daily living.
Arthrodesis to provide stability and correct osseous deformity may be indicated, particularly in the foot. However, if dynamic balance is established before the development of structural deformity, arthrodesis may be unnecessary. When it is necessary to combine arthrodesis with tendon transfer, muscle reeducation must be delayed until adequate bony union has taken place.
Management of the Hip
Soft Tissue Contracture
The common deformity of the hip secondary to soft tissue contracture consists of flexion, abduction, and external rotation. Several factors must be considered in its pathogenesis. During the acute and convalescent stages of poliomyelitis, the patient lies supine in the so-called frog-leg attitude with the hips flexed, abducted, and externally rotated; the knees are flexed, and the feet are in equinovarus posture. This position is assumed because of spasm of the hamstrings, hip flexors, tensor fasciae latae, and hip abductor muscles and because of the force of gravity acting on the flail lower limbs. Maintenance of the lower limbs in malposture results in permanent shortening of the soft tissues. Contracture of the intermuscular septa and enveloping fasciae occurs first. This can easily be observed at surgery. On sectioning of the contracted fasciae that cover normal muscle fibers and retraction of the cut edges of the fascia 2 to 3 cm, the underlying muscle tissue is found to be in a relaxed condition when it is elevated with tissue forceps. Partially paralyzed muscle becomes shortened because of contracture of the involved fibrosed muscle fibers scattered throughout the normal muscle tissue. Adaptive shortening of normal muscle occurs later. Structural bony deformity develops with growth in the presence of soft tissue contracture and dynamic muscle imbalance.
The iliotibial band (or tract) is the thickened lateral portion of the fascia lata; it is located along the entire lateral aspect of the thigh and extends from the greater trochanteric region to below the knee. Superiorly, the iliotibial band is attached to the iliac crest by three prongs: a middle one through the aponeurosis over the gluteus medius, an anterior one through the tensor fasciae latae, and a posterior one through the gluteus maximus ( Fig. 33.3 ).
Throughout its extent on the lateral aspect of the thigh, the iliotibial tract is continuous on its deep surface with the lateral intermuscular septum, through which it is firmly attached to the linea aspera on the posterior aspect of the femur. At the knee joint level, fascial expansions from the anterior border of the iliotibial tract join expansions that emanate from the quadriceps muscle to form the lateral patellar retinaculum. The lower end of the iliotibial band is attached to the lateral condyle of the tibia and the head of the fibula. Proximally the iliotibial band is located in a plane that is anterior and lateral to the axis of the hip joint, whereas distally in a normal limb the iliotibial tract inserts on the tibia in front of the axis of the knee joint. However, Irwin stated that the lower part of the iliotibial tract lies in a plane posterior and lateral to the axis of the knee joint. Contracture of the iliotibial band may contribute directly or indirectly to development of the deformities described in the following subsections. , , , ,
Lower Limb
Flexion, Abduction, and External Rotation Contracture of the Hip
The shortened iliotibial band, which is in a plane anterior and lateral to the hip joint, draws the femur into flexion and abduction at the hip, with the pelvis as the fixed point. External rotation deformity results from maintenance of the malposture of the frog-leg position. The related muscles—the tensor fasciae latae, reflected head of the rectus femoris, sartorius, and external rotators of the hip—will undergo myostatic contracture if the fascial contracture is not corrected. The fixed soft tissue contracture causes anteversion of the proximal end of the femur.
Flexion and Valgus Deformity of the Knee and External Torsion of the Tibia
The iliotibial band crosses lateral to the axis of the knee. When it is contracted, a force is exerted on the lateral aspect of the joint and the tibia is gradually abducted on the femur. Its deforming action resembles that of a taut string on the concavity of an archer’s bow. Irwin proposed that flexion deformity of the knee develops as a result of the location of the band in a plane posterior to the axis of motion of the knee joint. However, subsequent studies did not support this observation. The short head of the biceps takes its origin in part from the intermuscular septum, which in turn is attached to the iliotibial band. Flexion deformity of the knee develops as a result of spasm and subsequent myostatic contracture of the short head of the biceps. Prolonged maintenance of the knee in flexion causes contracture of the patellar retinacula and soft tissues behind the knee.
External Torsion of the Tibia and Subluxation of the Knee Joint
The pull of the laterally located iliotibial band and the short head of the biceps femoris gradually rotates the tibia and fibula externally on the femur. When the contracture is not controlled, the deforming forces cause posterolateral subluxation of the knee with displacement of the fibular head into the popliteal space.
Positional Pes Varus
Positional pes varus results from an ill-fitted orthosis that fails to compensate for the external tibial torsion. The axes of the knee and ankle joints do not occupy the same horizontal plane in external torsion of the tibia. When an above-knee orthosis manufactured with these joints in the same horizontal plane is fitted to a limb with external tibial torsion, the appliance forces the foot into varus position so that the ankle is in line with the knee joint. Initially, the varus deformity is purely functional (the foot assumes normal alignment when the lateral upright of the orthosis is allowed to rotate externally on the thigh); it later becomes fixed because of permanent shortening of the soft tissues and adaptive osseous changes in the tarsal bones.
Pelvis and Trunk
Pelvic Deformity, Lumbar Scoliosis, and Subluxation of the Contralateral Hip
In abduction deformity of the hip secondary to contracture of the iliotibial band, the pelvis is level with or at a right angle to the vertical axis of the trunk as long as the affected hip is maintained in abduction; however, when it is brought parallel to the vertical axis of the body in the weight-bearing position, the pelvis is forced to assume an oblique position. This pelvic obliquity results from contracture below the iliac crest. Lumbosacral scoliosis, convex to the low side of the pelvis, simultaneously develops. The contralateral hip subluxates.
Exaggerated Lumbar Lordosis
Exaggerated lumbar lordosis is produced by bilateral flexion contracture of the hips. It is a compensatory response to the increased pelvic inclination when the trunk assumes an upright position.
Pelvic Obliquity
Fixed pelvic obliquity is a common deformity after poliomyelitis and may be caused by suprapelvic, intrapelvic, or infrapelvic abnormalities. In an extensive study conducted in Korean patients, pelvic obliquity was classified into two major types and four subtypes relative to the resultant scoliosis. In major type I, the pelvis is lower on the short-leg side, and we recommended ipsilateral abductor fasciotomy and, at times, contralateral lumbodorsal fasciotomy to correct the deformity. In type II deformities, the pelvis is high on the short-limb side as a result of adduction contracture of the ipsilateral hip, abduction contracture of the contralateral hip, or ipsilateral lumbodorsal fascial contracture.
Treatment
Bivalved Casts
Static malpostural deformities of the lower limbs in the acute and subacute stages of poliomyelitis can be prevented by the use of bivalved casts to maintain the joints in neutral position. A horizontal bar in the posterior half of the cast or a rotational strap controls malrotation at the hips. The knees should be in slight flexion to prevent genu recurvatum. Passive exercises are performed to maintain full range of joint motion.
Passive Stretching Exercises
Minimal contracture of the iliotibial band can be corrected by passive stretching exercises, which follow the same steps as in the Ober test. These exercises can also be performed with the patient supine and the hip that is to be stretched hanging over the edge of the bed. In an older patient the iliotibial band can be stretched by the following exercise: the patient should stand sideways approximately 2 feet away from the wall with the hip that is to be stretched placed facing it. With the feet on the ground and the legs together, the hip is brought toward the wall to the count of 10 and is then returned to the original position. This exercise should be performed for 20 repetitions, three times a day.
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