Pediatric Annals

Cervical Spine Injuries in Children

E Shannon Stauffer, MD; John M Mazur, MD

Abstract

INTRODUCTION

The cervical spine in a child is not simply a small adult cervical spine. Its anatomy, physiology, radiographic appearance and response to trauma differ greatly from the mature cervical spine. Some of these differences and the principles of diagnosis and management of cervical spine injuries in children will be discussed here. An understanding of normal development and anatomy is essential to recognize normal developmental variations radiographically and the pathologic anatomic variations created by injuries. The first section of this article will review the embryology and development of the cervical spine. Normal variations and congenital anomalies are often confused radiographically with traumatic injuries. A discussion of common injuries with regard to mechanism of injury, associated physical signs, radiographic findings and treatment recommendations will follow. Finally, section three will be devoted to consideration of rehabilitation and prevention of complications in the pediatric population with residual permanent paralysis.

EMBRYOLOGY, DEVELOPMENT, AND COMMON VARIATIONS OF THE CERVICAL SPINE

The development of the cervical spine can be divided into three stages; the notocord, mesenchymal segmentation, and the ossification of the vertebrae.1 Growth and development is a continuous process and therefore these arbitrary stages overlap. The notocord develops about day IS and at about day 21, segmentation of the mesoderm begins from the occiput and proceeds caudally. These segments fuse and separate again at their centers so that by the time chondrification begins at about six weeks, each vertebra consists of one-half of each of two original adjacent segments (Figure 1).

Each segment consists of a ventral and a dorsal mass. The ventral mass forms a vertebral body while the dorsal mass surrounds the neural tube and forms the neural arch. Disorders of segmentation arise in this early stage of development, since no further changes in position occur during chondrification or ossification.2

Ossification begins during the second month and by the fourth month all the vertebral bodies have ossification centers. In the C-3 through C-7 vertebrae there are three ossification centers per segment (Figure 2), one for the centrum (the body), and one for each half of the neural arch which includes the transverse, costal and spinous processes. Variations of ossification and persistent separate centers may be misinterpreted on radiographs as fractures. The seventh cervical vertebra usually has a separate center of ossification for each costal process, which occasionally does not fuse to the body of the transverse process until the fifth or sixth year. This may remain separate in adult life and form a cervical rib. Complete ossification of the neural arch occurs during the first two years of life. The ossification centers from each side unite posterior to the cord, forming the single spinous process. Six secondary ossification centers appear by the 16th year. These secondary centers fuse with the rest of the vertebrae in the early part of the third decade. Variations of ossification such as persistence of separate ossification centers may occur and be misinterpreted on radiographs as fractures during growth of the child and occasionally in the adult.

The ossification centers of the atlas and axis (C-I and C-2) differ from the lower cervical spine and therefore require special consideration. There are three primary centers in the atlas (Figure 3): one for each lateral mass appears during the seventh week of fetal life, and one for the anterior arch at one year of life. The ossification center for the anterior arch fuses with the anterior end of each lateral mass by the eighth year. The posterior arch fuses by the fourth year. When the ring of C- 1 fails to fuse in any of these three areas it may be…

INTRODUCTION

The cervical spine in a child is not simply a small adult cervical spine. Its anatomy, physiology, radiographic appearance and response to trauma differ greatly from the mature cervical spine. Some of these differences and the principles of diagnosis and management of cervical spine injuries in children will be discussed here. An understanding of normal development and anatomy is essential to recognize normal developmental variations radiographically and the pathologic anatomic variations created by injuries. The first section of this article will review the embryology and development of the cervical spine. Normal variations and congenital anomalies are often confused radiographically with traumatic injuries. A discussion of common injuries with regard to mechanism of injury, associated physical signs, radiographic findings and treatment recommendations will follow. Finally, section three will be devoted to consideration of rehabilitation and prevention of complications in the pediatric population with residual permanent paralysis.

EMBRYOLOGY, DEVELOPMENT, AND COMMON VARIATIONS OF THE CERVICAL SPINE

The development of the cervical spine can be divided into three stages; the notocord, mesenchymal segmentation, and the ossification of the vertebrae.1 Growth and development is a continuous process and therefore these arbitrary stages overlap. The notocord develops about day IS and at about day 21, segmentation of the mesoderm begins from the occiput and proceeds caudally. These segments fuse and separate again at their centers so that by the time chondrification begins at about six weeks, each vertebra consists of one-half of each of two original adjacent segments (Figure 1).

Each segment consists of a ventral and a dorsal mass. The ventral mass forms a vertebral body while the dorsal mass surrounds the neural tube and forms the neural arch. Disorders of segmentation arise in this early stage of development, since no further changes in position occur during chondrification or ossification.2

Ossification begins during the second month and by the fourth month all the vertebral bodies have ossification centers. In the C-3 through C-7 vertebrae there are three ossification centers per segment (Figure 2), one for the centrum (the body), and one for each half of the neural arch which includes the transverse, costal and spinous processes. Variations of ossification and persistent separate centers may be misinterpreted on radiographs as fractures. The seventh cervical vertebra usually has a separate center of ossification for each costal process, which occasionally does not fuse to the body of the transverse process until the fifth or sixth year. This may remain separate in adult life and form a cervical rib. Complete ossification of the neural arch occurs during the first two years of life. The ossification centers from each side unite posterior to the cord, forming the single spinous process. Six secondary ossification centers appear by the 16th year. These secondary centers fuse with the rest of the vertebrae in the early part of the third decade. Variations of ossification such as persistence of separate ossification centers may occur and be misinterpreted on radiographs as fractures during growth of the child and occasionally in the adult.

The ossification centers of the atlas and axis (C-I and C-2) differ from the lower cervical spine and therefore require special consideration. There are three primary centers in the atlas (Figure 3): one for each lateral mass appears during the seventh week of fetal life, and one for the anterior arch at one year of life. The ossification center for the anterior arch fuses with the anterior end of each lateral mass by the eighth year. The posterior arch fuses by the fourth year. When the ring of C- 1 fails to fuse in any of these three areas it may be misinterpreted radiographically as a fracture (Figure 4).

Figure 1. Scheme showing the manner in which each vertebral center is developed from portions of two adjacent segments. (A) The early segmental provertebrae. (B) Fusion of the early segments with formation of the costal process from the caudal portion of the original schlerotome. (C) Segmentation of the vertebra occurs in such a manner that the costal process, the neural arch and its process, and the anterior and posterior longitudinal ligaments are derived from the caudal portion of each prevertebral centrum which shifts backwards to fuse with the cranial half of the provertebra immediately caudal to it. (D) Final adult form.

Figure 1. Scheme showing the manner in which each vertebral center is developed from portions of two adjacent segments. (A) The early segmental provertebrae. (B) Fusion of the early segments with formation of the costal process from the caudal portion of the original schlerotome. (C) Segmentation of the vertebra occurs in such a manner that the costal process, the neural arch and its process, and the anterior and posterior longitudinal ligaments are derived from the caudal portion of each prevertebral centrum which shifts backwards to fuse with the cranial half of the provertebra immediately caudal to it. (D) Final adult form.

There are five primary and two secondary ossification centers in the axis (Figure 5). The odontoid represents the embryological centrum of the atlas. During the sixth month bilateral centers of ossification occur in the odontoid. The summit of the odontoid is formed by a bridge of cartilage. At birth the odontoid is separated from the body of the axis by a cartilaginous line representing the growth plate. This epiphyseal line is present in nearly all children at age three, 50% of children at age four, and closed by age six.3 When open, this growth plate can be misinterpreted radiographically as a fracture. However, most fractures occur at the base of the odontoid, whereas this epiphyseal line lies lower within the body of the axis below the level of the superior articular facets (Figure 6).

Persistent congenital anomalies of the odontoid, such as failure of fusion to the axis, can lead to an unstable atlantoaxial complex with serious potential neurologic sequelae. Paralysis, and even death, may occur due to spinal cord injury or pressure secondary to minor trauma. Several variations of anomalies exist, ranging from aplasia (complete absence) to os odontoidium (apical segment remains separated from the base). The anomalies are relatively rare, but occur more frequently in conditions such as Down's syndrome, Morquio's syndrome, and Klippel-Feil syndrome. A congenital or developmental etiology of these anomalies has always been assumed. Hypoplasia or os odontoidium may be acquired secondary to trauma or infection.4 It is assumed that an insult occurs damaging the growth plate at the base of the odontoid. this insult could compromise the blood supply to the developing odontoid, resulting in either partial or complete absorption. it is thought that failure of fusion of the apex of the odontoid results in os odontoidium (figure 7). the distinction of aplasia or hypoplasia from os odontoidium is somewhat academic, since each of these conditions leads to atlantoaxial instability. these patients may present clinically with neck pain, episodes of weakness following trauma, unexplained spasticity or with signs of brain stem ischemia due to vertebral artery compression, with symptoms of seizures, syncope, vertigo or visual disturbances. treatment of symptomatic patients is cervical fusion of c-i to c-2 by means of posterior wiring and bone graft. considerable controversy exists as to the role of prophylactic stabilization in the asymptomatic patient with radiographic evidence of instability. the safety of stabilization, and with it, the ability to lead a normal, active life, must be weighed against the potential complications of surgery. if there is greater than 5 mm of instability, as seen on lateral flexion /extension radiographs, surgical fusion should be performed in the pediatric population to prevent the possible catastrophic results of acute or chronic spinal cord compression.5

Figure 2. Primary ossification center of typical C-3 through C-7 vertebrae: one for the body and one for each vertebral arch. Secondary ossification centers of a typical C-3 through C-7 vertebrae: two for the bifid spinous process one for each transverse process and ring apophysis.

Figure 2. Primary ossification center of typical C-3 through C-7 vertebrae: one for the body and one for each vertebral arch. Secondary ossification centers of a typical C-3 through C-7 vertebrae: two for the bifid spinous process one for each transverse process and ring apophysis.

Figure 3. Three primary ossification centers of C-1, atlas: the two lateral mass centrums appear during the seventh week of fetal life while the anterior arch appears at the end of one year of life.

Figure 3. Three primary ossification centers of C-1, atlas: the two lateral mass centrums appear during the seventh week of fetal life while the anterior arch appears at the end of one year of life.

in children below the age of eight, there normally exists hypermobility and laxity of the cervical spinal ligaments. this can mimic radiographic evidence of serious cervical injury with ligamentous rupture and apparent dangerous spinal instability. cattell3 found in a study of 160 normal children a 19% incidence of marked subluxation of c-2 on c-3 vertebra (figure 8). this anterior pseudosubluxation can be seen as a loss of normal lordosis on a neutral cervical spine radiograph, or as an anterior displacement (up to 3 mm) of c-2 on c-3 as seen on a flexion /lateral radiograph. the reasons for this normal pseudosubluxation seen only in children are: ligamentous laxity, relative horizontal configuration of the facet joints, lack of the development of the joints of luschka and the anterior wedged configuration of the growing vertebral bodies. as children mature beyond the age of eight, most achieve the adult configuration, and the pseudosubluxation disappears.

children frequently complain of pain in the neck following falls or automobile accidents. physical examination frequently reveals only tenderness, pain on motion of the neck, or muscle spasm, with no other evidence to localize the site of injury. as a result, there is a tendency to rely on radiographic evidence to identify the exact area of an injury to the cervical spine. physicians concerned with diagnosing and treating such injuries should have a thorough knowledge of the normal variations seen during growth and development to avoid misdiagnoses. The frequent pitfalls are: 1) Children with neck pain believed to have traumatic subluxation of C-2 on C-3 vertebra, which is later proven to be a normal range of motion;' 2) Children thought to have fractures of the odontoid process which were later proven to have a vestigial basilar growth plate; 3) Children thought to have fractures of the atlas which fail to heal, and were later found to be failure of fusion of the ossification centers. The limited ability of the child in pain to cooperate in obtaining satisfactory radiographic examinations, including flexion and extension radiographs, frequently compounds the problem. There are no contralateral comparison views which can be obtained to aid in a diagnostic dilemma. Therefore, the recognition of true radiographic abnormality depends upon the thorough knowledge of normal radiographic appearance and developmental variations. The clinical care of a child with a symptom of neck pain, non-specific physical findings, and radiographs that reveal questionable trauma or developmental variations should consist of proper immobilization of the cervical spine and symptomatic treatment and evaluation of the response to that treatment. Rapid remission of symptoms with persistence of the radiographic variation, as a rule, identifies the radiographic finding as a normal variation. Conversely, persistent symptoms and signs such as pain, torticollis, limitation of motion, and muscle spasm associated with a radiographic alteration imply an injury, and the appropriate treatment should be instituted. Following these principles, fewer children are likely to be overtreated, and the more serious error of not treating a true fracture or dislocation can be avoided.

Figure 4. CAT Scan of C-1 in an eight-year-old girl with neck pain secondary to trauma. Note break in anterior ring. Although originally thought to be a fracture, this proved to be a nontraumatic variant, a failure to fuse the primary ossification centers anteriorly.

Figure 4. CAT Scan of C-1 in an eight-year-old girl with neck pain secondary to trauma. Note break in anterior ring. Although originally thought to be a fracture, this proved to be a nontraumatic variant, a failure to fuse the primary ossification centers anteriorly.

Figure 5. Ossification center of the axis: three for the dens and one for each vertebral arch, one for the body and one for the under surface of the body.

Figure 5. Ossification center of the axis: three for the dens and one for each vertebral arch, one for the body and one for the under surface of the body.

Figure 6. Open odontoid radiograph of a child approximately two years of age, demonstrating the persistence of growth plate of the dens (large arrows). This could commonly be confused as a fracture of the dens.

Figure 6. Open odontoid radiograph of a child approximately two years of age, demonstrating the persistence of growth plate of the dens (large arrows). This could commonly be confused as a fracture of the dens.

Figure 7. Open-mouth radiograph showing os odontoidium.

Figure 7. Open-mouth radiograph showing os odontoidium.

FRACTURES AND DISLOCATIONS OF THE CERVICAL SPINE IN CHILDREN

Of primary importance in the evaluation of injuries of the vertebral column is the status of the spinal cord and nerve roots. Care must be taken to avoid injury to the neural elements from the time of the patient's accident until treatment is completed. If any injury to the neural elements exists, the neck must be appropriately immobilized, and the exact nature of the neurologic disturbance interpreted accurately and quickly. Treatment is aimed at restoring a stable spine free of pain with normal function.

Vehicular accidents account for the majority of the injuries to the cervical spine. Most commonly, at vehicular impact the child passenger is hurdled forward through the interior of the car, striking headfirst against the auto's interior. The type of fracture or dislocation depends upon the forces and position of the head-neck-body complex at the time of this second impact. Cervical injuries to children also occur as a result of diving or falls on the head. Obstetrical injuries have been reported in difficult deliveries resulting in atlanto-occipital separations, odontoid fractures, and transsections of the spinal cord. The upper cervical spine is not resistant to major torsional stresses under these circumstances, and the injury occurs proximal to the tethering of the large brachial plexus nerve roots. Similar types of injuries may occur in infancy and early childhood with violent manual shaking. The heavy, infantile head is poorly supported by weak cervical musculature, and the upper cervical spine is highly vulnerable to the repeated shaking as occurs in a battered child syndrome.6-9

If a cervical spine or spinal cord injury is suspected during the evaluation of an injured child, all efforts should be made to provide emergency management which prevents further spinal cord injury. The well-known priorities of cardio-respiratory resuscitation should be followed, with maintenance of an adequate airway assuming priority. Careful evacuation of the child from the site of trauma and transportation to a medical facility may avoid permanent paralysis and life-long catastrophic disability. In handling such a child, the spine must be kept in neutral alignment, preventing flexion, extension, or rotation of the neck. The supine position is preferable on a firm board with rolls of towels, sheets or blankets, or sandbags beside the head to prevent rotation. Once the child arrives at the emergency ward, the neck can be better immobilized by gentle head-halter traction, which maintains the normal alignment of the head with the body. Undressing the child is undesirable, since it may require manipulative movement in undesirable directions. Open wounds should be dressed and extremity fractures splinted. Determination of a cervical spine and /or spinal cord injury should then be assessed by means of appropriate physical and radiographic examination. Careful attention must be paid to prevent further injury to the cord during the radiographic examination; therefore, only lateral and anterior/ posterior films are taken initially. If a fracture or dislocation exists as documented by the radiograph, the spine should be stabilized with a brace or traction. If no obvious injury of the cervical spine is seen radiographically, then the spine may be gently positioned for a complete series of radiographs, including obliques and open-mouth views. Treatment will depend upon the type of injury. If no injury is seen radiographically, then gentle active flexion and extension lateral radiographs are taken to assess ligamentous stability.

Figure 8. Demonstration of pseudoSubluxation of C-2 on C-3.

Figure 8. Demonstration of pseudoSubluxation of C-2 on C-3.

Figures. (A) Open-mouth radiograph of 1 1-year-old boy involved in an automobile accident. Arrows demonstrate spread of lateral masses of C-1. (B) CAT Scan of same fracture.

Figures. (A) Open-mouth radiograph of 1 1-year-old boy involved in an automobile accident. Arrows demonstrate spread of lateral masses of C-1. (B) CAT Scan of same fracture.

Figure 10. Patient with Jefferson fracture demonstrated in Figure 9 being treated in a halo-cast.

Figure 10. Patient with Jefferson fracture demonstrated in Figure 9 being treated in a halo-cast.

Fractures of the atlas (Figure 9) occur in children either by a fall or direct blow on the head, or in an automobile accident where the head strikes the car's interior. Sir Geoffrey Jefferson described this fracture, postulating the mechanism of injury to be a vertical force applied alongthe axis of the spine with the force being dissipated on the relatively weak atlas.10 The patients with this injury usually present with a severe headache, with pain being referred along the course of the greater occipital nerve. Marked rigidity of the neck with limitation of motion, especially rotation of the neck, is frequently found associated with marked muscle spasm. Neurological findings are seldom present. Treatment of this fracture in childhood should be immobilization in a Minerva jacket (body cast including the head) or a halo-cast11 (Figure 1 0). These fractures usually heal without complications and surgery is rarely indicated.

In children, fractures of the odontoid with displacement almost always occur at the level of the growth plate between the odontoid and the axis vertebral body, with the odontoid displaced anteriorly. A transoral radiograph is of little value, particularly when the child is apprehensive and in pain, so that a good lateral view should usually suffice in making the diagnosis. I2 The anteriorly displaced odontoid process can almost always be easily reduced by gentle manipulation into extension with traction. The reduction can be held with either a halo-cast or Minerva cast until healing occurs.13'14 Prompt healing generally occurs, offering a good prognosis; however, the odontoid fracture may not be totally benign if initially unrecognized. There are reported cases in which the injury to the odontoid was not recognized and resorption of the basilar portion of the odontoid occurred, producing the appearance of the absent odontoid, or an os odontoidium.4 Late atlantoaxial instability may thus complicate even minimally displaced odontoid process fractures because of resorption of all or part of the odontoid process. Followup of these patients with periodic radiographic evaluation is necessary until stability is assured.

Figure 11. Patient with atlantoaxial rotatory displacement demonstrating the "cock-robin" position.

Figure 11. Patient with atlantoaxial rotatory displacement demonstrating the "cock-robin" position.

Figure 12A: Tomogram of patient seen in Figure 11, demonstrating the medial and lateral offset of the lateral masses.

Figure 12A: Tomogram of patient seen in Figure 11, demonstrating the medial and lateral offset of the lateral masses.

Figure 12B: CAT Scan of patient seen in Figure 12A, demonstrating the rotatory displacement with the absence of any anterior displacement of C-1 on C-2.

Figure 12B: CAT Scan of patient seen in Figure 12A, demonstrating the rotatory displacement with the absence of any anterior displacement of C-1 on C-2.

Atlantoaxial rotary displacement is one of the most common causes of childhood torticollis, yet the diagnosis is commonly delayed or missed because of a lack of understanding of the underlying pathology. This is predominantly a lesion of childhood. The onset may be spontaneous, or it may follow an upper respiratory infection or be caused by minor or major trauma. The torticollis position is typically similar to that of a robin listening for a worm (Figure 11), or the "cock-robin" position. The head is tilted to one side and rotated to the opposite side with slight flexion. The child resists attempts to move the head, complaining of marked pain with any passive attempts to do so. Associated muscle spasm is on the side to which the chin points, since these muscles are attempting to correct the deformity. This is unlike spasmodic muscular torticollis, which has the muscle spasm on the side away from which the chin points, since the muscle spasm in spasmodic torticollis causes the rotatory deformity. Neurologic findings are rarely present in atlantoaxial rotary displacement.

Rotary displacement of C 1-2 is often difficult to identify radiographically, due to the difficulty in positioning the child with pain and rotational deformity. The diagnosis should be suspected if, in an open-mouth anterior/ posterior radiograph (Figure 12), the lateral mass of C-I has rotated forward, appearing to be wider and closer to the midline (medial offset), while the opposite lateral mass is narrower and away from the midline (lateral offset). Tomograms and CAT scans are often helpful, but a cineradiograph offers the only sure way to make the diagnosis. On the lateral projection the cineradiograph demonstrates the axis and atlas move as a unit with rotation.

The treatment of atlantoaxial rotary displacement must be tailored to the degree of seventy of the individual case. If complaints are mild and there is a simple rotary displacement without anterior shift (Figure 12B), the child may be treated with a cervical collar and analgesic medication (Figure 13). Moderately severe cases may require a period of halter traction. If no anterior displacement is demonstrated, support need only be continued until symptoms have subsided. If the atlas is displaced anteriorly on the axis, immobilization should be continued for six weeks to allow ligamentous healing to occur. Careful followup is necessary in these patients because of potential permanent atlantoaxial instability. These deformities rarely become fixed, but if they do, a fusion of C-2 to C- 1 may be indicated if there is anterior C1 facet dislocation causing compromise of the neural canal by the arch of C-I.

Injuries of the lower cervical spine may occur at all ages in the pediatric population. Obstetrical trauma may cause serious injuries.15 Most birth injuries result from breech presentations with excessive traction being applied, producing either meningeal bleeding, spinal cord lesions, nerve root tears or disruption of the vertebral arteries. Intrauterine hyperextension of the head in breech deliveries carries a particularly poor prognosis, with 25% of such patients developing a significant degree of neurologic deficit.15 If diagnosed prenatally, these children should be delivered by Cesarean section.

Figure 13. Same patient as Figure 11, demonstrating complete resolution with treatment in Philadelphia collar.

Figure 13. Same patient as Figure 11, demonstrating complete resolution with treatment in Philadelphia collar.

The osseous pathologic change in lower cervical spine lesions in infants and young children is less significant than the degree of neural injury. Quadriplegia may occur in patients with negative cervical spine radiographs, including negative myélographie studies. The spinal cord is more likely to be damaged by torsion or longitudinally applied forces permitted to act on the weak muscles and supporting soft tissues of children. Radiographs may appear normal in the face of serious injury, as the fractures may occur in the cartilaginous zones between the end plates and the primary ossification centers, producing serious cervical instability. Treatment of fractures or dislocations of the lower cervical spine should consist of reduction of the fracture or dislocation with skeletal traction and then stabilizing the spine in a halo-cast or body cast to include the head (Figure 14). Surgical stabilization is rarely required in children, as stability is restored by bony healing if the neck is held in the reduced position. Unstable fractures and dislocations occur more frequently in the older pediatric population. The adolescent cervical spine responds more like the adult spine to trauma, and, therefore, may suffer fractures and ligamentous disruptions leading to instability and may require surgical stabilization. Teenage children who suffer pure unilateral or bilateral facet dislocations with complete posterior ligamentous rupture frequently will require internal posterior interspinous process wiring and fusion to provide stability. External immobilization and ligamentous healing by scar frequently leads to persistent flexion-extension instability. These patients may develop progressive kyphotic deformities and late onset neurologic changes. The indications for early surgical treatment in fractures and dislocations of the lower cervical spine include: 1) Inability to reduce a unilateral or bilateral facet dislocation with an existing neurological deficit. These patients should have an open reduction performed through the posterior approach if a sufficient trial of traction has not been effective in reducing the dislocated facets; and 2) An incomplete spinal cord lesion demonstrating a progressive neurologic deficit may be due to an epidural hematoma, or interposition of bone fragments in the spinal canal, and warrants posterior exploration. If a laminotomy or complete laminectomy is performed, fusion with bone grafting over the lateral facet joints should be performed. The treatment of fractures and fracture dislocations in the lower cervical spine in children should not include multiple level laminectomies. These routinely result in progressive late kyphotic deformities and have not been proven to improve neurologic function.10

Figure 14. A 12-year-old girl with a fractured C-7 in body cast including the head.

Figure 14. A 12-year-old girl with a fractured C-7 in body cast including the head.

REHABILITATION AND LONG TERM MANAGEMENT OF THE CHILD WITH CERVICAL SPINAL CORD INJURY

Prognosis and realistic planning for the future of the child with a cervical spinal cord injury is based on an accurate neurologic assessment. If paralysis is present, the first phase of examination is to ascertain whether the injury to the spinal cord is a complete or an incomplete transverse lesion.17 Cord concussion may result in temporary paralysis followed by a rapid return of function. This temporary loss may last for several minutes to several hours. More serious injuries which cause incomplete motor and sensory transverse lesions may demonstrate progressive recovery over a long period of time. During the initial evaluation perianal sensation and voluntary toe flexion or sphincter control may be the only evidence that there is neural transmission across the injured area of the spinal cord, thereby classifying the injury as incomplete. The prognosis of incomplete injuries cannot be accurately predicted, as recovery may vary from little functional recovery to complete recovery, depending upon the individual case. If there is complete motor paralysis and absolute absence of sensation in the extremities below the level of injury and perianal sacral area, the injury is diagnosed as a complete transverse lesion. If this complete loss persists for 24 hours from the time of injury, one can expect no future improvement in spinal cord transmission of impulses across the injured segment to provide return of functional muscle power distal to the injury. Immediately following a severe spinal cord injury, the patient may be in a state of neural spinal shock, manifested by flaccid paralysis and complete loss of all reflexes. Spinal shock may last for several hours to several days, but in most instances lasts less than 24 hours. The earliest evidence of the end of the spinal shock period is the appearance of the bulbocavernosus reflex. With a gloved finger in the rectum, the examiner squeezes the glans penis or clitoris simultaneously, feeling a contraction of the anal sphincter. If the reflex is absent, the patient is still in spinal shock. If the reflex is present and there is no evidence of voluntary motor power or sensory perception around the perianal area, spinal shock is over and the patient has a confirmed, complete lesion.

The management of a patient with a traumatic quadriplegia is based on his altered functional physiology and the remaining voluntary muscle power. The child can be expected to have a normal intellect with full control of cranial nerves, head-neck, and voluntary muscles of the upper extremity above the level of the lesion. The involuntary functions of the cardiovascular, gastrointestinal, urinary tract and endocrine systems continue by reflex activity mediated by the spinal cord centers, altered only by the loss of the inhibitory and coordinating impulses from the higher cerebral centers. The goal of treatment is to prevent medical complications secondary to the altered physiology and to develop the remaining functional muscle power to return the child to as near a normal lifestyle as possible. This requires a coordinated, comprehensive program addressing the realistic physical, psychological and educational objectives based on residual motor function.

The normal physiology of most organ systems is altered by a spinal cord lesion. There are several serious complications which, if not prevented, may at least inhibit rehabilitation or, at most, be fatal. The complication which causes the most difficulty during the first week following a spinal cord injury is pulmonary atelectasis and pneumonia. The quadriplegic patient has only the diaphragm with which to breathe, providing only voluntary inhalation and passive exhalation. With paralysis of the abdominal muscles and intercostal muscles, the patient cannot voluntarily exhale, cough, or sigh. Aggressive, preventive respiratory therapy consisting of intermittent positive pressure breathing of humidified air is necessary to prevent recurring atelectasis and pneumonia during the first several weeks.

The patient's anesthetic skin requires diligent nursing care and observation to protect it from pressure necrosis and ulceration. Frequent log rolling from the supine to the lateral position and bridging of bony prominences with pillows is necessary to prevent pressure sores until the patient's cervical spine is stable to allow sleeping in the prone position. Constant vigilance is necessary to detect early red marks as a sign of impending pressure sores, and these areas must be carefully bridged to remove all pressure while the patient is in bed. As the patient is mobilized to the sitting position in the wheelchair, the accurately measured wheelchair must be prescribed, along with an appropriate seat cushion designed to minimize constant pressure over the bony prominences of the ischial tuberosities and femoral trochanters.

The paralyzed bladder must be aseptically drained with intermittent catheterization until a reflex emptying program is established. A baseline intravenous pyelogram and pharmacologic manipulation of sphincter detrusor muscle imbalance will usually result in automatic reflex emptying of the bladder, and its capacity should not be allowed to be greater than 400 or 500 milliliters, with residual bladder urine following reflex emptying not more than 100 milliliters. An annual intravenous pyelogram is necessary to monitor progressive, occult, possibly fatal conditions, such as hydroureter and hydronephrosis. The goal of the rehabilitation program is to attain the child's maximum physical, psychological and developmental potential and to return him to the community as an active member of the family unit. This requires a health team, including a pediatrician, urologist, and an orthopaedist, as well as rehabilitation nurses, respiratory therapists, physical therapists, occupational therapists, medical psychologist, medical social worker and an orthotist. The central theme of each team member's responsibility is education of the child and parents regarding the potential abilities of the child and prevention of the potential medical complications.

The long term management of the child with a cervical spinal cord injury requires periodic followup of physical capabilities and monitoring to prevent complications. Severe spasticity may restrict joint motion and cause significant deformity and disability. Joint contractures must be prevented by knowledgeable range of motion exercises by the child and parents. Spinal deformity, particularly scoliosis, develops in almost every child who suffers a quadriplegia prior to the age of 10. Preventive bracing of the spine is difficult due to the muscle paralysis and potential of pressure sores on the anesthetic skin; however, body jackets can be used to provide spinal stability unless a progressive curvature occurs which cannot be controlled with orthotics. Many of these patients will require spinal instrumentation and fusion to correct a progressive paralytic scoliosis.

Since these children have a normal intellect, it is preferable to provide rehabilitation services with the aim of discharging the child home to the care of his family, rather than to permanent institutionalization in a nursing home. The latter almost always leads to progressive deterioration of physical function, psychological deterioration, and major medical complications resulting in early demise of the patient.

Along with reintegration of the paralyzed child into the family, it is important to reintegrate him into the normal school activity in regular school. Home-bound tutoring and education in classes for the handicapped which frequently are geared for the mentally retarded and learning disabled child do not provide the education that the quadriplegic child needs to compete for college entrance and vocational or professional training to become an independent adult.

After successful management of the unstable injured spine and rehabilitation of the quadriplegic resulting in reintegration into home and school, annual outpatient révaluations are necessary for constant vigilance to prevent deterioration of kidney function, progressive spinal deformity and the occurrence of pressure sores. This care and support, along with psychological support for the child and family, will help the paralyzed child mature into a healthy adult, as independent as possible, based on his abilities rather than his disability.

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