Spinal Cord Injuries
Spinal Cord Injuries
OBJECTIVES:
By the end of this lecture, the student will be able to:
1. Identify etiologic factors involved in traumatic and non-traumatic spinal cord injuries (SCI).
2. Describe the clinical features following damage to the spinal cord.
3. Describe the potential secondary complications associated with SCI.
4. Identify the anticipated functional expectations for spinal cord patients at various lesion levels.
5. Describe appropriate assessment and treatment procedures of both acute and chronic phases of management.
Introduction:
Spinal cord injury (SCI) has been identified as a low-incidence, high-cost disability requiring tremendous changes in the patient's lifestyle.
Etiology:
Spinal cord injuries can be divided into two main etiological categories; traumatic and non-traumatic injuries. Traumatic SCI are the most common, which may result from motor vehicle accident, fall or gunshot wound. Non-traumatic injuries may be due to tumors, transverse myelitis and vascular causes.
Functional classification of spinal cord injuries: [pic]
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Spinal cord injuries are divided typically into two broad functional categories; quadriplegia and paraplegia. "Quadriplegia" refers to partial or complete paralysis of all four extremities and trunk, including respiratory muscles. It results from lesion of the cervical cord. "Paraplegia" refers to partial or complete paralysis of both lower extremities with or without trunk involvement. It results from lesion of the thoracic or lumber cord or sacral roots.
|[pic] |[pic] |
|Quadriplegia |Paraplegia |
Designation of lesion level:
The most commonly used method to determine the level of SCI is to indicate the most distal uninvolved or partially involved nerve root i.e. the power of muscles supplied by that root is at least grade 3+ according to manual muscle testing.
Classification of SCI according to the severity of the lesion:
* Complete lesion:
It is characterized by loss of sensory and motor functions below the level of lesion. It is caused by complete transaction, severe compression or extensive vascular impairment of the cord.
* Incomplete lesion:
It is characterized by preservation of some sensory or motor functions below the level of injury. Preservation of function indicates that some viable neural tissue is crossing the area of the injury to more distal segments. Incomplete lesions often result from contusions produced by pressure on the cord from displaced bone and/or soft tissues or from swelling within the spinal canal.
Clinical picture:
- Spinal shock:
Immediately following SCI, there is a period of a-reflexia. It results from abrupt withdrawal of connections between higher centers and the spinal cord. It is characterized by absence of all reflex activity, flaccidity and loss of sensation below the level of lesion.
- Motor deficits and sensory loss:
Following spinal cord injury, there will be either complete or partial loss of muscle function below the level of the lesion. Disruption of the ascending sensory fibers following SCI results in impaired or absent sensation below the lesion level. The clinical presentation of motor and sensory deficits is dependent on the specific features of the lesion. These include the neurologic level, the completeness of the lesion, the symmetry of the lesion (transverse or oblique) and the presence or absence of sacral sparing.
- Impaired temperature control:
After damage to the spinal cord, the hypothalamus can no longer control cutaneous blood flow or level of sweating. This autonomic (sympathetic) dysfunction results in loss of internal thermoregulatory responses. The ability to shiver is lost; vasodilatation does not occur in response to heat nor vasoconstriction in response to cold.
- Respiratory impairment:
Respiratory dysfunction varies depending on the level of the lesion. In lesions between Cl and C3, phrenic nerve innervation and spontaneous respiration are significantly impaired or lost. An artificial ventilator or phrenic nerve stimulation is required to sustain life. In contrast, lumber lesions present with full innervation of both primary (diaphragm) and secondary (neck, intercostals and abdominal) respiratory muscles. All patients with quadriplegia and those with high level paraplegia demonstrate some compromise in respiratory function. The level of respiratory impairment is directly related to the lesion level and the residual respiratory muscle function.
Patients with a complete lesion at C4 will have loss of vasomotor control. As a result of paralysis of the vasoconstrictors, there is a marked vasodilatation. This causes blockage of the nasal air passages, which adds to the difficulties of respiration. This phenomenon is known as "Guttmann's sign".
Spasticity:
Spasticity results from release of intact reflex arcs from the central nervous system control and is characterized by hypertonicity, hyperactive stretch reflexes and clonus. It typically occurs below the level of lesion after spinal shock subsides. There is a gradual increase in spasticity during the first six months and usually reaches a plateau one year after injury. It is increased by multiple internal and external stimuli, including positional changes, cutaneous stimuli, environmental temperatures, tight clothing, bladder or kidney stones, catheter blockage, urinary tract infections and emotional stress. Spasticity varies in degree of severity.
- Bladder dysfunction:
The effect of bladder dysfunction following SCI is a serious medical complication, requiring consistent and long-term management. Urinary tract infection (UTI) is the most frequent medical complication during the initial medical/rehabilitation period. During the stage of spinal shock, the bladder is flaccid. All muscle tone and bladder reflexes are absent. Medical considerations during this period are focused on establishing an effective system of drainage and prevention of urinary retention and infection.
The spinal integration center for micturation is the conus medullaris. Primary reflex control originates from the sacral segments of S2,3,4. Following spinal shock, one of two types of bladder conditions will develop, depending on location of the lesion. Patients with lesions that occur within the spinal cord above conus medullaris typically develop a reflex neurogenic bladder. Following a lesion of the conus medullaris or cauda equina, an autonomous, or non-reflex neurogenic bladder develops. Reflex (upper motor neuron) bladders reflexly empty in response to a certain level filling pressure. The reflex arc is intact. Autonomous or non-reflex (lower motor neuron) bladders are essentially flaccid because there is no reflex action of the detrusor muscle.
Secondary complications:
1. Pressure sores:
Pressure sores are ulcerations of skin or subcutaneous tissue, caused by unrelieved shearing forces. They are subject to infection which may migrate to bone. It is a major cause of delayed rehabilitation and may lead to death. Impaired sensory function and the inability to make appropriate positional changes are the most important factors in the development of pressure sores. Other factors include:
a) Loss of vasomotor control, which lowers tissue resistance to pressure.
b) Spasticity, with resultant shearing forces between bony surfaces.
c) Skin maceration from exposure to moisture (e.g. urine).
d) Nutritional deficiencies as low serum protein and anemia.
e) Secondary infections.
2. Autonomic dysreflexia:
Autonomic dysreflexia (hyper-reflexia) is a pathologic autonomic reflex that occurs in lesions above T6 (above sympathetic outflow). This clinical syndrome produces an acute onset of autonomic activity from noxious stimuli below the level of the lesion. Afferent input from these stimuli reach the lower spinal cord areas, initiating a mass reflex response, resulting in elevation of blood pressure. Normally, the impulses stimulate the receptors in the carotid sinus and aorta, which signal the vasomotor center to readjust peripheral resistance. Following SCI, impulses from the vasomotor center can not pass the site of the lesion to counteract the hypertension. Owing to lack of inhibition from higher centers, hypertension will persist if not treated promptly. The most common stimuli for this pathologic reflex are bladder or rectal distention, pressure sores, urinary stones, bladder infections and noxious cutaneous stimuli. [pic]
3. Postural hypotension:
Postural hypotension is a decrease in blood pressure, which occurs when a patient is moved from a horizontal to a vertical position. It is caused by a loss of sympathetic vasoconstriction control. The problem is enhanced by lack of muscle tone, causing peripheral venous blood pooling. Reduced cerebral flow and decreased venous return to the heart also may occur. In many patients who are immobilized for up to 6 to 8 weeks, episodes of postural hypotension are a fairly common occurrence during early progression to a vertical position. They tend to occur more frequently with lesions of the cervical and upper thoracic regions. Patients will often describe the onset as feelings of dizziness, faintness or impending "blackout". Although the exact mechanism is not clearly understood, the cardiovascular system, over time, gradually reestablishes sufficient vasomotor tone to allow assumption of the vertical position.
4. Heterotopic (Ectopic) bone formation:
Heterotopic bone formation is osteogenesis in soft tissues below the level of the lesion, which is of an unknown etiology. However, multiple theories have been proposed, including tissue hypoxia secondary to circulatory stasis, abnormal calcium metabolism, local pressure and micro trauma related to aggressive range of motion exercises. Heterotopic bone formation is always extra-articular and extra-capsular. It may develop in tendons, in connective tissue between muscles or in the peripheral aspects of muscle. It must be differentiated from myositis ossificans, which results from injury to a muscle and is characterized by bony deposits within muscle tissue. No relationships have been found between the development of heterotopic bone formation and level of injury, amount of exercise or degree of spasticity or flaccidity. Heterotopic bone formation typically occurs adjacent to large joints, with the hips and knees most commonly involved. Other joints include the elbows, shoulders and spine. Early symptoms of heterotopic ossification resemble those of thrombophlebitis, including swelling, decreased range of motion, erythema and local warmth near a joint.
5. Contractures:
Contractures develop with prolonged shortening of structures across and around a joint, resulting in limitation in motion. Contractures initially produce alterations in muscle tissue but rapidly progress to involve capsular and pericapsular changes. Factors place the patient with SCI at risk for developing joint contractures are lack of muscle function, flaccidity, spasticity, faulty positioning, ectopic bone formation and imbalances in muscle pull.
The hip joint is particularly prone to flexion, internal rotation and adduction. The shoulder may develop flexion or extension, depending on early positioning. Both patterns at the shoulder are associated with internal rotation and adduction.
6. Deep venous thrombosis (DVT):
Deep venous thrombosis (DVT) results from development of a thrombus (abnormal blood clot) within a vessel. It has the potential to break free of its attachment and float freely within the venous blood stream. Such mobile clots are known as emboli. They may block pulmonary vessels and result in death. In SCI, DVT is due to loss of the normal pumping mechanism provided by active contraction of lower extremity musculature. This slows the flow of blood, allowing higher concentrations of pro-coagulants (thrombin) to develop in localized areas.
Prognosis:
The potential for recovery from SCI is directly related to the extent of damage to the spinal cord and/or nerve roots. There are three main factors that affect potential for recovery: (1) the degree of pathologic changes imposed by the trauma. (2) The precautions taken to prevent further damage during rescue. (3) prevention of additional compromise of neural tissue from hypoxia and hypotension during acute management.
Formulation of a prognosis is initiated after spinal shock has subsided and is guided by whether or not the lesion is complete. Following spinal shock, a lesion is generally considered complete in the absence of any sensory or motor function below the level of damage. With incomplete lesions some evidence of sensory and/or motor function is noted below the level of the lesion after spinal shock subsides. The rate of recovery will decrease, and a plateau will be reached. When the plateau is reached; and no new muscle activity is observed for several months, no additional recovery can be expected in the future.
MANAGEMENT
Acute Phase
It starts from the onset of injury until the fracture site is stable and upright activities can be initiated.
I- Emergency Care
Management of SCI begins at the location of the accident. Techniques used in moving and managing the patient immediately following the trauma can influence prognosis significantly. When a spinal injury suspected, efforts should be made to avoid both active and passive movements of the spine by strapping the patient to a spinal back board, use of a supporting cervical collar, and assistance from multiple personnel in moving the patient safely. On arrival at the emergency room, initial attention is focused on stabilizing the patient medically. Attention is directed toward preventing progression of neurologic impairment by restoration of vertebral alignment and early immobilization of the fracture site.
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II – Fracture stabilization
Cervical Injuries
Immobilization of unstable cervical fractures is achieved via skeletal traction. Traction can be applied by use of tongs attached to the outer skull from supine lying position (Fig. 1).
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|Fig.(1):Cervical Tongs. | |
Thoracic and Lumber Injuries
Fractures of these sites are immobilized through bed rest or by application of a body cast or jacket .The expanded use of spinal orthotics also allows earlier mobility activities.
III - Surgical Intervention
Surgery may be indicated to restore bony anatomic alignment, to prevent further damage to the cord and to stabilize the fracture site. Compared with spontaneous healing times, surgical stabilization allows earlier initiation of rehabilitation activities.
Surgical interventions for cervical fractures include decompression and fusion by bone grafting. Frequently, surgery for thoracic and lumbar injuries requires use of an internal fixation device, which may be used in combination with bone grafts. The patient is immobilized by spinal orthosis after surgery for at least 3 months.
IV – Physical therapy assessment
• Respiratory assessment (muscle strength of intercostals; diaphragm; and abdominals, chest expansion, breathing pattern, and cough).
• Skin assessment: Skin inspection combines both visual observation and palpation. Particular attention should be paid to areas most susceptible to pressure. Patient education related to skin care is crucial and should be initiated early.
• Sensory assessment: Superficial and deep sensations are fully assessed.
• Tone and deep reflexes.
• Manual muscle testing and ROM test: Caution should be taken when resisting shoulder muscles in cervical injuries i.e. quadriplegia and around lower trunk and hip in paraplegia.
• Functional assessment.
V – Physical Treatment
1. Respiratory management and Skin care.
2. ROM and positioning: Full ROM should be completed daily except for those areas that are contraindicated. With paraplegia, SLR greater than 60 degrees or hip and knee flexion more than 90 degrees are avoided. With quadriplegia movement of the head and neck or stretching of shoulder should be avoided.
3. Selective strengthening: All remaining muscles should be maximally strengthened. Stress at fracture sites is avoided e.g. musculature around shoulder and scapula in quadriplegia and those of the hip and trunk in paraplegia. Bilateral exercises are carried out for upper extremities to avoid rotational stresses on the spine.
4. Orientation to the vertical position after radiographic stability of the fracture site. Gradual acclimation to upright posture is effective with the use of abdominal binder to prevent venous pooling.
5. Bladder training programs: The primary goal of bladder training is to allow the patient to be free from a catheter and to control bladder function.
Automatic bladder, intermittent catheterization is the most frequently used program. Its aim is to establish reflex bladder emptying at regular and predictable intervals in response to a certain limits of filling. It involves restricted fluid intake to 2000 ml/day. It is taken about 150 – 180 ml/hour from morning to early evening. Initially the patient is catheterized every 4 hours before which the patient should try to void bladder by one of the manual techniques (such as stroking, kneading, or tapping the surapubic region or thigh and lower abdominals). Calculation of the residual and voided urine volumes should be recorded. As bladder emptying becomes more effective, the residual volume decreases and time interval between catheterization is expanded.
Autonomous bladder, one of the previously mentioned techniques can be used to help voiding. In addition, give strengthening exercises to lower abdominals, pelvic floor and glutei muscles. Interferential and faradic stimulation are of great benefit in such cases. Finally, in sensory atonic bladder, pulling of pubic hair or allowing the patient to listen to the sound of water will increase the sensory awareness of bladder fullness.
Subacute Stage
All the assessment procedures performed during the acute stage will be continued with completion of all avoided muscle testing and ROM.
Physical therapy management
a) Emphasis will remain on respiratory management, ROM exercises and positioning.
b) Resisted exercises for all innervated muscles especially shoulder depressors that will help in independent transfer. Different methods can be used such as PNF, progressive resisted exercises, weights, dumbles, pulley system and suspension therapy. Also before encountering patient into ADL training, balance and endurance exercises are stressed.
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c) ADL training includes bed and mat activities, transfer, wheel chair activities, and exercises in between parallel bars.
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d) Gait training with or without walking aids such as walkers, crutches either elbow or axillary or cane. Patients who become functionally ambulators are those whose trunk muscles (abdominals and erector spinae) are at least grade fair. Full hip extension ROM is essential in attaining balance in upright position.
Gait expectations of complete paraplegics:
Above T10 ----------- Swing to gait.
T10 – L1 -------------- Four point gait.
Below L1 ------------- Swing through gait.
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e) Elevation activities: The easiest pattern of ascent is with stairs backward to the patient and descent with stairs forward.
f) Training for controlled falling.
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