C Spinal cord injuries
Spinal cord transection is the description of spinal cord injury that is manifested as paralysis of the lower extremities (paraplegia) or of all extremities (quadriplegia). Spinal cord transection above the level of C2 to C4 is incompatible with survival because innervation to the diaphragm is likely to be destroyed.
The most common cause of spinal cord transection is the trauma associated with a motor vehicle or diving accident that results in fracture dislocation of cervical vertebrae. Occasionally, rheumatoid arthritis of the spine leads to spontaneous dislocation of the C1 vertebra on the C2 vertebra, producing progressive quadriparesis. These patients can suddenly become quadriplegic. The most frequent nontraumatic cause of spinal cord transection is multiple sclerosis. In addition, infections or vascular and developmental disorders may be responsible for permanent damage to the spinal cord.
2. Preoperative assessment
Spinal cord transection initially produces flaccid paralysis with total absence of sensation below the level of injury. Temperature regulation and spinal cord reflexes are lost below the level of injury. The phase after the acute transection of the spinal cord is known as spinal shock and typically lasts 1 to 3 weeks. Several weeks after acute transection of the spinal cord, the spinal cord reflexes gradually return, and patients enter a chronic stage characterized by overactivity of the sympathetic nervous system and involuntary skeletal muscle spasms. Mental depression and pain are pressing problems after spinal cord injury.
a) History and physical examination
(1) Cardiovascular: Electrocardiograph abnormalities are common during the acute phase of spinal cord transection and include ventricular premature beats and ST–T-wave changes suggestive of myocardial ischemia. Decreased systemic blood pressure and bradycardia are also common secondary to a loss of sympathetic tone. Generally, this condition can be treated effectively with crystalloid and colloid infusion vasopressor and atropine to increase the heart rate. Around 85% of patients with spinal cord transection above T6 exhibit autonomic hyperreflexia, a disorder that appears after the resolution of spinal shock and in association with the return of the spinal cord reflexes.
(2) Respiratory: A transection between the levels of C2 and C4 may result in apnea from denervation of the diaphragm. The ability to cough and clear secretions from the airway is often impaired because of decreased expiratory reserve volume. Vital capacity also is significantly decreased if the transection of the spinal cord is at the cervical level. Furthermore, arterial hypoxemia is a consistent early finding during the period after cervical spinal cord injury. Tracheobronchial suctioning has been associated with bradycardia and cardiac arrest in these patients secondary to vasovagal reflex, a finding emphasizing the importance of establishing optimal arterial oxygenation before undertaking this maneuver. Acute respiratory insufficiency and the inability to handle oropharyngeal secretions necessitate immediate tracheal intubation. Before intubation is initiated, the neck must be stabilized.
(3) Neurologic: Whereas patients with spinal cord trauma at the T1 level are paraplegic, traumas above C5 may result in quadriplegia and loss of phrenic nerve function. Injuries between these two levels result in varying loss of motor and sensory functions in the upper extremities. Careful assessment and documentation of preoperative sensory and motor deficits are important.
(4) Musculoskeletal: Prolonged immobility leads to osteoporosis, skeletal muscle atrophy, and the development of decubitus ulcers. Pathologic fractures can occur when these patients are moved. Pressure points should be well protected and padded to minimize the likelihood of trauma to the skin and the development of ulcers.
(5) Renal: Renal failure is the leading cause of death in patients with chronic spinal cord transection. Chronic urinary tract infections and immobilization predispose to the development of renal calculi. Amyloidosis of the kidney can be manifested as proteinuria, leading to a decrease in the concentration of albumin in the plasma.