Spinal Cord Injury

Spinal Cord Injury

Chapter 32 Spinal Cord Injury Katharine Hunt  •  Rodney Laing Pathophysiology Nervous System Respiratory System Cardiovascular System Gastrointestin...

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Chapter 32

Spinal Cord Injury Katharine Hunt  •  Rodney Laing

Pathophysiology Nervous System Respiratory System Cardiovascular System Gastrointestinal and Genitourinary Systems Temperature Diagnosis and Management in the Intensive Therapy Unit Assessment of Spinal Cord Injury Associated Injury Immobilization

Airway and Respiratory Support Cardiovascular Support Other Early Steroid Intervention Autonomic Dysreflexia Pathophysiology Signs and Symptoms Treatment Anesthesia Postoperative Care

Pathophysiology The pathophysiology of spinal cord injury (SCI) can be divided into primary and secondary components. Primary injury may be caused by stretching of the spinal cord secondary to hyperextension or hyperflexion of the spinal column. If the force is great enough, tearing of the spinal cord can result. The cord may become compromised as a result of compression from fractured and disrupted bony structures and may occasionally be damaged by a direct, penetrating injury. Primary injury leads to disruption of neural tissues, as well as interruption of the vascular supply with hemorrhage, vasospasm, and local ischemia. Whatever the mechanism of primary injury, the pattern of the ongoing or secondary injury is similar in all cases and involves a complex cascade of events, including release of cytokines and amino acids from injured tissue that generate an inflammatory cascade ultimately leading to free radical formation, cellular edema, and cellular apoptosis. These events may be compounded by systemic hypotension and hypoxia, as well as local cord edema, and result in the destruction of axons nerve cell bodies and the supporting glia. SCI not only results in neurologic dysfunction but also causes important disturbances in the body’s other systems.

Nervous System Damage to the spinal cord causes an interruption in both somatic and visceral sensation that results in absent somatic and autonomic reflexes and flaccid paralysis. This phenomenon is often termed “spinal shock.” Spinal shock may last for up to 6 weeks, but in most cases it resolves within 24 hours of the initial injury. As spinal shock 211



resolves, the initial neurologic findings are replaced by progressive spasticity of the affected segments below the level of injury.

Respiratory System The degree of airway and respiratory compromise depends on the level of the SCI, as well as the presence of concomitant injuries. In cervical cord injuries, the level of spinal cord edema and hence dysfunction may ascend and make respiratory support necessary. In addition, injuries below the fifth cervical vertebra (C5) affect the intercostal muscles, which may decrease alveolar ventilation and also limit the effectiveness and strength of cough. In unstable thoracic spine injuries, particularly those associated with rib fractures and lung contusions, there is a high risk for the development of respiratory complications. In lesions at the C4/C5 level, voluntary respiration is maintained but vital capacity is reduced by as much as 20% to 25%. These patients often require ventilatory support. In any lesion above C4, accessory, diaphragmatic, and intercostal muscle function may be lost and require total ventilatory support.

Cardiovascular System Although patients are often hypertensive at the moment of injury, they quickly become hypotensive because of interruption of sympathetic pathways. Compensatory reflexes are lost, particularly if the lesion is above T1, and a profound bradycardia may occur as a result of unopposed parasympathetic activity.

Gastrointestinal and Genitourinary Systems Both bladder and bowel atony may occur and are manifested as paralytic ileus, gastric distention, and urinary retention.

Temperature v

The ability to control body temperature is lost because of an inability to initiate sweating, coupled with profound cutaneous vasodilation.

Diagnosis And Management In The Intensive Therapy Unit Assessment of Spinal Cord Injury The initial clinical examination should begin with assessment of airway, breathing, and circulatory status. The neck should be immobilized in a rigid cervical collar, and during transport the patient should be immobilized on a spinal board. The spinal board should be removed as soon as possible once the patient is in the hospital and under specialist supervision. The skin over the spine must be inspected and palpated for deformity and tenderness. Sensory and motor function and tendon reflexes should be examined and documented via the American Spinal Injury Association (ASIA) chart as soon as possible. Radiographs are taken to screen the vertebral column, but any area of suspected injury should be scanned with computed tomography (CT). CT also allows proper imaging of the cervicothoracic (C7-T1) junction, where injury 212


is ­ common and can be missed with standard radiographs. Imaging should be reviewed by radiologists and by a spinal surgeon to assess the clinical implications of any abnormality. It is possible for a patient with negative findings on plain radiographs or CT scans to have a soft tissue or ligamentous injury. If despite negative radiologic findings a patient experiences pain or tenderness, particularly with movement, flexion-­extension views of the neck or magnetic resonance imaging should be considered. Uncooperative patients should undergo CT scanning of the whole spine.

Associated Injury Twenty percent to 50% of patients have other systemic injuries, the most common being traumatic brain or major chest injuries. Traumatic brain injury occurs in up to 50% of patients with SCI and is more likely after a motor vehicle accident. The possibility of other injuries may present several problems. First, other major injuries may cause hypoxia and hypotension, which can result in considerable secondary injury to the spinal cord. Second, the presence of a spinal injury makes secondary injuries harder to diagnose and treat. The airway may also be more difficult to secure because fear of exacerbating a cord injury in the presence of an unstable spine may hinder proper assessment and resuscitation.

Immobilization During initial transport from the scene to the hospital, patients are commonly immobilized in a rigid cervical collar and placed on a spinal board. Once in an intensive care unit, the neck may be immobilized by continuation of rigid cervical collar support or the use of two sandbags secured on either side of the head. Patients should not be kept on a spinal board in intensive care because of the risk for the development of pressure sores, particularly in areas with diminished or absent sensation. Patients can be log-rolled to allow examination and relief of pressure areas. Immobilization can in itself cause complications, including pressure sores, pain, and atelectasis. Rigid cervical collars are associated with raised intracranial pressure; airway compromise, which can lead to pulmonary aspiration; and pressure necrosis of the underlying skin. Assessment of the stability of the vertebral column and permitted range of movement should be done as soon as possible by experienced clinicians so that immobilization can be discontinued.

Airway and Respiratory Support It is common for patients with spinal injury to require intubation. Indications for intubation in SCI are

• Pao2 <10 kPa (75 mm Hg) • Paco2 >6.5 kPa (50 mm Hg) • Vital capacity <20 mL/kg • Pulmonary edema • Pulmonary aspiration • Chest or lung injuries

To minimize movement of the cervical cord, manual in-line stabilization should be used during laryngoscopy and endotracheal intubation. If the patient is awake and cooperative, awake fiberoptic intubation may be considered. In the acute phase of 213



injury (<24 hours), succinylcholine may be administered safely without concern for triggering hyperkalemia.

Cardiovascular Support Hypotension coupled with bradycardia secondary to loss of cardiac accelerator function and unopposed parasympathetic activity is common after high SCI but can occur after injury at any level. Hypotension may be compounded by active hemorrhage from other associated injuries. Hypotension and hypovolemia should be initially managed with volume replacement guided by central venous pressure measurements. Pulmonary edema commonly occurs after SCI, and although it is probably sympathetically mediated and occurs independently of fluid overload, care must still be taken when optimizing fluid balance. If perfusion remains inadequate despite fluid resuscitation, treatment with vasoconstrictors or inotropes should be commenced and a pulmonary artery catheter inserted. The bradycardia seen in spinal injury responds to atropine.

Other Bladder and bowel atony is managed by urinary catheterization and insertion of a nasogastric tube, respectively. Prophylaxis against deep venous thrombosis should be given once patients are stabilized and all sources of hemorrhage have been controlled, provided that surgical intervention to decompress the cord or stabilize the spine (or both) is not imminent.

Early Steroid Intervention


Corticosteroids have been extensively investigated in both animals and humans. Although their precise mechanism of action is unknown, effects may include stabilization of membrane structures, reduction of vasogenic edema, free radical scavenging, enhancement of spinal cord blood flow, and limitation of the inflammatory response. The largest human trials, the National Acute Spinal Cord Injury Studies (NASCIS I, II, and III), concluded that early steroid intervention improves neurologic outcome in SCI patients. The NASCIS II study recommended the use of methylprednisolone given as an initial bolus of 30 mg/kg followed by an infusion at 5.4 mg/kg over the next 23-hour period. The NASCIS studies have, however, been criticized on several levels, the most important being that the conclusions of the trial were driven by results taken from subpopulations of patients rather than from the patient study group as a whole. The results have also not been reproducible in any subsequent studies using the same drug and dosage regimens, and the improvement seen in the neurologic level of injury in the NASCIS trials did not equate with an improvement in survival or quality of life. These criticisms, coupled with the potential side effects associated with high-dose steroid therapy, have led several neurosurgical organizations to suggest that steroid therapy should be used only as an option in SCI treatment with the full knowledge that the risks of administration may outweigh the potential benefits of its actions.

Autonomic Dysreflexia Autonomic dysreflexia is a phenomenon seen after SCI. It typically occurs weeks and months after the initial insult and is characterized by a massive autonomic response to stimuli below the level of the spinal cord lesion. 214

Autonomic dysreflexia is seen in 60% to 80% of patients with complete SCI above T6 (splanchnic outflow), but it may occur in up to 90% of patients with higher thoracic or cervical cord lesions. The response is rarely seen in those with complete injuries below T10. The widespread inappropriate sympathetic response causes profound vasoconstriction. Increased sensitivity to endogenous catecholamines may also develop. Many stimuli can trigger autonomic dysreflexia, the most common of which is pelvic visceral stimulation. Bladder distention, fecal impaction, uterine contractions, urinary tract infections, long-bone fractures, deep venous thrombosis, pressure sores, and even tight clothing can initiate the reaction. Surgical stimuli can also induce the reflex.



Signs and Symptoms The most concerning clinical feature of autonomic dysreflexia is paroxysmal hypertension. Blood pressure can reach systolic levels of greater than 260 mm Hg and diastolic pressure ranging from 170 to 220 mm Hg. The rise in blood pressure is commonly accompanied by headache, profuse sweating, and flushing or pallor above the level of the spinal cord lesion. Cardiac function may be disturbed by arrhythmias (especially bradycardia), myocardial ischemia, and in severe cases, congestive cardiac failure. Other features include nausea and vomiting, pupillary changes, nasal obstruction, Horner’s syndrome, paresthesias, and anxiety. If left untreated, the precipitous rise in blood pressure may lead to cerebral, retinal, or subarachnoid hemorrhage, seizures, coma, myocardial infarction, and death.

Treatment The most important aspect in the management of autonomic dysreflexia is awareness and recognition of the phenomenon. Initial treatment involves identifying and removing the precipitating stimulus, loosening all tight clothing and shoes, and when safe, sitting the patient upright. These measures alone may reduce the blood pressure. If an episode occurs under anesthesia, deepening the anesthesia or providing extra analgesia may alleviate the problem. A rapid-onset, short-acting vasodilator is the next drug of choice. Sublingual nifedipine and sublingual, intravenous, or dermal patch glyceryl trinitrate are the most commonly used agents. Intravenous phentolamine and hydralazine have also been used in the acute treatment of this disorder. Long-term therapy with other antihypertensive agents can be considered. Prazosin, guanethidine, clonidine, and calcium channel blockers have all been used with some success in preventing episodes of the condition from occurring.

Anesthesia Surgery is a potent stimulus for autonomic dysreflexia, even in patients with no previous history of this disorder. It is generally thought that spinal anesthesia is superior to epidural or general anesthesia in reducing occurrences during surgery. Before a decision about the type of anesthesia is made, a thorough assessment of renal, cardiac, and respiratory (forced expiratory volume in 1 second [FEV1]/forced vital capacity [FVC] ratio) function should be undertaken to enable planning of both intraoperative and postoperative care. It is also common to premedicate patients who may be at risk for autonomic dysreflexia with antihypertensives. It is common practice to preload patients with up to a liter of crystalloid before anesthesia to reduce the likelihood of severe hypotension. 215



Careful monitoring of patient temperature should take place in all but the shortest of procedures because patients with SCI are unable to generate heat and are therefore at much higher risk for hypothermia. General Anesthesia Propofol is the induction agent of choice, and a short-acting, nondepolarizing muscle relaxant can be administered to aid tracheal intubation. Succinylcholine is known to produce hyperkalemia in SCI patients, which if severe may lead to cardiac arrest. Its use should, when possible, be avoided for 72 hours to 9 months after injury. Local Anesthesia Regional techniques may be used alone or in conjunction with general anesthesia. As well as preventing episodes of autonomic dysreflexia, spinal anesthesia maintains good overall cardiovascular stability in these patients and has therefore become the anesthetic of choice, especially for urologic surgery. In addition to instilling standard local anesthetic agents into the epidural space, opioids can be used. Meperidine, in particular, may prevent autonomic dysreflexia by producing selective blockade of spinal opioid receptors and hence blocking the nociceptive reflexes below the level of cord injury.

Postoperative Care Autonomic dysreflexia may occur for the first time in the postoperative period. Careful monitoring for this, as well as respiratory function and temperature, is therefore essential. It is wise to allow an extended time for recovery and provide postoperative high-dependency care for these patients.

Key Points


• Initial management of SCI should begin with assessment of the airway, breathing, and circulation. • Patients should be immobilized until vertebral column injury and stability have been assessed. • Up to 50% of patients have other associated injuries. • High-dose corticosteroid therapy is not routinely indicated in early management. • Autonomic dysreflexia may occur in both the acute and late stages of SCI. Further Reading Guidelines of the American Association of Neurologic Surgeons and the Congress of Neurologic Surgeons. Pharmacological therapy after cervical spinal cord injury. Neurosurgery 2002; 50(Suppl):63-72. Hambly PR, Martin B: Anaesthesia for chronic spinal cord lesions. Anaesthesia 1998; 3:273-289. Smith M, Hunt K: Neurosurgery. In Emergencies in Anaesthesia. London, Oxford University Press, 2005. Stevens RD, Bhardwaj A, Kirsch JR, Mirski MA: Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol 2003; 15:215-229.