Acute management of the patient with spinal cord injury

Acute management of the patient with spinal cord injury

REVIEW PAPER Acute Management of the Patient with Spinal Cord Injury Mary C. Karlet, CRNA, PhD Spinal cord injuries are not as common as many other ...

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REVIEW PAPER

Acute Management of the Patient with Spinal Cord Injury Mary C. Karlet, CRNA, PhD

Spinal cord injuries are not as common as many other types of injuries. The victims are often young, the injury debilitating, and the effects devastating and incalculable. The acute management of patients with spinal cord injury can significantly affect the patient’s eventual neurologic and functional outcome and ultimately their quality of life. Early interventions are aimed at reestablishing physiologic homeostasis, lessening the amount of secondary injury, and preserving neurologic function. (Int J Trauma Nurs 2001;7:43-8.)

n the United States, 10,000 to 15,000 new cases of spinal cord injury (SCI) occur each year, most in men 16 to 30 years of age (81%).1-3 SCIs are the result of motor vehicle crashes (37%), acts of violence (26%), falls (22%), and sports accidents (7%) (Fig 1).2 The mean age at the time of injury has increased since 1973, and today 9% of victims of SCI are more than 60 years of age.2,4 Elderly persons with preexisting degenerative vertebral disorders can sustain an SCI from even minor trauma.5-7 In the older trauma victim, mortality is higher and complications are more severe.7 Most patients (60%) with SCI have multiple injuries; therefore, all patients with multiple injuries are initially treated with the presumption that SCI might be present.8,9 Only 40% of patients with SCI have an isolated cord injury.8,9 The overall hospital mortality rate for patients with SCI is 17%.10 Deaths are most common in patients with multiple injuries and most hospital deaths occur within 24 hours of injury.1

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Mary C. Karlet, CRNA, PhD, is the program director of the Nurse Anesthesia Program at Duke University School of Nursing, Durham, North Carolina. Reprint requests: Mary C. Karlet, CRNA, PhD, 206 Country Club Dr, Greensboro, NC 27408. Copyright © 2001 by the Emergency Nurses Association. 1075-4210/2001/$35.00 + 0 65/1/115349 doi:10.1067/mtn.2001.115349 APRIL-JUNE 2001

MECHANISM Injuries to the spine can involve the vertebral column, spinal cord, spinal nerves, and blood vessels that supply the cord. SCIs tend to occur in conjunction with vertebral injuries. The vertebral column is constructed as a circumferential bony ring around the spinal cord, protecting the cord from minor trauma. Severe flexion, extension, compression, and rotation forces can cause fracture and dislocation of the vertebral column.

Shortly after spinal cord trauma, localized hemorrhage and edema occur at the level of injury. Vertebral injuries occur most often at the cervical vertebrae regions C1 to C2 and C4 to C7 and in thoracic-lumbar regions T11 to L2.5 The cervical cord is most vulnerable to injury because in that region the spine lacks the support provided by the ribs and large muscles of the back. Cervical SCI occurs in approximately 52% of patients with multiple injuries that include the spine and in 65% of patients with isolated spinal cord trauma.1 PATHOPHYSIOLOGY The damage to the spinal cord and nerves is largely the result of direct mechanical insult to the INTERNATIONAL JOURNAL OF TRAUMA NURSING/Karlet 43

Table 1. Cellular and subcellular alterations associated with SCI*

Time after injury First few minutes

Within 2 h

Within 4 h

Within 24 h

First few days

3 to 4 wk

Cellular and subcellular alterations Microscopic hemorrhages in central gray matter, vasospasm, hypotension, loss of autoregulation Edema in white matter impairs microcirculation of the spinal cord Disruption of myelin, axonal degeneration, and endothelial cell ischemia Necrosis consumes 70% of the cross-sectional area of the spinal cord Progressive axonal changes; cavitation and coagulation necrosis at site of injury Traumatized cord replaced by acellular collagenous scar tissue

*Adapted from Boss.5

cord at the time of injury and is called primary injury (Table 1). In the hours and days after trauma, a cascade of local biochemical and hemodynamic processes can cause additional SCI and nerve cell death, known as secondary injury.4,11-14 Secondary injury is a destructive process caused by ischemia, tissue hypoxia, and delayed axonal and neuronal degeneration.11,12,14 Shortly after spinal cord trauma, localized hemorrhage and edema occur at the level of injury. This is followed by reduced vascular perfusion, the development of local ischemic areas, and decreased oxygen tension in the tissue at the injury site.5,14,15 Chemical and metabolic changes occur as part of the injury response and include release of toxic excitatory amino acids, accumulation of endogenous opiates, lipid peroxidation (a destructive chemical reaction), elevated intracellular calcium concentration, and local free radical release.5,13,16 Pathochemical changes may contribute to vasospasm, edema formation, and tissue hypoxia, which exacerbate neuronal death and increase the person’s degree of dysfunction.14,17 CLINICAL MANIFESTATIONS AND MANAGEMENT The acute care rendered to the patient with SCI has a profound effect on the patient’s eventual out44

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come.18 The patient should be assessed for immediate life-threatening conditions and the spine immobilized to protect it from further injury. A careful neurologic examination must be completed to determine a baseline of function, followed by frequent repeat checks to detect any change. Radiologic studies are done to identify areas of injury. The neurologic examination consists of motor, sensory, and reflex testing. Motor function is assessed by asking the patient to move muscles in the upper and lower extremities and determining their strength. The loss of motor function can be correlated to the level of SCI (Table 2). Sensory testing uses light touch and pinprick to all of the major dermatomes and vibration and joint position in the upper and lower extremities. The various sensory stimuli are carried by different ascending (sensory) tracts in the spinal cord. A loss or sparing of a tract can help determine the crosssectional area of the cord that is injured. When doing a neurologic assessment of the spinal cord, the examiner will begin with the motor exam and move from head to toe. Sensory is assessed by moving from the lower to upper body regions because it is easier for the patient to recognize the onset of a sensory stimulus rather than the cessation. The information obtained from the motor, sensory, and reflex testing is used to determine the type and extent of SCI. An incomplete SCI has spared a portion of the cross-section of the cord at the level of injury. There will be some residual motor or sensory function below the level of injury. Approximately 60% of patients with acute SCI are admitted with incomplete lesions; 59% of these patients develop significant recovery of function.4 A patient with a complete SCI loses all voluntary motor and sensory function below the injury level, with preservation of spinal reflexes. Approximately 3% of patients with complete SCI on initial examination develop significant neurologic recovery within 24 hours. Persistent complete SCI after 48 hours portends a poorer outcome with little likelihood of recovering lost function.8,19,20 SPINAL SHOCK If a patient has no voluntary motor function, no identifiable sensory function, and a total loss of spinal reflexes, the spinal cord may be in a state of dysfunction referred to as “spinal shock.” Spinal shock is a term that is often misunderstood because “shock” is generally considered a reference to blood pressure, and most patients with SCI do have VOLUME 7, NUMBER 2

Table 2. Guide to determining neurologic function of the spinal cord according to motor and sensory function* Spinal nerve Cervical 1-4 Cervical 5 Cervical 6 Cervical 7 Cervical 8 Thoracic 1-10

Motor function Breathe with diaphragm Flex biceps

Lumbar 2

Extend wrist Flex triceps Extend finger Breathe with intercostals muscles Flex hip

Lumbar 4

Dorsiflex ankle

Sacral 1

Flex knee and ankle Constrict rectal sphincter

Sacral 4-5

Sensory function Top of shoulders Skin over anterior upper arm Thumb Third finger Fifth finger T 4–nipple line T 10–umbilicus Middle of anterior thigh Medial part of lower leg Lateral ankle Perineal area

*Lesions above T3 are considered quadriplegic.

a severe drop in arterial blood pressure. However, spinal shock is a specific term that relates to the loss of all neurologic activity below the level of injury, resulting in flaccidity, paralysis, poikilothermy, areflexia, and anesthesia to all modalities.3 It is a temporary physiologic disorganization of spinal cord function that starts within 30 to 60 minutes after injury and typically lasts 7 to 20 days after onset.5 Table 3 lists the characteristics of spinal shock. Spinal shock is more severe in patients with higher SCI because injuries that occur in the lower thoracic or lumbar regions spare the sympathetic nervous system at these levels. As spinal shock subsides the patient gradually regains somatic and autonomic reflex activity below the level of the lesion. SIGNIFICANT COMPLICATIONS Major problems encountered in the postinjury period include respiratory insufficiency, hemodynamic instability, autonomic hyperreflexia, gastrointestinal problems, skin breakdown, and inability to regulate body temperature.

Respiratory Insufficiency The extent of respiratory system involvement with SCI depends in large part on the level of injury. Injuries that affect the abdominal wall musAPRIL-JUNE 2001

Table 3. Characteristics of spinal shock* Flaccid paralysis at and below the level of lesion Bladder paralysis Loss of autonomic and spinal reflex function at and below the level of lesion Loss of vasomotor tone Unstable blood pressure Disturbed temperature control Venous pooling Paralytic ileus with distention Anesthesia to all modalities below the level of lesion *Adapted from Boss.5

cles will decrease the ability to cough. Lesions that involve the spinal cord above T 5-9 will cause loss of ability to use intercostal muscles, and lesions above C 3,4,5 nerve roots will cause loss of diaphragm function and potentially respiratory arrest.4,5,21 A cervical SCI often compromises the respiratory status of the patient because progressively ascending cord edema may impair the phrenic nerve. Lu et al reported that respiratory failure, manifesting as sudden apnea, may develop days or even weeks after cervical SCI. It appears that patients who are asleep are most at risk for delayed apnea.21 Patients with SCI require close monitoring of respiratory drive, ventilation, ability to cough, pulse oximetry, and arterial blood gases. Hypoxia

Spinal shock is a term that is often misunderstood because “shock” is generally considered a reference to blood pressure.

can exacerbate the pathophysiologic cascade in injured neurologic tissue and must be prevented by supplemental oxygen, mechanical ventilation, or both.3 Chest physiotherapy, incentive spirometry, “quad coughing,” (using pillows to push against the abdomen to help generate intra-abdominal pressure to cough), position changes, and suctioning are used to enhance mobilization of secretions.4 If the patient requires endotracheal intubation, the neck is maintained in a neutral position to establish an airway. The heart rate should be monitored during intubation because there is a risk of asystole from excessive stimulation of the vagus nerve. INTERNATIONAL JOURNAL OF TRAUMA NURSING/Karlet 45

Table 4. Differentiating neurogenic from hypotensive shock in the patient with SCI Type of shock Neurogenic

Mechanism Loss of vascular tone Venous pooling

Hypovolemic

Hemorrhage

Hemodynamic Instability SCI.4,22 The

Hypotension is common with sympathetic nervous system innervates blood vessels and the heart, which are controlled by vasomotor centers in the brain stem. If an SCI lesion is above T4, there is interruption of vasomotor center influence and the peripheral vessels vasodilate. The inability to exert neurologic control of vascular smooth muscle is referred to as “neurogenic shock.” It may be difficult to keep an adult’s systolic blood pressure above 90 mm Hg; therefore, the aim of therapy is to maintain adequate tissue perfusion and not an absolute pressure. The blood

The vagus nerve is a cranial nerve that innervates many smooth muscles, including the heart, bronchi, esophagus, and stomach. pressure can be very sensitive to changes in body position and patients may have orthostatic hypotension just from being turned from one body position to another. Hypoperfusion should be treated with intravenous crystalloid solutions, such as normal saline, and if needed, vasopressors, such as dopamine. Dopamine is especially useful in counteracting bradycardia and protecting renal blood flow. Invasive monitoring of mean arterial pressure and central venous pressure may help guide fluid management. A urinary catheter is inserted to monitor urine output and assure emptying of the bladder. In the multiinjured patient, it may not be easy to dif46

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Signs and Symptoms Hypotension Bradycardia Warm, hyperemic skin

Hypotension Tachycardia Cool, clammy skin

Treatment Inotropic support (dobutamine) Vasopressors (dopamine) Moderate volume infusion Control blood loss Aggressive blood and fluid replacement

ferentiate neurogenic hypotension from hypotension of other origins (Table 4).10,18 Bradycardia is seen in SCI and is caused by loss of vasomotor center influence. The unopposed vagal nerve stimulation slows the heart rate and may contribute to hypotension and an unstable cardiovascular state. The vagus nerve is a cranial nerve that innervates many smooth muscles, including the heart, bronchi, esophagus, and stomach. When the sympathetic fibers are blocked by a high SCI, unopposed parasympathetic tone leads to overt stimulation of the vagus nerve and bradycardia.4,23 In susceptible patients, manipulating the endotracheal tube, suctioning, or inserting a nasogastric tube may trigger severe bradycardia and even cardiac asystole. Intravenous atropine should be available at the bedside at all times and sensitive patients should be premedicated with atropine before high-risk procedures. Venous thromboembolism may develop in the SCI patient because of venous pooling and loss of movement below the injury.4,10 Because patients are insensate or receiving steroids, edema and inflammation may not be visible. Patients with SCI need to have thrombosis prevention started early.4 Methods used may include antiembolus stockings, sequential compression devices, and anticoagulant therapy (in the absence of contraindications). In some instances, patients with SCI are treated with an inferior vena caval filter to prevent emboli from reaching the pulmonary circulation.

Autonomic Hyperreflexia Also referred to as autonomic dysreflexia, autonomic hyperreflexia may occur any time after spinal shock resolves. Patients with high SCI lesions (T6 or above5) react to a stimulus, such as a distended bladder or rectum. As the impulses are transmitted up the spinal cord, neurons of the symVOLUME 7, NUMBER 2

pathetic nervous system located in the thoracolumbar region of the cord are triggered and produce vasoconstriction and increased blood pressure. A person with an intact spinal cord would respond to the hypertension with immediate nerve transmission from the brainstem vasomotor control centers, causing peripheral vessels to dilate. Unfortunately, the patient with a high SCI is unable to conduct efferent signals (from the brain) and the condition continues. Signs of autonomic hyperreflexia are sudden hypertension (greater than 200 mm Hg, systolic), severe head-ache, blurred vision, nasal congestion, flushed skin, and sweating above the level of the lesion, pallor below the level of the lesion, and a compensatory bradycardia (as low as 30-40 beats/min).5 Autonomic hyperreflexia and the associated hypertension is a life-threatening situation and requires immediate intervention. Removing the source of the noxious stimuli (eg, kinked urinary catheter, emptying the bladder or bowel) usually relieves the symptoms. If a distended bowel or bladder is suspected, introducing irrigation fluid into a catheter or finger to examine the bowel may worsen the condition. If irrigation is mandated, a topical anesthetic should be used to anesthetize the area before introducing more volume to a body cavity. Raising the head of the bed (considering stability of the injury) may also produce relief. If more conservative measures fail, rapidacting antihypertensive medications, such as nifedipine, nitrogylcerine, or nitroprusside, may be required.5

Gastrointestinal System After trauma, it is common for patients to experience delayed gastric emptying and an ileus. Abdominal distention can prevent the diaphragm from fully descending. Patients with SCI are at risk for tracheal aspiration of gastric contents. During the acute care stage, the stomach should be decompressed with a nasogastric tube connected to low suction. After the ileus has resolved, the patient will need a bowel regimen of stool softeners and laxatives. Patients with SCI are at risk for stress ulceration and are given H2 receptors and antacids to maintain a gastric pH of more than 5.

Skin Breakdown There are multiple reasons that patients with SCI are prone to pressure damage to the skin. They are unable to shift their weight or sense pressure or pain. Decreased skin perfusion, altered nutrition, the use of steroids, and the stress of trauma impair APRIL-JUNE 2001

wound healing. Skin care should be a primary concern for all health care providers, starting with emergency personnel. Skin breakdown occurs within hours and is a preventable and costly complication.

Inability to Regulate Body Temperature Because patients have loss of sympathetic nervous system control of the vascular system below the level of the injury, they do not have the ability to conserve body heat through vasoconstriction. Poikilothermy is a state in which the body has lost the ability to generate or preserve a core temperature. They become dependent on the environmental temperature. Patients with acute SCI should be kept warm with passive warming devices and monitored carefully to avoid thermal injury to insensate skin.

Poikilothermy is a state in which the body has lost the ability to generate or preserve a core temperature. PREVENTING SECONDARY INJURY TO THE SPINAL CORD The reduction of a secondary injury to the spinal cord can have a profound effect on a patient’s ultimate level of function.11,18 Early immobilization and stabilization of the spinal column and decompression of the spinal cord 1,3,4,18 help to prevent cord compression caused by misalignment. This is accomplished by skeletal traction or surgery.10,11 Glucocorticoids have been the focus of much attention as potential modulators of secondary insult.4,12 The National Acute Spinal Cord Injury studies24-26 have shown that secondary injury can be mitigated with high-dose methylprednisolone started within 8 hours of injury. An initial bolus dosage of 30 mg/kg intravenously, followed by 5.4 mg/kg per hour continuous infusion for 23 hours, enhances both motor and sensory neurologic outcomes following traumatic injury.24-26 This neuroprotective steroid has several mechanisms of action, such as acting as a free radical scavenger, inhibiting lipid peroxidation, stabilizing lysosomal membranes, and reducing the breakdown of supportive and nutritive neural glial cells.11,12 INTERNATIONAL JOURNAL OF TRAUMA NURSING/Karlet 47

CONCLUSION The initial, acute management of patients with SCI affects the patient’s eventual neurologic and functional outcomes and ultimately the patient’s quality of life. Early interventions are aimed at reestablishing physiologic homeostasis, lessening the amount of secondary injury, and preserving neurologic function. Normalizing vital signs, maintaining sufficient blood oxygen levels, reestablishing and stabilizing the spinal column, and incorporating pharmacologic interventions to reduce secondary injury are key acute care goals. REFERENCES 1. Burney RF, Maio RF, Maynard, Karunas R. Incidence, characteristics, and outcome of spinal cord injury at trauma centers in North America. Arch Surg 1993;128:596-9. 2. Spinal Cord Injury Information Network. Facts and figures at a glance. Available at: http://www.spinalcord.uab.edu. Accessed January 2001. 3. Amar AP, Levy ML. Surgical controversies in the management of spinal cord injury. J Am Coll Surg 1999;188:550-66. 4. Buckley DA, McKenna, Guanci M. Spinal cord trauma. Nurs Clin North Am 1999;34:661-87. 5. Boss BJ. Alterations of neurologic function. In: McCance KL, Huether SE, editors. Pathophysiology: the biologic basis for disease in adults and children. 3rd ed. St Louis: Mosby; 2000. p. 510-73. 6. Kannus P, Niemi S, Palvanen M, Parkkari J. Continuously increasing number and incidence of fall induced, fracture-associated, spinal cord injuries in elderly persons. Arch Intern Med 2000;160:2145-9. 7. Lovasik D. The older patient with a spinal cord injury. Crit Care Nurs Q 1999;22:20-30. 8. Chapman JR, Anderson PA. Thoracolumbar spine fractures with neurologic deficit [abstract]. Orthop Clin North Am 1994;25:595-612. 9. Reiss SJ, Raque GH, Shields CB, Garretson HD. Cervical spine fractures with major associated trauma. J Neurosurg 1986;18:327-30. 10.King B, Gupta R, Narayan RK. Critical care of the trauma patient. The early assessment and intensive care unit management of patients with severe traumatic brain and spinal cord injuries. Surg Clin North Am 2000;80:855-67. 11. University of Washington, Department of Rehabilitation. Current and future management of SCI. Available at: http://www.depts.washington.edu/rehab. Accessed January 2001.

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12. Seidl EC. Promising pharmacological agents in the management of acute spinal cord injury. Crit Care Nurs Q 1999; 22:44-50. 13. Braughler JM, Hall ED. Involvement of lipid peroxidation in CNS injury. J Neurotrauma 1992;9:S1-6. 14. Tator CH, Fehlings MG. Review of the secondary injury theory of acute spinal cord trauma with emphasis on vascular mechanisms. J Neurosurg 1991;75:15-26. 15. Dubendorf P. Spinal cord injury pathophysiology. Crit Care Nurs Q 1999;22:31-5. 16. Hall ED, Yonders PA, Andrus PK, Cox JW, Anderson DK. Biochemistry and pharmacology of lipid antioxidants in acute brain and spinal cord injury. J Neurotrauma 1992;9:S425-42. 17. Moriya T, Hassan AZ, Young W, Chesler M. Dynamics of extracellular calcium activity following contusion of the rat spinal cord. J Neurotrauma 1994;11:255-63. 18. Dyson-Hudson TA, Stein AB. Acute management of traumatic cervical spinal cord injuries. Mt Sinai J Med 1999;66: 170-8. 19. Greenberg MS. Spine injuries. In: Greenberg MS, editor. Handbook of neurosurgery. 4th ed. Lakeland (FL): Greenberg Graphics; 1997. p. 754-96. 20. Stauffer ES. Neurological recovery following injuries to the cervical spinal cord and nerve roots. Spine 1984;9:532-4. 21. Lu K, Lee TC, Liang CL, Chen HJ. Delayed apnea in patients with mid- to lower cervical spinal cord injury. Spine 2000;5:1332-8. 22. Lehmann KG, Lane JG, Piepmeier JM, Batsford WP. Cardiovascular abnormalities accompanying acute spinal cord injury in humans: incidence, time course, and severity. J Am Coll Cardiol 1987;10:46-52. 23. Levi L, Wolf A, Belzgerg H. Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome. J Neurosurg 1993;33:1007-16. 24. Bracken MB, Shepard MJ, Collins WF, Holford TR, Young W, Baskin DS, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury. Results of the second national acute spinal cord injury study. N Engl J Med 1990;322:1405-11. 25. Bracken MB, Shepard MJ, Collins WF, Holford TR, Baskin DS, Eisenberg HM, et al. Methylprednisolone or naloxone treatment after acute spinal cord injury: 1-year follow-up data. J Neurosurg 1992;76:23-31. 26. Bracken MB, Shepard MJ, Holford TR, Leo-Summers L, Aldrich EF, Fazl M, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazid mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the third national acute spinal cord injury randomized controlled trial. JAMA 1997;277:1597-604.

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