spinal cord injury(redirected from Spinal-cord injury)
Spinal Cord Injury
Causes and symptoms
- C1-8. These nerves enter from the eight cervical or neck vertebrae.
- T1-12. These nerves enter from the thoracic or chest vertebrae.
- L1-5. These nerves enter from the lumbar vertebrae of the lower back.
- S1-5. These nerves enter through the sacral or pelvic vertebrae.
- Coccygeal. These nerves enter through the coccyx or tailbone.
- C1-C4: head and neck.
- C3-C5: diaphragm (chest and breathing).
- C5-T1: shoulders, arms and hands.
- T2-T12: chest and abdomen (excluding internal organs).
- L1-L4: abdomen (excluding internal organs), buttocks, genitals, and upper legs.
- L4-S1: legs.
- S2-S4: genitals and muscles of the perineum.
Paralysis and loss of sensation
Spasticity and contracture
Loss of bladder and bowel control
spinal cord injurySpinal cord compression, spinal cord trauma Neurology Traumatic damage to the spinal cord resulting in a significant or complete loss of voluntary control of extremities or autonomic nervous system at and below the level of injury Epidemiology 10,000 to 15,000 new cases/yr; 200,000 currently with chronic SCI–US; MVAs cause 45%, falls 22%, acts of violence 16%, sports–eg, diving into shallow water 13%, etc–industrial accidents, gunshot wounds, assault; ♂:♀ ratio 4:1; mean age = 31; 59% occur at age 16-30 Clinical SC compression due to fluid or blood in sub- and epidural spaces, paralysis, loss of bladder, bowel control Complications-2nd yr UTI 59%, spasticity 38%, chills and fever 19%, pressure sore 16%, autonomic hyperreflexia, contractures Complications-≥ 30 yrs Pressure sores 17%, muscle and joint pain 16%, GI or cardiovascular problems, UTIs or other infections Management Depending on the severity; surgical if acute or unstable; physical therapy for chronic SCI. See SCIWORA.
Spinal Cord Injury
|Mean LOS:||3.5 days|
|Description:||MEDICAL: Spinal Disorders and Injuries Without CC or Major CC|
Spinal cord injury (SCI), trauma to the spinal cord, affects approximately 12,000 Americans every year. Half of the injuries produce paraplegia and half quadriplegia. A physiological cascade of events occurs at the time of an SCI and leads to neuronal damage and neurological deficit.
The initial injury causes a release of glutamate, which causes cellular damage and petechial hemorrhages at the injury site. Calcium influx into the neuron is caused by thrombus formation. This alteration in calcium triggers the arachidonic acid cascade to be initiated, leading to free radical formation, lactic acidosis, and lipid peroxidation. This final series of events hastens ischemia of the white matter and microvasculature destruction, with resultant neuronal damage and permanent neurological deficit. This series of physiological and chemical events associated with acute SCI lead to the permanent neurological deficit. With aggressive medical interventions and nursing management, approximately 90% of patients with acute SCI survive.
SCI can be classified by a variety of methods: complete and incomplete cord injury, mechanism of injury, and the level of injury. In a complete SCI, the patient loses all function below the neurological injury level (the lowest neurological segment with intact motor and sensory function). In an incomplete SCI, some motor or sensory function below the neurological injury level remains intact (Table 1).
|INJURY||MECHANISM||DESCRIPTION||FUNCTIONS PRESERVED||FUNCTIONS IMPAIRED|
|Brown-Séquard syndrome||Penetrating trauma||One side of the cord is affected||Opposite-side pain and temperature sensation||Opposite-side movement, proprioception, light touch|
|Same-side movement, proprioception, light touch||Same-side pain and temperature sensation|
|Posterior cord syndrome||Extension||Loss of posterior column sensory function; motor paralysis|
|Anterior cord syndrome||Flexion||Hypalgesia; hypesthesia, motor paralysis, posterior column sensory function preserved||Light touch, proprioception, vibratory sensation||Pain sensation, motor function, temperature sensation|
|Central cord syndrome||Flexion or extension||Injury to central gray matter||Motor functions of lower extremities||Motor functions of upper extremities|
Leading causes of SCI include motor vehicle crashes (MVCs), falls, acts of violence, and sporting injuries. SCIs caused by violence have increased dramatically in the last decade. The mechanism of injury influences the type of SCI and the degree of neurological deficit.
No clear genetic contributions to susceptibility have been defined.
Gender, ethnic/racial, and life span considerations
Acute SCIs occur in both children and adults, although the majority occur between the ages of 16 and 18. The vast majority, approximately 80%, involve men. The financial impact of acute SCIs is tremendous, but it is related to the age of most patients and the degree of disability. Older adults have greater functional and mental status decline after a SCI as compared to their younger counterparts. There are no known racial or ethnic considerations.
Global health considerations
Experts estimate that each year, there are approximately 225,000 cases globally of traumatic SCI from injuries and violence. Transportation injuries from motor vehicle crashes are decreasing in developed regions but increasing in developing regions due to the growing number of vehicles on the road, poor infrastructure, and difficulty enforcing laws. As populations age, traumatic SCI from falls among older adults is increasing in developed and developing regions; falls from heights of less than 5 meters are the leading cause of injury overall, and in developing countries, falls are common from trees, roofs, and balconies, and at construction sites. Traumatic SCI occurs in young people in developing regions from carrying heavy loads on their heads.
Determine the mechanism of injury in addition to taking a detailed report from prehospital professionals about the patient with an acute SCI. Question the prehospital care provider, significant others, or witnesses about the situation surrounding the injury. If the patient was in an MVC, determine the speed and type of the vehicle, whether the patient was restrained, the patient’s position in the vehicle, and if the patient was thrown from the vehicle on impact. If the patient fell, the distance of the fall is important to know during the initial assessment and evaluation phase. A key component of the history in the patient with a suspected acute SCI is information about the patient’s motor and sensory function at the scene of the injury.
Common symptoms include pain, changes in strength and motion of the extremities, changes in sensation, and changes in bowel and bladder function. Changes may be an autonomic response (urinary retention, constipation, paralytic ileus, hypotension, hypothermia, and bradycardia), a motor response (hemiplegia or hemiparesis, paraplagia or paraparesis, tetraplegia or tetraparesis), or sensory changes at a particular cord level. Assess the patient as soon as possible after the primary injury and again each hour during the acute period. Neurological assessments usually include the Glasgow Coma Scale and pupil reflexes.
The initial assessment is conducted at the injury site. This primary survey generally takes about 30 seconds and focuses on assessing airway, breathing, and circulation (ABCs) and implementing life-saving intervention. Stabilizing the cervical spine prevents an incomplete SCI from progressing to a complete one. The secondary survey is a complete head-to-toe assessment. Sometime during the first 48 hours, a tertiary survey is performed to discover any subtle injuries that may have been missed during the initial assessment.
Assess the patient’s injury level. Test the patient’s ability to distinguish a pinprick from dull pain at each level of the dermatomes. Rectal examination helps determine if the sphincter tone is normal and if the SCI is complete or incomplete. Normal sphincter tone and anal winking indicate an incomplete SCI. Evaluate the patient’s motor strength to help determine the injury level. Test the patient’s motor movement.
Examine the patient for signs of neurogenic shock, which usually occurs within 30 to 60 minutes after the SCI when sympathetic nerves have lost their normal connections to the central nervous system (CNS). Signs to look for include decreased heart rate and pronounced hypotension (systolic pressure below 90 mm Hg).
Acute SCI is catastrophic and alters not only the lives of patients but also the lives of their families, friends, and the community they live in. Physiological alterations are significant in patients with acute SCIs, as are the psychosocial adjustments. Ongoing assessment of the patient’s and family’s coping skills is critical in planning meaningful support and interventions to assist the patient in reaching her or his functional potential.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Spine x-rays||Normal body structures||May show spine fractures or injury such as dislocation or subluxation||Determines the integrity of bony structures of spine|
|Computed tomography scan||Normal body structures||Determines degree and extent of injury; may show spine fractures or injury such as dislocation or subluxation||Determines the integrity of bony structures of spine|
|Magnetic resonance imaging||Normal body structures||Determines degree and extent of injury; may show spine fractures or injury such as dislocation or subluxation||Determines the integrity of bony structures of spine|
Other Tests: Electromyography, somatosensory-evoked potentials, motor-evoked potentials, complete blood count, urinalysis, arterial blood gases
Primary nursing diagnosis
DiagnosisIneffective airway clearance related to hypoventilation or airway obstruction
OutcomesRespiratory status: Gas exchange and ventilation; Safety status: Physical injury
InterventionsAirway insertion; Airway management; Airway suctioning; Oral health promotion; Respiratory monitoring; Ventilation assistance
Planning and implementation
Maintenance of ABCs is the highest priority in patients with SCI. The patient with a cervical or high thoracic injury is at risk for developing pulmonary insufficiency, problems with airway clearance, and ineffective breathing patterns. The patient may require endotracheal intubation or tracheostomy with mechanical ventilation. Assess tidal volume and vital capacity every 2 hours in the patient who is not endotracheally intubated. Hydration may be provided by intravenous (IV) crystalloid fluids or by dextran, a plasma expander that may be used to increase capillary blood flow.
The benefits of early spinal stabilization are decreased morbidity and decreased length of hospital stay, but the neurological benefits are controversial. Although this is a temporary intervention, external stabilization may be accomplished by Gardner-Wells tongs, which can be applied until surgical stabilization can be performed. A halo apparatus can be applied either as a primary intervention or to protect a surgical repair. This device immobilizes the cervical spine but allows the patient increased mobility. Patients with stable thoracolumbar spine fractures require only support with a rigid external brace for several months. Timing for surgical (internal) stabilization of cervical spine injuries is controversial. Some suggest that early surgical stabilization enhances neurological recovery and decreases morbidity, but others believe that early stabilization may increase biochemical alterations and vascular instability.
Patients with unstable thoracolumbar spine fractures are managed with metal rods and surgical decompression. Neurological outcome may be improved by postponing surgery until spinal cord edema is decreased.
Postoperative patients may require a rigid cervical collar or rigid external brace to protect the surgical repair. Patients with acute SCI from penetrating trauma may require surgical intervention for débridement and closure of the dura if cerebrospinal fluid leakage persists. If x-ray films demonstrate that a bullet or other foreign body is within the spinal cord, surgical removal may be recommended to decrease the likelihood of chronic radicular pain.
|Medication or Drug Class||Dosage||Description||Rationale|
|Methylprednisolone||30 mg/kg IV as a loading dose, followed by a 48-hr IV infusion of 5.4 mg/kg per hr||Corticosteroid; dexamethasone may also be used||Reduces inflammation and improves motor and sensory function|
|Inotropic agents||Varies by drug||Dopamine, dobutamine||Improve systemic vascular resistance and blood pressure|
|Atropine||1 mg IV as needed||Anticholinergic||Manages symptomatic bradycardia|
Other Drugs: Prophylactic anticoagulants may prevent the formation of deep vein thrombosis when the patient is no longer at risk for hemorrhage. Histamine-receptor antagonists decrease gastric acid secretion by inhibiting the receptor sites in the parietal cells and reducing the risk of stress ulcers. Antacids may be administered to neutralize gastric acid.
The most critical nursing intervention for the patient with an acute SCI is to maintain airway, breathing, and circulation. Maintain cervical alignment and immobilization. An abdominal binder may be beneficial in patients with SCIs to provide additional support of the abdominal musculature, a major contributor to respiratory excursion. A potentially life-threatening complication associated with acute SCI is autonomic dysreflexia. This dysfunction may occur after the acute phase and is characterized by a hypersympathetic response to some noxious stimuli; this response is commonly found in patients with SCIs above the T8 level (Box 1). Deep vein thrombosis may also occur. Apply sequential compression devices or foot pumps as prescribed.Autonomic Dysreflexia
Check bony prominences and areas under the brace or jacket for skin breakdown. Aggressive physical and occupational therapy early in the acute phase may be beneficial to the patient’s overall rehabilitation. Joint range-of-motion exercises prevent contractures and severe muscle wasting. Some patients may require splints for the upper and lower extremities to prevent flexion contractures and footdrop.
Prevent urinary tract infections by instituting an intermittent catheterization protocol early. Protocols vary, but most begin with catheterizing every 4 hours. Monitor the residual urine volume; when it is less than 400 mL, catheterization can be done every 6 hours. Record the amount of urine voided and the postvoid residuals. As the amount of residual volume decreases, increase the time intervals between catheterizations. Before catheterization, assist the patient in emptying the bladder by Crede’s method or by gently tapping or percussing the bladder. Establish bowel continence early in the acute phase.
When the patient is eating by mouth or is being tube fed, administer stool softeners as ordered. If the patient has not had a bowel movement, administer bisacodyl (Dulcolax) suppository. If the patient is NPO (nothing by mouth), administer bisacodyl every other night. Digital stimulation is used in conjunction with the bowel program. Adequate fluid volume status is important for a successful bowel and bladder program.
Provide diversionary activities to help pass the time. Arrange for the patient or family to consult with a clinical nurse specialist, chaplain, or social worker to assist in coping with anxiety and stress if it is deemed necessary. If the patient has little hope for recovery, consider speaking with the family about donating the patient’s organs if appropriate.
If the patient is scheduled for discharge, teach the patient and family about the recommended activity level and rehabilitative exercises. Explain how to recognize the signs and symptoms of infection or a deteriorating level of consciousness. Instruct the patient and family in the name, dosage, action, and potential adverse effects of all prescribed medications. Show them the proper care for wounds and lacerations. Make sure the patient and family are aware of the schedule for follow-up medical care.
Evidence-Based Practice and Health Policy
Krassioukov, A., Eng, J.J., Claxton, G., Sakakibara, B.M., & Shum, S. (2010). Neurogenic bowel management after spinal cord injury: A systematic review of the evidence. Spinal Cord, 48(10), 718–733.
- Investigators conducted a systematic review of 52 studies reporting strategies for neurogenic bowel management in patients with an SCI and evaluated them according to the following levels of evidence: level 1 includes randomized controlled trials (RCTs) with good to excellent methodological quality; level 2 includes RCTs with fair to good methodological quality and nonrandomized cohort studies; level 3 includes case-control studies; and level 4 includes pretest and posttest or case series.
- There is level 4 evidence that support the use of multifaceted bowel management programs to reduce gastrointestinal transit time and the duration of time required for bowel management. There is also level 4 evidence that support the use of digital rectal stimulation to increase motility as well as the use of abdominal massage to shorten colonic transit time, reduce abdominal distension, and increase the frequency of bowel movements per week.
- Additionally, there is level 1 evidence that supports the use of polyethylene glycol-based suppositories to decrease total bowel care time, and there is level 2 evidence that supports the use of cisapride, prucalopride, and intravenous metoclopramide to decrease constipation, improve stool consistency, and correct impairment in gastric emptying. However, level 4 evidence from one case series revealed that the use of a high-fiber diet increased rather than decreased the colonic transit time among SCI patients in that study.
- Lastly, there is level 4 evidence that supports the placement of a colostomy to simplify bowel care routines, reduce the number of hours spent on bowel care, reduce the number of gastrointestinal-related hospitalizations, and improve patients’ health-related and psychosocial quality of life.
- Physical findings: Vital signs, hemodynamic parameters, urinary output, tidal volumes, vital capacity, level of consciousness
- Presence of complications: Pulmonary infections, urinary tract infection, deep vein thrombosis, alterations in skin integrity, autonomic dysreflexia
- Presence of bowel and bladder continence
Discharge and home healthcare guidelines
Encourage the patient to participate in therapies. Instruct the patient to communicate any abnormalities that are recognized. Explain the use of compression stockings as prescribed, with correct application. Teach the patient to maintain the bowel and bladder program. Verify that the patient and family understand the causes and symptoms of autonomic dysreflexia. Be sure the patient understands any medication prescribed. Verify that the patient and family have demonstrated safe use of all assistive devices: wheelchair, transfers, adaptive feeding equipment, and toileting practices. Review with the patient and family all follow-up appointments that are arranged. Verify that all at-home arrangements have been completed.