We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy

Factor Contributes to Student Absenteeism

The whole doc is available only for registered users

A limited time offer! Get a custom sample essay written according to your requirements urgent 3h delivery guaranteed

Order Now

Patients with spinal cord injury (SCI) usually have permanent and often devastating neurologic deficits and disability. According to the National Institutes of Health, “among neurological disorders, the cost to society of automotive SCI is exceeded only by the cost of mental retardation.”The goals for the emergency physician are to establish the diagnosis and initiate treatment to prevent further neurologic injury from either pathologic motion of the injured vertebrae or secondary injury from the deleterious effects of cardiovascular instability or respiratory insufficiency.PathophysiologyThe spinal cord is divided into 31 segments, each with a pair of anterior (motor) and dorsal (sensory) spinal nerve roots. On each side, the anterior and dorsal nerve roots combine to form the spinal nerve as it exits from the vertebral column through the neuroforamina. The spinal cord extends from the base of the skull and terminates near the lower margin of the L1 vertebral body.

Thereafter, the spinal canal contains the lumbar, sacral, and coccygeal spinal nerves that comprise the cauda equina. Therefore, injuries below L1 are not considered SCIs because they involve the segmental spinal nerves and/or cauda equina. Spinal injuries proximal to L1, above the termination of the spinal cord, often involve a combination of spinal cord lesions and segmental root or spinal nerve injuries.The spinal cord itself is organized into a series of tracts or neuropathways that carry motor (descending) and sensory (ascending) information. These tracts are organized anatomically within the spinal cord. The corticospinal tracts are descending motor pathways located anteriorly within the spinal cord. Axons extend from the cerebral cortex in the brain as far as the corresponding segment, where they form synapses with motor neurons in the anterior (ventral) horn. They decussate (cross over) in the medulla prior to entering the spinal cord.The dorsal columns are ascending sensory tracts that transmit light touch, proprioception, and vibration information to the sensory cortex. They do not decussate until they reach the medulla. The lateral spinothalamic tracts transmit pain and temperature sensation. These tracts usually decussate within 3 segments of their origin as they ascend.

The anterior spinothalamic tract transmits light touch. Autonomic function traverses within the anterior interomedial tract. Sympathetic nervous system fibers exit the spinal cord between C7 and L1, while parasympathetic system pathways exit between S2 and S4.Injury to the corticospinal tract or dorsal columns, respectively, results in ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. Unlike injuries of the other tracts, injury to the lateral spinothalamic tract causes contralateral loss of pain and temperature sensation. Because the anterior spinothalamic tract also transmits light touch information, injury to the dorsal columns may result in complete loss of vibration sensation and proprioception but only partial loss of light touch sensation. Anterior cord injury causes paralysis and incomplete loss of light touch sensation.Autonomic function is transmitted in the anterior interomedial tract. The sympathetic nervous system fibers exit from the spinal cord between C7 and L1. The parasympathetic system nerves exit between S2 and S4. Therefore progressively higher spinal cord lesions or injury causes increasing degrees of autonomic dysfunction.

Neurogenic shock is characterized by severe autonomic dysfunction, resulting in hypotension, relative bradycardia, peripheral vasodilation, and hypothermia. It does not usually occur with SCI below the level of T6. Shock associated with an SCI involving the lower thoracic cord must be considered hemorrhagic until proven otherwise. In this article, spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from autonomic dysfunction and the interruption of sympathetic nervous system control in acute SCI.The blood supply of the spinal cord consists of 1 anterior and 2 posterior spinal arteries. The anterior spinal artery supplies the anterior two thirds of the cord. Ischemic injury to this vessel results in dysfunction of the corticospinal, lateral spinothalamic, and autonomic interomedial pathways. Anterior spinal artery syndrome involves paraplegia, loss of pain and temperature sensation, and autonomic dysfunction.

The posterior spinal arteries primarily supply the dorsal columns. The anterior and posterior spinal arteries arise from the vertebral arteries in the neck and descend from the base of the skull. Various radicular arteries branch off the thoracic and abdominal aorta to provide collateral flow.The primary watershed area of the spinal cord is the midthoracic region. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. For example, a lower cervical spine fracture may result in disruption of the vertebral artery that ascends through the affected vertebra. The resulting vascular injury may cause an ischemic high cervical cord injury. At any given level of the spinal cord, the central part is a watershed area. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome.SCIs may be primary or secondary. Primary SCIs arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary SCI may occur in the absence of spinal fracture or dislocation.

Penetrating injuries due to bullets or weapons may also cause primary SCI. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.Extradural pathology may also cause a primary SCI. Spinal epidural hematomas or abscesses cause acute cord compression and injury.Spinal cord compression from metastatic disease is a common oncologic emergency.Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary SCI without spinal fracture or dislocation. The term SCIWORA (spinal cord injury without radiologic abnormality) was first coined in 1982 by Pang and Wilberger. The spinal cord is tethered more securely than the vertebral column. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in SCIWORA.Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary SCI. Anoxic or hypoxic effects compound the extent of SCI.One of the goals of the emergency physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete.

A complete cord syndrome is characterized clinically as complete loss of motor and sensory function below the level of the traumatic lesion. Incomplete cord syndromes have variable neurologic findings with partial loss of sensory and/or motor function below the level of injury. Incomplete cord syndromes include the anterior cord syndrome, the Brown-Séquard syndrome, and the central cord syndrome. Other cord syndromes include the conus medullaris syndrome, the cauda equina syndrome, and spinal cord concussion.In most clinical scenarios, the emergency physician should use a best-fit model to classify the SCI syndrome.The incomplete SCI syndromes are further characterized clinically as follows: * Anterior cord syndrome involves variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception. * Brown-Séquard syndrome involves a relatively greater ipsilateral loss of proprioception and motor function, with contralateral loss of pain and temperature sensation.

* Central cord syndrome usually involves a cervical lesion, with greater motor weakness in the upper extremities than in the lower extremities. The pattern of motor weakness shows greater distal involvement in the affected extremity than proximal muscle weakness. Sensory loss is variable, and the patient is more likely to lose pain and/or temperature sensation than proprioception and/or vibration. Dysesthesias, especially those in the upper extremities (eg, sensation of burning in the hands or arms), are common. Sacral sensory sparing usually exists.Other cord syndromes are clinically described as follows: * Conus medullaris syndrome is a sacral cord injury with or without involvement of the lumbar nerve roots. This syndrome is characterized by areflexia in the bladder, bowel, and to a lesser degree, lower limbs. Motor and sensory loss in the lower limbs is variable. * Cauda equina syndrome involves injury to the lumbosacral nerve roots and is characterized by an areflexic bowel and/or bladder, with variable motor and sensory loss in the lower limbs. Because this syndrome is a nerve root injury rather than a true SCI, the affected limbs are areflexic.

This injury is usually caused by a central lumbar disk herniation. * A spinal cord concussion is characterized by a transient neurologic deficit localized to the spinal cord that fully recovers without any apparent structural damage.SCI, as with acute stroke, is a dynamic process. In all acute cord syndromes, the full extent of injury may not be apparent initially. Incomplete cord lesions may evolve into more complete lesions. More commonly, the injury level rises 1 or 2 spinal levels during the hours to days after the initial event. A complex cascade of pathophysiologic events related to free radicals, vasogenic edema, and altered blood flow accounts for this clinical deterioration. Normal oxygenation, perfusion, and acid-base balance are required to prevent worsening of the SCI.FrequencyUnited StatesThe incidence is approximately 50 cases per million population, or about 14,000 patients, per year.SexThe male-to-female ratio is approximately 2.5-3.0:1.Age * About 80% of males with SCIs are aged 18-25 years.

* SCIWORA occurs primarily in children. A high incidence of complete cord injuries associated with SCIWORA has been reported in children younger than 9 years.History * Clinical evaluation of a patient with suspected SCI begins with careful history taking, focusing on symptoms related to the vertebral column (most commonly pain) and any motor or sensory deficits. * Complete bilateral loss of sensation or motor function below a certain level indicates a complete SCI. * Ascertaining the mechanism of injury is also important in identifying the potential for spinal injury. * Hemorrhagic shock may be difficult to diagnose because the clinical findings may be affected by autonomic dysfunction. * * Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure the emergency physician. * Occult internal injuries with associated hemorrhage may be missed.

* In all patients with SCI and hypotension, a diligent search for sources of hemorrhage must be made before hypotension is attributed to neurogenic shock. In acute SCI, shock may be neurogenic, hemorrhagic, or both. * The following clinical pearls are useful in distinguishing hemorrhagic shock from neurogenic shock: * * Neurogenic shock occurs only in the presence of acute SCI above T6. Hypotension and/or shock with acute SCI at or below T6 is caused by hemorrhage. * Hypotension with a spinal fracture alone, without any neurologic deficit or apparent SCI, is invariably due to hemorrhage. * Patients with an SCI above T6 may not have the classic physical findings associated with hemorrhage (eg, tachycardia, peripheral vasoconstriction). This vital sign confusion attributed to autonomic dysfunction is common in SCI. * The presence of vital sign confusion in acute SCI and a high incidence of associated injuries requires a diligent search for occult sources of hemorrhage. * A careful neurologic assessment is required to establish the presence or absence of SCI and to classify the lesion according to a specific cord syndrome.

Determine the level of injury and try to differentiate nerve root injury from SCI but recognize that both may be present. * The American Spinal Injury Association has established pertinent definitions. The neurologic level of injury is the lowest (most caudal) level with normal sensory and motor function. For example, a patient with C5 quadriplegia has, by definition, abnormal motor and sensory function from C6 down. * The American Spinal Injury Association recommends use of the following scale of findings for the assessment of motor strength in SCI: * 0 – No contraction or movement * 1 – Minimal movement * 2 – Active movement, but not against gravity * 3 – Active movement against gravity * 4 – Active movement against resistance * 5 – Active movement against full resistance * Assessment of sensory function helps to identify the different pathways for light touch, proprioception, vibration, and pain. Use a pinprick to evaluate pain sensation. * Differentiating a nerve root injury from SCI can be difficult. The presence of neurologic deficits that indicate multilevel involvement suggests SCI rather than a nerve root injury. In the absence of spinal shock, motor weakness with intact reflexes indicates SCI, while motor weakness with absent reflexes indicates a nerve root lesion.

PhysicalAs with all trauma patients, initial clinical evaluation begins with a primary survey. The primary survey focuses on life-threatening conditions. Assessment of airway, breathing, and circulation takes precedence. An SCI must be considered concurrently.The clinical assessment of pulmonary function in acute SCI begins with careful history taking regarding respiratory symptoms and a review of underlying cardiopulmonary comorbidity such as chronic obstructive pulmonary disease or heart failure.Carefully evaluate respiratory rate, chest wall expansion, abdominal wall movement, cough, and chest wall and/or pulmonary injuries. Arterial blood gas (ABG) analysis and pulse oximetry are especially useful because the bedside diagnosis of hypoxia or carbon dioxide retention may be difficult. * The degree of respiratory dysfunction is ultimately dependent on preexisting pulmonary comorbidity, the level of SCI, and any associated chest wall or lung injury. Any or all of the following determinants of pulmonary function may be impaired in the setting of SCI: *

* Loss of ventilatory muscle function from denervation and/or associated chest wall injury * Lung injury, such as pneumothorax, hemothorax, or pulmonary contusion * Decreased central ventilatory drive that is associated with head injury or exogenous effects of alcohol and drugs * A direct relationship exists between the level of cord injury and the degree of respiratory dysfunction. * * With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent. * With lesions at C3 through C6, vital capacity is 20% of normal, and cough is weak and ineffective. * With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and cough is weak. * With lower cord injuries, respiratory function improves. * With injuries at T11, respiratory dysfunction is minimal. Vital capacity is essentially normal, and cough is strong.

* Other findings of respiratory disfunction include the following: * * Agitation, anxiety, or restlessness * Poor chest wall expansion * Decreased air entry * Rales, rhonchi * Pallor, cyanosis * Increased heart rate * Paradoxic movement of the chest wall * Increased accessory muscle use * Moist cough * In all patients, assessment of deep tendon reflexes and perineal evaluation is critical. The presence or absence of sacral sparing is a key prognostic indicator. * The sacral roots may be evaluated by documenting the following: * Perineal sensation to light touch and pinprick * Bulbocavernous reflex (S3 or S4) * Anal wink (S5) * Rectal tone * Urine retention or incontinence * Priapism * The reader is referred to any textbook of neuroanatomy or emergency medicine for a table outlining the important muscle groups, dermatomes, and reflexes to determine the level of the spinal cord lesion (see Image 1).Other Problems to be ConsideredTransverse myelitis Acute intervertebral disk herniation

Extradural spinal cord compressionLab Studies * Hemoglobin and/or hematocrit levels may be measured initially and monitored serially to detect or monitor sources of blood loss. * Perform urinalysis to detect associated genitourinary injury.Imaging Studies * Diagnostic imaging begins with the acquisition of standard radiographs of the affected region of the spine. However, in some centers, CT scanning has supplanted plain radiographs. * * The standard 3 views of the cervical spine are recommended: anteroposterior, lateral, and odontoid. * Anteroposterior and lateral views of the thoracic and lumbar spine are recommended. * Radiographs must adequately depict all vertebrae. * The cervical spine radiographs must include the C7-T1 junction to be considered adequate. * A common cause of missed injury is the failure to obtain adequate images. * CT scanning is reserved for delineating bony abnormalities or fracture. Some studies have suggested that CT scanning with sagittal and coronal reformatting is more sensitive than plain radiography for the detection of spinal fractures. * * Radiography is insensitive to small fractures of the vertebra. To confirm SCI without radiologic abnormality (SCIWORA), a CT scan documenting the absence of fracture often is necessary.

* Perform CT scanning in the following situations: * Plain radiography is inadequate. * Convenience and speed: If a CT scan of the head is required, then it is usually simpler and faster to obtain a CT of the cervical spine at the same time. Similarly, CT images of the thoracic or lumbar spine might be easier and faster to obtain than plain radiographs. * Radiography depicts suspicious and/or indeterminate abnormalities. * Radiography depicts fracture or displacement: CT scanning provides better visualization of the extent and displacement of the fracture. * Recently published clinical criteria have established guidelines for cervical spine radiography in symptomatic trauma patients with neck pain. The NEXUS criteria and the Canadian C-spine rules have recently been validated in large clinical trials. * Adequate spinal radiography supplemented by CT scanning through areas that are difficult to visualize or are suspicious detects the vast majority of fractures with a reported negative predictive value between 99% and 100%. * Dynamic flexion/extension views are safe and effective for detecting occult ligamentous injury of the cervical spine in the absence of fracture. The negative predictive value of a normal 3-view cervical spine series and flexion/extension views exceeds 99%.

The incidence of occult injury in the setting of normal findings on cervical spine radiography and CT scanning is low, so clinical judgment and the mechanism of injury should be used to guide the decision to order flexion/extension views. * MRI is best for suspected spinal cord lesions, ligamentous injuries, or other soft tissue injuries or pathology. * * MRI should be used to evaluate nonosseous lesions, such as extradural spinal hematoma; abscess or tumor; and spinal cord hemorrhage, contusion, and/or edema. * Neurologic deterioration is usually caused by secondary injury, resulting in edema and/or hemorrhage. MRI is the best diagnostic image to depict these changes.TREATMENTPrehospital Care * Most prehospital care providers recognize the need to stabilize and immobilize the spine on the basis of mechanism of injury, pain in the vertebral column, or neurologic symptoms. * Patients are usually transported to the ED with a cervical hard collar on a hard backboard. * * Commercial devices are available to secure the patient to the board. * The patient should be secured so that in the event of emesis, the backboard may be rapidly rotated 90 degrees while the patient remains fully immobilized in neutral position.

Spinal immobilization protocols should be standard in all prehospital care systems.Emergency Department CareMost patients with SCIs have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation takes precedence.Airway management in the setting of SCI, with or without a cervical spine injury, is complex and difficult. The cervical spine must be maintained in neutral alignment at all times. Clearing of oral secretions and/or debris is essential to maintain airway patency and to prevent aspiration. The modified jaw thrust and insertion of an oral airway may be all that is required to maintain an airway in some cases. However, intubation may be required in others. Failure to intubate emergently when indicated because of concerns regarding the instability of the patient’s cervical spine is a potential pitfall.Hypotension may be hemorrhagic and/or neurogenic in acute SCI. Due to the vital sign confusion in acute SCI and the high incidence of associated injuries, a diligent search for occult sources of hemorrhage must be made.The most common causes of occult hemorrhage are chest, intra-abdominal, or retroperitoneal injuries and pelvic or long bone fractures.

Appropriate investigations, including radiography or CT scanning, are required. In the unstable patient, diagnostic peritoneal lavage or bedside FAST (focused abdominal sonography for trauma) ultrasonographic study may be required to detect intra-abdominal hemorrhage.Once occult sources of hemorrhage have been excluded, initial treatment of neurogenic shock focuses on fluid resuscitation. Judicious fluid replacement with isotonic crystalloid solution to a maximum of 2 liters is the initial treatment of choice. Overzealous crystalloid administration may cause pulmonary edema because these patients are at risk for the acute respiratory distress syndrome. * The therapeutic goal for neurogenic shock is adequate perfusion with the following parameters:* Systolic blood pressure (BP) should be 90-100 mm Hg. Systolic BPs in this range are typical for patients with complete cord lesions. The most important treatment consideration is to maintain adequate oxygenation and perfusion of the injured spinal cord. Compelling animal and human studies recommend maintenance of systolic blood pressure higher than 90 and prevent any hypotensive episodes. * Heart rate should be 60-100 beats per minute in normal sinus rhythm. * Hemodynamically significant bradycardia may be treated with atropine.

* Urine output should be more than 30 mL/h. Placement of a Foley catheter to monitor urine output is essential. Rarely, inotropic support with dopamine is required. It should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation. Usually, low doses of dopamine in the 2- to 5-mcg/kg/min range are sufficient. * Prevent hypothermia. * Associated head injury occurs in about 25% of SCI patients. A careful neurologic assessment for associated head injury is compulsory. The presence of amnesia, external signs of head injury or basilar skull fracture, focal neurologic deficits, associated alcohol intoxication or drug abuse, and a history of loss of consciousness mandates a thorough evaluation for intracranial injury, starting with noncontrast head CT scanning. * Ileus is common. Placement of a nasogastric tube is essential. Aspiration pneumonitis is a serious complication in the SCI patient with compromised respiratory function. Antiemetics should be used aggressively.

* The patient is best treated initially in the supine position. Occasionally, the patient may have been transported prone by the prehospital care providers. Logrolling the patient to the supine position is safe to facilitate diagnostic evaluation and treatment. Use analgesics appropriately and aggressively to maintain the patient’s comfort if he or she has been lying on a hard backboard for an extended period. * Prevent pressure sores. Denervated skin is particularly prone to pressure necrosis. Turn the patient every 1-2 hours. Pad all extensor surfaces. Undress the patient to remove belts and back pocket keys or wallets. Remove the spine board as soon as possible. * The National Acute Spinal Cord Injury Studies (NASCIS) II and III, a Cochrane review of all randomized clinical trials and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete SCIs who were treated with high doses of methylprednisolone within 8 hours of injury.The NASCIS II study evaluated methylprednisolone administered within 8 hours of injury.

The NASCIS III study evaluated methylprednisolone 5.4 mg/kg/h for 24 or 48 hours versus tirilazad 2.5 mg/kg q6h for 48 hours. (Tirilazad is a potent lipid preoxidation inhibitor.) High doses of steroids or tirilazad are thought to minimize the secondary effects of acute SCI. In the NASCIS III trial, all patients (n = 499) received a 30-mg/kg bolus of methylprednisolone intravenously. The study found that in patients treated earlier than 3 hours after injury, the administration of methylprednisolone for 24 hours was best. In patients treated 3-8 hours after injury, the use of methylprednisolone for 48 hours was best. Tirilazad was equivalent to methylprednisolone for 24 hours.Both NASCIS studies evaluated the patients’ neurologic status at baseline on enrollment into the study, at 6 weeks, and at 6 months. Absolutely no evidence from these studies suggests that giving the medication earlier (eg, in the first hour) provides more benefit than giving it later (eg, between hours 7 and 8). The authors only concluded that there was a benefit if given within 8 hours of injury following the NASCIS trials. * The use of high-dose methylprednisolone in nonpenetrating acute SCI had become the standard of care in North America.

Nesathurai and Shanker revisited these studies and questioned the validity of the results. These authors cited concerns about the statistical analysis, randomization, and clinical endpoints used in the study. Even if the benefits of steroid therapy are valid, the clinical gains are questionable. Other reports have cited flaws in the study designs, trial conduct, and final presentation of the data. The risks of steroid therapy are not inconsequential. An increased incidence of infection and avascular necrosis has been documented. * A number of professional organizations have therefore revised their recommendations pertaining to steroid therapy in SCI. The Canadian Association of Emergency Physicians is no longer recommending high-dose methylprednisolone as the standard of care. The Congress of Neurological Surgeons has stated that steroid therapy “should only be undertaken with the knowledge that the evidence suggesting harmful side effects is more consistent than any suggestion of clinical benefit.”

The American College of Surgeons has modified their Advanced Trauma Life Support guidelines to state that methylprednisolone is “a recommended treatment” rather than “the recommended treatment.” * In a recent survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroids in SCI, but only 24% believed that they were of any clinical benefit. Note that the authors discovered that approximately 7% of spine surgeons do not recommend or use steroids at all in acute SCI. The authors reported that most centers werefollowing the NASCIS II trial protocol. * Overall the benefit from steroids is considered modest at best, but for patients with complete or incomplete quadriplegia, a small improvement in motor strength in one or more muscles can provide important functional gains. * The administration of steroids remains an institutional and physician preference in spinal cord injury. Nevertheless, the administration of high-dose steroids within 8 hours of injury for all acute SCI patients is practiced by most physicians.

* The current recommendation is to treat all SCI patients according to the local/regional protocol. If steroids are recommended, they should be initiated within 8 hours of injury with the following steroid protocol: methylprednisolone 30 mg/kg bolus over 15 minutes and an infusion of methylprednisolone at 5.4 mg/kg/h for 23 hours beginning 45 minutes after the bolus. * Local policy will also determine if the NASCIS II or NASCIS III protocol is to be followed. * Two North American studies have addressed the administration of GM-1 ganglioside following acute SCI. The available medical evidence does not support a significant clinical benefit. It was evaluated as a treatment adjunct after the administration of methylprednisolone. * Treatment of pulmonary complications and/or injury in patients with SCI includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax and/or hemothorax. * The ideal technique for emergent intubation in the setting of SCI is fiberoptic intubation with cervical spine control. This, however, has not been proven better than orotracheal with in-line immobilization.

Furthermore, no definite reports of worsening neurologic injury with properly performed orotracheal intubation and in-line immobilization exist. If the necessary experience or equipment is lacking, blind nasotracheal or oral intubation with in-line immobilization is acceptable. Indications for intubation in SCI are acute respiratory failure, decreased level of consciousness (Glasgow score <9), increased respiratory rate with hypoxia, PCO2 more than 50, and vital capacity less than 10 mL/kg. * In the presence of autonomic disruption from cervical or high thoracic SCI, intubation may cause severe bradyarrhythmias from unopposed vagal stimulation. Simple oral suctioning can also cause significant bradycardia.

Preoxygenation with 100% oxygen may be preventive. Atropine may be required as an adjunct. Topical lidocaine spray can minimize or prevent this reaction.Consultations * Consultation with a neurosurgeon and/or orthopedist is required, depending on local preferences. * Because most patients with SCI have multiple associated injuries, consultation with a general surgeon or trauma specialist may be required. * Depending on the patient’s associated injuries, other consultations may be required. MEDICATIONThe goal of therapy is to improve motor function and sensation in patients with SCIs.Drug Category: GlucocorticoidsHigh-dose steroids are thought to reduce the secondary effects of acute SCI. Studies have shown limited but significant improvement in the neurologic outcome of patients treated within 8 h of injury. Drug Name| Methylprednisolone (Solu-Medrol)| Description| Used to reduce the secondary effects of acute SCI.| Adult Dose| 30 mg/kg IV bolus over 15 min, followed by 5.4 mg/kg/h over 23 h; begin IV infusion 45 min after conclusion of bolus| Pediatric Dose| Administer as in adults|

Contraindications| Documented hypersensitivity; viral, fungal, or tubercular skin infections| Interactions| Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogen use may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when administered with diuretics| Pregnancy| C – Safety for use during pregnancy has not been established.| Precautions| Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications| FOLLOW-UPFurther Inpatient Care * Admit all patients with an acute SCI. Depending on the level of neurologic deficit and associated injuries, the patient may require admission to the ICU, neurosurgical observation unit, or general ward. * Orthopedic and/or neurosurgical consultants should determine the need for and timing of any surgical intervention. * * Studies from the 1960s and 1970s showed that the patients experienced no improvement with emergent surgical decompression.

In the only recent (1997) prospective, randomized, controlled study to determine whether functional outcome is improved in patients with SCI, Vaccaro reported no significant difference between early ( <3 d, mean 1.8 d) or late (>5 d, mean 16.8 d). * Emergent decompression of the spinal cord is recommended in those select patients with extradural lesions, such as epidural hematomas or abscesses. * The role of immediate surgical intervention is limited. Impingement of spinal nerves or if acute neurologic deterioration requires emergent surgical intervention. Emergent surgical decompression is recommended in specific injuries such as facet dislocation, bilateral locked facets, or cauda equina syndrome.Transfer * Depending on local policy, patients with acute SCI are best treated at a regional SCI center. * Once stabilized, early referral to a regional SCI center is best. The center should be organized to provide ongoing definitive care. * Other reasons to transfer the patient include the lack of appropriate diagnostic imaging (CT scanning or MRI) and/or inadequate spine consultant support (orthopedist or neurosurgeon).Deterrence/Prevention

* Many patients experience SCI as a result of incidents involving drunk driving, assaults, and alcohol or drug abuse. * Industrial hazards, such as equipment failures or inadequate safety precautions, are potentially preventable causes. * Unfenced, shallow, or empty swimming pools are known hazards.Complications * The neurologic deficit often increases during the hours to days following acute SCI, despite optimal treatment. * One of the first signs of neurologic deterioration is the extension of the sensory deficit cephalad. Careful repeat neurologic examination may reveal that the sensory level has risen 1 or 2 segments. Repeat neurologic examinations to check for progression are essential. * Careful and frequent turning of the patient is required to prevent pressure sores. Denervated skin is particularly prone to this complication. Remove belts and objects from back pockets such as keys and wallets. * Try to remove the patient from the backboard as soon as possible. Some patients may require spinal immobilization in a halo vest or a Stryker frame. Many patients with acute SCI have stable vertebral fractures yet needlessly spend hours on a hard backboard.

* Patients with SCI are at high risk for aspiration. Nasogastric decompression of the stomach is mandatory. * Prevent hypothermia by using external rewarming techniques and/or warm humidified oxygen. * Pulmonary complications in SCI are common. Pulmonary complications are directly correlated with mortality, and both are related to the level of neurologic injury. Pulmonary complications of SCI include the following: * * Atelectasis secondary to decreased vital capacity and decreased functional residual capacity * Ventilation-perfusion mismatch due to sympathectomy and/or adrenergic blockade * Increased work of breathing because of decreased compliance * Decreased coughing, which increases the risk of retained secretions, atelectasis, and pneumonia * Muscle fatiguePrognosis * Patients with a complete cord injury have a less than 5% chance of recovery. If complete paralysis persists at 72 hours after injury, recovery is essentially zero. * The prognosis is much better for the incomplete cord syndromes. * If some sensory function is preserved, the chance that the patient will eventually be able walk is greater than 50%.

* Ultimately, 90% of patients with SCI return to their homes and regain independence. * Providing an accurate prognosis for the patient with an acute SCI usually is not possible in the ED and is best avoided. * In the early 1900s, the mortality rate 1 year after injury in patients with complete lesions approached 100%. Much of the improvement since then can be attributed to the introduction of antibiotics to treat pneumonia and urinary tract infection. * Currently, the 5-year survival rate for patients with a traumatic quadriplegia exceeds 90%. The hospital mortality rate for isolated acute SCI is low.Patient Education * As part of inpatient therapy, patients with SCI should receive a comprehensive program of physical and occupational therapy. * For excellent patient education resources, see the eMedicine Consumer Health Web site.MISCELLANEOUSMedical/Legal Pitfalls * Failure to establish the diagnosis of incomplete cord injury or radiculopathy when the neurologic findings are subtle * Failure to adequately immobilize the spine when the mechanism of injury is consistent with the diagnosis * * Agitated intoxicated patients are often the most difficult to manage properly.

* Pharmacological restraint may be required to allow proper assessment. Haldol and intravenous droperidol have been used successfully, even in large doses, without hemodynamic or respiratory compromise. Occasionally, rapid-sequence intubation and pharmacologic paralysis is required to treat these patients. * Physical examination and radiographic studies could be delayed until the patient is more cooperative, if his or her overall condition permits. * Attributing hypotension to neurogenic shock in the setting of SCI – A potentially devastating error * Failure to interpret the radiographs correctly * * On cervical radiography, subtle findings (eg, increased prevertebral soft tissue swelling or widening of the C1-C2 preodontoid space) indicate potentially unstable cervical spine injuries that could have serious consequences if they are not detected. * In many EDs, radiology support is limited. If unsure of a finding, request a formal interpretation or immobilize the patient appropriately, pending formal review of the studies. * Radiographs are only as good as the first and last vertebrae seen. Incomplete radiographs (eg, cervical spine radiograph that incompletely depicts the C7-T1 junction) are common in missed injuries.MULTIMEDIA Media file 1: Spinal cord injuries. Dermatome map.

Related Topics

We can write a custom essay

According to Your Specific Requirements

Order an essay
Materials Daily
100,000+ Subjects
2000+ Topics
Free Plagiarism
All Materials
are Cataloged Well

Sorry, but copying text is forbidden on this website. If you need this or any other sample, we can send it to you via email.

By clicking "SEND", you agree to our terms of service and privacy policy. We'll occasionally send you account related and promo emails.
Sorry, but only registered users have full access

How about getting this access

Your Answer Is Very Helpful For Us
Thank You A Lot!


Emma Taylor


Hi there!
Would you like to get such a paper?
How about getting a customized one?

Can't find What you were Looking for?

Get access to our huge, continuously updated knowledge base

The next update will be in:
14 : 59 : 59