Drstroiavictoria.ro

Spinal injuries eMedicine
Pathophysiology
The 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 spinal cord injuries (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 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 Neurogenic shock is characterized by severe autonomic dysfunction, resulting in hypotension, relative bradycardia, peripheral vasodilation, and hypothermia. It does not usually occur with spinal cord injury below the level of T6. Shock associated with a spinal cord injury 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 spinal cord injury.
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.
Spinal cord injuries may be primary or secondary. Primary spinal cord injuries arise from mechanical disruption, transection, or distraction of neural elements. This injury usually occurs with fracture and/or dislocation of the spine. However, primary spinal cord injury may occur in the absence of spinal fracture or dislocation. Penetrating injuries due to bullets or weapons may also cause primary spinal cord injury. More commonly, displaced bony fragments cause penetrating spinal cord and/or segmental spinal nerve injuries.
Extradural pathology may also cause a primary spinal cord injury. Spinal epidural hematomas or abscesses cause acute cord compression and injury.
Spinal cord compression from a common oncologic emergency.
Longitudinal distraction with or without flexion and/or extension of the vertebral column may result in primary spinal cord injury without spinal fracture or dislocation. 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. The term SCIWORA (spinal cord injury without radiologic abnormality) was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or CT evidence of fracture or dislocation. However with the advent of MRI, the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury. SCIWORA should now be more correctly renamed as "spinal cord injury without neuroimaging abnormality" and recognize that its prognosis isactually better than patients with spinal cord injury and radiologic evidence of traumatic injury.
Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock are the major causes of secondary spinal cord injury. Anoxic or hypoxic effects compound the extent 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 and the central cord syndrome. Other cord syndromes include the conus medullaris syndrome, the and spinal cord concussion.
In most clinical scenarios, the emergency physician should use a best-fit model to classify the SCI 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 spinal cord injury (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.
Spinal cord injury, 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 spinal cord injury.
Frequency
United States
The incidence of spinal cord injury is approximately 40 cases per million population, or about 12,000 patients, per year based on data in the National Spinal Cord Injury database. However, this estimate is based on older data from the 1970s as there has not been any new overall incidence studies completed.
Mortality/Morbidity
Originally the leading cause of death in patients with spinal cord injury who survived their initial injury was renal failure, but, currently, the leading causes of death are pneumonia, pulmonary embolism, or septicemia. Life expectancies for patients with spinal cord injury continues to increase but are still below the general population. Based on 2003 US Life Tables, a healthy 20-year-old would have a life expectancy of 78.4 years, whereas a quadriplegic who was injured at age 20 would have a life expectancy of only 60.
A significant trend over time has been observed in the racial distribution of persons with spinal cord injury.
Since 2000, 63% are Caucasian, 22.7% are African American, 11.8% are Hispanic, and fewer than 2% areAsian.
The male-to-female ratio is approximately 4:1.
Since 2005, the average age at injury is 39.5 years, reflecting the rise in the median age of the general population in the United States.
About 50% of spinal cord injuries (SCIs) occurred between the ages of 16 and 30.
Of SCIs, 3.5% occur in children aged £ 15 years, while there has been an increasing incidence of spinal cord injury in persons older than 60 years (11.5%).
Clinical
Clinical evaluation of a patient with suspected spinal cord injury (SCI) begins with careful history taking, focusing on symptoms related to the vertebral column (most commonly pain) and any motor 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.
be difficult to diagnose because the clinical findings may be affected by Disruption of autonomic pathways prevents tachycardia and peripheral vasoconstriction that normally characterizes hemorrhagic shock. This vital sign confusion may falsely reassure the 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 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 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 2 - Active movement, but not against gravity 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 Physical
As 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. Aspinal cord injury (SCI) must be considered concurrently., The clinical assessment of pulmonary function in acute spinal cord injury 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 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 With high thoracic cord injuries (ie, T2 through T4), vital capacity is 30-50% of normal, and With lower cord injuries, respiratory function improves.
With injuries at T11, respiratory dysfunction is minimal. Vital capacity is essentially normal, and Other findings of respiratory disfunction include the following: In all patients, a complete detailed neurological assessment including motor function, sensory evaluation, deep tendon reflexes, and perineal evaluation is critical. The presence or absence of sacral sparing is a key prognostic indicator.
In 1982, the American Spinal Injury Association (ASIA) first published standards for neurological classification of patients with spinal injury. Since then, further refinements have been made to definitions of neurological levels, key muscles and sensory points were identified corresponding to specific neurological levels, and the Frankel scale was validated. In 1992, the International Medical Society of paraplegia adopted these guidelines to create true international standards. Further refinements have been adopted. A standardized ASIA method for classifying spinal cord injury (SCI) by neurologic level has been developed and is included here to serve as a useful educational and reference tool. (See The key muscles that need to be tested to establish neurologic level are as follows: The sacral roots may be evaluated by documenting the following: Perineal sensation to light touch and pinprick The axial skeleton should be examined to identify and provide initial treatment of potentially unstable spinal fractures from both a mechanical and a neurologic basis. The posterior cervical spine and paraspinal tissues should be evaluated for pain, swelling, bruising, or possible malalignment.
Logrolling the patient to systematically examine each spinous process of the entire axial skeleton from the occiput to the sacrum can help identify and localize injury.
Differential Diagnoses
Other Problems to Be Considered
Laboratory Studies
Arterial blood gas measurements may be useful to evaluate adequacy of oxygenation and ventilation.
Lactate levels to monitor perfusion status can be helpful in the presence of shock. Hemoglobin and/or hematocrit levels may be measured initially and monitored serially to detect or 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. Recent investigators have shown that CT scanning is exquisitely sensitive for the detection ofspinal fractures and is cost effective.However, a properly performed lateral radiograph of the cervical spine that includes the C7-T1 junction can provide sufficient information to allow the multiple trauma victim to proceed emergently to the operating room if necessary without additional intervention other than maintenance of full spinal immobilization and a hard cervical collar. In some centers, CT scanning has supplanted plain radiographs.
The standard 3 views of the cervical spine are recommended: anteroposterior, lateral, and 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 forthe detection of spinal fractures.
Radiography is insensitive to small fractures of the vertebra.
Perform CT scanning in the following situations: When plain radiography is inadequate or fails to visualize segments of the axial skeleton 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.
To provide further evaluation when radiography depicts suspicious and/or indeterminate When 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. These algorithms may be used to guidephysicians to determine whether or not imaging of the cervical spine is required., 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 negativepredictive 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 MRI is best for suspected spinal cord lesions, ligamentous injuries, or other soft tissue injuries or MRI should be used to evaluate nonosseous lesions, such as extradural spinal hematoma; abscess or tumor; disk rupture; 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.
Noncontiguous spinal fractures are defined as spinal fractures separated by at least one normal vertebra. Noncontiguous fractures are common and occur in 10-15% of patients with spinal cord injury. Therefore, once a spinal fracture is identified, the entire axial skeleton must be imaged,preferably by CT, to assess for noncontiguous fractures.
Emergency Department Care
Most patients with spinal cord injuries (SCIs) have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation takes precedence.
Airway management in the setting of spinal cord injury, 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 spinal cord injury. Because of the vital sign confusion in acute spinal cord injury 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 anyhypotensive 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.
Associated head injury occurs in about 25% of patients with spinal cord injury. 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 Ileus is common. Placement of a nasogastric tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury 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 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.
Use of steroids in spinal cord injury
The National Acute Spinal Cord Injury Studies (NASCIS) II and III, a Cochrane Database of Systematic Reviews article of all randomized clinical trials and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete spinal cord injuries (SCIs) who were treated with high doses of methylprednisolone within 8 hours ofinjury.
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 spinal cord injury (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 wasequivalent 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 8hours of injury following the NASCIS trials.
The use of high-dose methylprednisolone in nonpenetrating acute spinal cord injury had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned thevalidity 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 spinal cord injury (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 clinicalbenefit."The American College of Surgeons has modified their Advanced Trauma Life Support guidelines to state that methylprednisolone is "a recommended treatment" rather than "the In a recent survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroidsin spinal cord injury (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 spinal cord injury. The authors reported that most centers were following the NASCIS II 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 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 patients with acute SCI is practiced by most physicians.
The current recommendation is to treat all patients with SCI 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 spinal cord injury. The available medical evidence does not support a significant clinical benefit. It wasevaluated as a treatment adjunct after the administration of methylprednisolone.
Treatment of pulmonary complications and injury in spinal cord injury
Treatment of pulmonary complications and/or injury in patients with spinal cord injury (SCI) includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax 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 spinal cord injury, 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 an orthopedist is required, depending on local preferences.
Because most patients with spinal cord injury have multiple associated injuries, consultation with a general surgeon or a trauma specialist may be required.
Depending on the patient's associated injuries, other consultations may be required.
Emergency Department Care
Most patients with spinal cord injuries (SCIs) have associated injuries. In this setting, assessment and treatment of airway, respiration, and circulation takes precedence.
Airway management in the setting of spinal cord injury, 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 spinal cord injury. Because of the vital sign confusion in acute spinal cord injury 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 anyhypotensive 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.
Associated head injury occurs in about 25% of patients with spinal cord injury. 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 Ileus is common. Placement of a nasogastric tube is essential. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury 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 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.
Use of steroids in spinal cord injury
The National Acute Spinal Cord Injury Studies (NASCIS) II and III, a Cochrane Database of Systematic Reviews article of all randomized clinical trials and other published reports, have verified significant improvement in motor function and sensation in patients with complete or incomplete spinal cord injuries (SCIs) who were treated with high doses of methylprednisolone within 8 hours ofinjury.
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 spinal cord injury (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 wasequivalent 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 8hours of injury following the NASCIS trials.
The use of high-dose methylprednisolone in nonpenetrating acute spinal cord injury had become the standard of care in North America. Nesathurai and Shanker revisited these studies and questioned thevalidity 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 spinal cord injury (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 clinicalbenefit."The American College of Surgeons has modified their Advanced Trauma Life Support guidelines to state that methylprednisolone is "a recommended treatment" rather than "the In a recent survey conducted by Eck and colleagues, 90.5% of spine surgeons surveyed used steroidsin spinal cord injury (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 spinal cord injury. The authors reported that most centers were following the NASCIS II 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 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 patients with acute SCI is practiced by most physicians.
The current recommendation is to treat all patients with SCI 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 spinal cord injury. The available medical evidence does not support a significant clinical benefit. It wasevaluated as a treatment adjunct after the administration of methylprednisolone.
Treatment of pulmonary complications and injury in spinal cord injury
Treatment of pulmonary complications and/or injury in patients with spinal cord injury (SCI) includes supplementary oxygen for all patients and chest tube thoracostomy for those with pneumothorax 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 spinal cord injury, 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 an orthopedist is required, depending on local preferences.
Because most patients with spinal cord injury have multiple associated injuries, consultation with a general surgeon or a trauma specialist may be required.
Depending on the patient's associated injuries, other consultations may be required.

Source: http://drstroiavictoria.ro/pdf/3.pdf