IntroductionThere are approximately 12,000 new cases of spinal cord injury (SCI) every year in the United States [1, 2]. This is typically a disease of young white males, though the incidence is rising in the middle-aged population [1, 3]. The causes of spinal cord injury are motor vehicle crash (42.1%), falls (26.7%), violent acts (15.1%), sports (7.6%), and other (8.6%), including medical and surgical causes. For those older than 60 years of age, falls are the most common cause of SCI. The cervical cord is most commonly injured (54.1%), compared with 45.2% for the thoracic, lumbar, and sacral levels combined [3]. The clinical signs of spinal cord injury are usually partial or complete muscular weakness, sensory loss, or both at and below the level of the lesion. Those with cervical injuries can have any degree of quadriplegia/paresis; those with thoracic lesions tend to have paraplegia/paresis. Of all patients with SCI, 20.9% have one of these clinical syndromes: anterior cord syndrome, central cord syndrome, Brown-Séquard syndrome, posterior cord syndrome, conus medullaris syndrome, and cauda equina syndrome [4]. The American Spinal Injury Association (ASIA) Impairment Scale (AIS) is used to document the severity of injury and has prognostic value when applied about 7 days after injury. AIS grades range from A (Complete—no motor or sensory function is preserved in sacral segment S4-S5) to E (Normal— motor and sensory function are normal). The numerical ASIA motor score can range from 100 (full/normal strength in all key muscle groups in the upper and lower extremities) to 0 (complete quadriplegia—complete absence of all motor function in key muscle groups in all four extremities). Diagnostic modalities used in spinal cord injury are plain x-rays (limited value), CT of the spine (for diagnosis of bony injury), MRI of the spinal cord (for diagnosis of cord and ligament pathology), and conventional and CT myelography (for diagnosis of spinal canal compromise in patients unable to undergo MRI). Show
Current acute treatment paradigms for these patients focus on stabilization of the spinal column to prevent further neurologic injury, good supportive management to prevent secondary injury, and measures to enhance cord perfusion. Some patients sustain an injury to the spinal vertebrae, disc, and/or the supporting ligaments without spinal cord injury. It is imperative that the spines of these patients are also stabilized, in order to prevent the development of neurologic injury. Acute care for these patients can be provided in the intensive care unit (ICU), an intermediate care unit, or a medical/surgical unit of a hospital, depending on the stability of the patient’s vital signs, the spinal level of the injury, the severity of injury, and other associated injuries. Pharmacologic agents such as methylprednisolone, administered in the acute phase of therapy, are controversial but have purported benefits in improving neurologic function in some patients [5–7]. Until research efforts targeted at therapies that can reverse injury and restore full neurologic function to these patients reach fruition, the mainstay of treatment will continue to focus on preventive measures (education, safer vehicles, and prevention of violence) and supportive critical care medicine. Although significant strides in its treatment have improved rates of mortality and morbidity, acute SCI continues to create an enormous societal burden related to the immeasurable detrimental psychological impact on survivors and the resource-intensive nature of their short-term and long-term care. In the United States, it is estimated that SCI has an annual cost exceeding $7 billion [8]. In addition, although the life expectancy for SCI patients is increasing with current multidisciplinary care, these patients still have a much shorter life expectancy than age-matched normals [1, 9]. Historically, renal failure was the leading cause of death for these patients, but current leading causes of early mortality in this population include pneumonias, pulmonary embolism, and septicemia [1, 9]. TreatmentAcute care
Critical care
Respiratory function
Heart and circulation
Other care considerations
Diet and lifestyle
Pharmacologic treatment
MethylprednisoloneStandard dosage:30 mg/k bolus, then 5.4 mg/kg per hour for 24 h if administered within 3 h of injury or for 48 h if started 3 to 8 h after injury [5–7, Class III]. Contraindications:Absolute contraindications for this drug are limited to hypersensitivity reactions to the drug, evidence of a systemic fungal infection, and recently receiving a live or live-attenuated vaccine. It is also contraindicated in penetrating traumatic spinal cord injury. Multiple drug interactions (e.g., antidiabetic agents) necessitate monitoring of therapy; consider dose adjustments in patients receiving CYP3A4 inhibitors. Main side effects:Immunosuppression (leading to increased incidence and severity of infections), gastrointestinal (GI) hemorrhage, hyperglycemia and psychosis are the notable adverse effects. Special points:The use of IV steroids is a matter of much debate. Increasingly it has been noted that it has an unfavorable risk-benefit ratio: Its use is associated with a modest improvement in motor function (improvement of motor level by one), but its adverse effects (increased infections and GI bleeds) may outweigh that benefit. Cost/cost-effectiveness::1 (40 mg) vial, USD $12.99. Although the actual drug itself is not expensive, it may not be cost-effective if its adverse effects are considered. Low molecular weight heparin (enoxaparin)Standard dosage:30 mg subcutaneous every 12 h, or 40 mg subcutaneous daily. Contraindications:In the immediate posttraumatic period when there is high risk for bleeding (concomitant traumatic brain injury), inadequate hemostasis, or coagulopathy, and in incomplete spinal cord injury associated with a spinal hematoma [12••, Class I]. Main drug interactions:Use caution when combined with certain antidepressants or other anticoagulants or antiplatelet agents. Main side effects:Bleeding. Special points:In patients who have undergone spinal operative manipulation, it is routine practice in our institution to wait for 72 h prior to using enoxaparin for thromboprophylaxis. Cost/cost-effectiveness:1 syringe (30 mL/0.3 mL), USD $23.99. Very cost-effective if its primary endpoint (prevention of thromboembolism) is achieved. Interventional procedures
Surgery
Assistive devices
Physical therapy, occupational therapy, speech therapy and exercise
Emerging therapies
Pediatric considerations
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Download references What kind of shock is spinal shock?Spinal shock is the altered physiologic state immediately after a spinal cord injury (SCI), which presents as loss of spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity.
How is neurogenic shock treated?How is neurogenic shock treated? Your provider will put a collar or neck brace on your neck to keep your injury from getting worse. First, your provider will treat your low blood pressure with fluids you receive through an IV. Next, your provider will treat your slow heart rhythm.
What is a neurogenic shock?Neurogenic shock is a combination of both primary and secondary injuries that lead to loss of sympathetic tone and thus unopposed parasympathetic response driven by the vagus nerve. Consequently, patients suffer from instability in blood pressure, heart rate, and temperature regulation.
What is the difference between hypovolemic shock and neurogenic shock?Hypovolemic shock (caused by too little blood volume) Anaphylactic shock (caused by allergic reaction) Septic shock (due to infections) Neurogenic shock (caused by damage to the nervous system)
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