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KEY POINTS

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  • After acute spinal cord injury (SCI), the primary injury sets limits (that are not always initially obvious) on the potential extent of recovery and the degree of secondary injury determines the extent of the potential recovery actually achieved.

  • Acute SCI patients, particularly those with cervical level and severe SCI, are at risk for respiratory arrest, hypoxemia, and cardiovascular instability.

  • The prevention of secondary injury or “neuroprotection” consists of spine immobilization, timely surgical intervention, and early recognition and treatment of hemodynamic instability, respiratory failure, and hypoxemia.

  • Hemodynamic instability is common after acute SCI and may be multifactorial, including due to hypovolemia secondary to blood loss, systemic inflammation from trauma or infection (vasodilation, decreased intravascular volume), neurogenic (vasodilation, inappropriate bradycardia), arrhythmias, myocardial stunning, pneumothorax, or cardiac tamponade from associated trauma.

  • The term “neurogenic shock” refers to hypotension due to vasodilation that may be accompanied by absolute (HR <60) or relative bradycardia caused by the loss of outflow from the sympathetic autonomic component of the spinal cord arising from the high thoracic and cervical regions, T1-T6 level and above.

  • The term “spinal shock” refers to the loss of sensation accompanied by motor paralysis and depression of spinal reflexes caudal to the level of acute SCI.

  • Among trauma patients, the risk of VTE is likely the highest after acute spinal cord injury and LMWH should be started as soon as safely possible after primary hemostasis is achieved; until that time intermittent pneumatic compression (IPC) devices should be used.

  • Pulmonary embolism (PE) is the third leading cause of death after acute SCI and after any sudden hemodynamic compromise, unexplained dyspnea, or hypoxemia, PE must be considered.

  • Patients with high cervical injury and prolonged ventilatory failure with tracheostomy are at a higher risk of malnutrition.84 The enteral route is preferred to preserve gut integrity. The current literature does not support the maintenance of strict normoglycemia in these critically ill patients.

  • Following spinal decompression and/or stabilization, and resolution of potentially life-threatening cardiac and respiratory events, the goal is for rehabilitation specialists to become involved early in the management.

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BACKGROUND

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Acute trauma to the spine may involve the neuronal (spinal cord and nerve roots) and/or skeletal and ligamentous structures of the vertebral column that normally protect the spinal cord. Vertebral fractures or dislocations can occur without damage to the spinal cord; however, acute traumatic spinal cord injury (SCI) often involves injury to the vertebral column. The manifestations of SCI may be immediate or delayed. The key to insuring the best outcome is rapid diagnosis and prevention of secondary injuries that can further worsen ischemic neurological damage. This includes rapid recognition and treatment of unstable fractures, fracture fragments, hematomas, or other lesions that can cause impingement or laceration of the spinal cord and critical care management that emphasizes maintenance of homeostasis and the detection of new or initially unrecognized injuries.

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Approximately 50% of spinal injuries occur in the cervical spine, the other half involve the thoracic, lumbar, and sacral areas.1 SCI may lead to significant neurological damage, including paraplegia, tetraplegia, or death. Patients with tetraplegia have injuries to one ...

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