The nurse is providing care to a patient with a spinal cord injury who has areflexic bladder

Spinal cord injury (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 spinal cord injury.

Spinal cord injury can be sustained through different mechanisms, with the following 3 common abnormalities leading to tissue damage:

• Destruction from direct trauma

• Compression by bone fragments, hematoma, or disk material

• Ischemia from damage or impingement on the spinal arteries

Edema could ensue subsequent to any of these types of damage.

Neurogenic shock refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction and the interruption of sympathetic nervous system control in acute spinal cord injury. Hypothermia is also characteristic. This condition does not usually occur with spinal cord injury below the level of T6 but is more common in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance, with the associated vascular dilatation. Neurogenic shock needs to be differentiated from spinal and hypovolemic shock. Hypovolemic shock tends to be associated with tachycardia.

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. That is, spinal shock is a state of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury, with associated loss of all sensorimotor functions.

An initial increase in blood pressure due to the release of catecholamines, followed by hypotension, is noted. Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. These symptoms tend to last several hours to days until the reflex arcs below the level of the injury begin to function again (eg, bulbocavernosus reflex, muscle stretch reflex [MSR]).

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 metastatic disease is 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 spinal cord injury without radiologic abnormality (SCIWORA).

SCIWORA was first coined in 1982 by Pang and Wilberger. Originally, it referred to spinal cord injury without radiographic or computed tomography (CT) scanning evidence of fracture or dislocation. However with the advent of magnetic resonance imaging (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 is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury. [7, 8, 9]

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 of spinal cord injury.

One of the goals of the physician is to classify the pattern of the neurologic deficit into one of the cord syndromes. Spinal cord syndromes may be complete or incomplete. In most clinical scenarios, physicians should use a best-fit model to classify the spinal cord injury syndrome.

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; these include the anterior cord syndrome, the Brown-Séquard syndrome, and the central cord syndrome.

Anterior cord syndrome involves a lesion causing variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception.

Brown-Séquard syndrome, which is often associated with a hemisection lesion of the cord, 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, with sacral sensory sparing. 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.

The conus medullaris syndrome, cauda equina syndrome, and spinal cord concussion are briefly discussed below.

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, whereas the sacral segments occasionally may show preserved reflexes (eg, bulbocavernosus and micturition reflexes). Motor and sensory loss in the lower limbs is variable.

Cauda equina syndrome involves injury to the lumbosacral nerve roots in the spinal canal 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, the affected limbs are areflexic. Cauda equina syndrome 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.

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Demographics profile of bladder management in spinal cord injury (n= 34).