Spinal Cord Injury (SCI)

Jessica

Etiopathophysiology
SCI 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

 Injury to the corticospinal tract or dorsal columns ipsilateral paralysis or loss of sensation of light touch, proprioception, and vibration. 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. 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 hypotension, relative bradycardia, peripheral vasodilation, and hypothermia. tends to occur more commonly 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 associated vascular dilatation. Therefore,shock associated with a spinal cord injury involving the lower thoracic cord must be considered hemorrhagic until proven otherwise.

 spinal shock is defined as 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]).

 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 primary watershed area of the spinal cord is the midthoracic region. At any level, the central part of SC is a watershed area. Vascular injury may cause a cord lesion at a level several segments higher than the level of spinal injury. Cervical hyperextension injuries may cause ischemic injury to the central part of the cord, causing a central cord syndrome.

 Primary SCI arise from mechanical disruption, transection, or distraction of neural elements. fracture and/or dislocation of the spine penetrating injuries due to bullets or weapons or displaced bony fragments. Extradural pathology, spinal epidural hematomas or abscesses, metastatic disease acute cord compression and injury. Longitudinal distraction of the spinal cord with or without flexion and/or extension of the vertebral column may result in SCIWORA (spinal cord injury without radiologic abnormality) Secondary SCI Vascular injury to the spinal cord caused by arterial disruption, arterial thrombosis, or hypoperfusion due to shock

 The extent of injury is defined by the ASIA Impairment Scale, using the following categories: A - Complete: No sensory or motor function is preserved in sacral segments S4-S5. B - Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5. C - Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade less than 3. D - Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have muscle grade greater than or equal to 3. E - Normal: Sensory and motor functions are normal.

 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.
anterior cord syndrome Brown-Squard syndrome central cord syndrome.

Other cord syndromes include the conus medullaris syndrome, the cauda equina syndrome, and spinal cord concussion.

 Anterior cord syndrome: variable loss of motor function and pain and/or temperature sensation, with preservation of proprioception. Brown-Squard syndrome: 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.
pattern of motor weakness shows greater distal involvement 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 are common. Sacral sensory sparing usually exists.

 Conus medullaris syndrome is a sacral cord injury with or without involvement of the lumbar nerve
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. 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.

Epidemiologi
US: incidence is 40 cases/million population, or about 12,000 patients/year 63% are Caucasian, 22.7% are African American, 11.8% are Hispanic, and < 2% are Asian. Male-to-female ratio is 4:1.[4] Average age at injury is 39.5 years About 50% of SCI occurred between 16-30 years the most common causes of SCI: motor vehicle accidents (42%), falls (27.1%), interpersonal violence primary gunshot wounds(15.3%), and sports (7.4%).

Assessment
Primary and secondary = spine fracture History 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. The presence of neurologic deficits that indicate multilevel involvement suggests SCI. In the absence of spinal shock, motor weakness with intact reflexes indicates SCI, while motor weakness with absent reflexes indicates a nerve root lesion.

 Physical exam: ABC RR, chest wall expansion, abdominal wall movement, cough, and chest wall and/or pulmonary injuries. With high lesions (ie, C1 or C2), vital capacity is only 5-10% of normal, and cough is absent. With lesions at C3-C6, vital capacity is 20% of normal, and cough is weak and ineffective. With high thoracic cord injuries (ie, T2-T4), vital capacity is 30-50% of normal, and cough is weak. a complete detailed neurological assessment: motor function, sensory evaluation, deep tendon reflexes, and perineal evaluation, presence or absence of sacral sparing (presence of motor function or sensation at the anal mucocutaneous junction on rectal exam) Sacral-sparing is evidence of the physiologic continuity of spinal cord long tract fibers (with the sacral fibers located more at the periphery of the cord). Logrolling the patient to systematically examine and palpate each spinous process of the entire axial skeleton from the occiput to the sacrum (pain, tenderness, swelling, bruising, or possible malalignment)

 Lab exam ABG, pulse oxymetry, CBC, urinalysis Lactate levels (in the presence of shock) Imaging Plain radiograph 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.

 CT scan When plain radiography is inadequate or fails to visualize segments of the axial skeleton Convenience and speed To provide further evaluation when radiography depicts suspicious and/or indeterminate abnormalities When radiography depicts fracture or displacement: visualization of the extent MRI evaluate nonosseous lesions, such as extradural spinal hematoma; abscess or tumor; disk rupture; ligamentous injuries, and spinal cord hemorrhage, contusion, and/or edema. Tatalaksana: lihat slide spine fracture