A combination of areflexia/hyporeflexia and autonomic dysfunction accompanies the spinal cord injury.
Initial hyporeflexia presents as a loss of cutaneous and deep tendon reflexes below the level of injury accompanied by loss of sympathetic flow, resulting in hypotension and bradycardia.
Reflexes usually return in a specific pattern, with skin reflexes that usually bear before deep tendon reflexes.
The first reflex to return is a delayed abnormal plantar reflex. The second reflex that produces is the cavernous bulb reflex. This reflex is checked to determine the end of spinal shock.
A cavernous bulb reflex is obtained by squeezing the penis glans or clitoris and the sensation of an involuntary contraction of the anus.
Pulling a Foley catheter can also cause this reflex. It usually comes back 1 to 3 days after the injury.
The autonomic dysfunction is worse with higher levels of injury. In cervical spinal cord lesions, the sympathetic flow decreases with persistent parasympathetic outflow by the vagus nerve, resulting in bradycardia and hypotension.
This autonomic dysfunction generally persists for months, and there is evidence to suggest that there is always some level of abnormality.
Sympathetic activity may be present and mediated by the spinal cord distal to the level of injury.
Due to this sympathetic/parasympathetic imbalance, patients with a complete spinal cord injury may have a hypertensive crisis resulting from a bladder or super-distended colon.
Due to this continuum of events after a spinal cord injury, the definition of spinal shock and the endpoint are variable.
The mechanism of injury that causes spinal shock is usually traumatic at the origin and occurs immediately. Still, the spinal shock has been described with injury mechanisms that progress for several hours.
The reflex arcs of the spinal cord immediately above the level of injury can also be severely depressed based on the Schiff-Sherrington phenomenon.
The spinal cord injury’s end of the spinal shock phase is indicated by the return of the weird rings of the cutaneous spinal arch or muscle spindle.
Autonomic reflex arcs involving secondary ganglionic neurons outside the spinal cord can be affected inconsistently, and their return after spinal shock decreases.
The reflex arcs of the spinal cord that return below the level of injury are irreversibly altered and are the substrate on which the rehabilitation efforts are based.
Signs and symptoms
The extent of the injury is defined by the impairment scale of the American Spinal Injury Association (ASIA) (modified from the Frankel classification), using the following categories:
A = Complete: No sensory or motor function in S4-S5 sacrum segments is preserved.
B = Incomplete: Sensory, but not motor, the function is preserved below the neurological level and extends through the sacral segments S4-S5.
C = Incomplete: Motor function is preserved below the neurological level, and most of the key muscles below the neurological level have a muscle grade below 3.
D = Incomplete: Motor function is preserved below the neurological level, and most of the key muscles below the neurological level have a muscle grade greater than or equal to 3.
E = Normal: Sensory and motor functions are normal.
Management of the respiratory tract
The cervical spine should be kept in neutral alignment at all times; cleaning oral secretions and debris is essential to maintain the patency of the respiratory tract and prevent aspiration.
Hypotension: Hypotension can be hemorrhagic and neurogenic in acute spinal cord injury; A diligent search should be made for hidden sources of bleeding.
Neurogenic shock: Replacement with isotonic crystalloid solution up to 2 liters is the initial treatment of choice. Maintain adequate oxygenation and perfusion of the injured spinal cord.
Supplemental oxygenation and mechanical ventilation may be necessary.
Amnesia, external signs of head injury or basilar cranial fracture, focal neurological deficit, associated alcohol intoxication or drug abuse, or history of loss of consciousness require a complete evaluation of the intracranial lesion.
The placement of a nasogastric tube (NG) is essential; Antiemetics should be used aggressively.
To prevent pressure sores, turn the patient every 1-2 hours, fill all extensor surfaces, undress the patient to remove the belts and keys or back pocket wallets, and remove the spine board as soon as possible.
The treatment of pulmonary complications and injuries in patients with spinal cord injury includes supplemental oxygen for all patients and thoracic thoracotomy for those with pneumothorax and hemothorax.
Emergent spinal cord decompression is suggested in the context of an acute spinal cord injury with progressive neurological deterioration, facet dislocation, or bilateral blocked facets.
The procedure is also suggested for establishing a spinal nerve shock with progressive radiculopathy in patients with extradural lesions such as hematomas or epidural abscesses and establishing cauda equina syndrome.
When a spinal cord injury is caused due to trauma, the body enters a state known as spinal shock.
While the spinal shock begins within a few minutes of the injury, it takes several hours before the full effects occur.
During spinal shock, the nervous system is unable to transmit signals, some of which may return once the spinal shock has subsided, the duration of the spine is approximately 4-6 weeks after the injury.