6 The Spinal Cord Injury Patient
Abstract
The management of spinal cord injuries is essentially no different than management of brain injuries. The goal of treatment is to prevent ischemia by decompressing the central nervous system, stabilizing the structures that support the spinal cord, and restoring blood flow. The examination of the spinal cord requires the same precision as the examination of the brain. The astute clinician should be able to distinguish a complete from an incomplete spinal cord injury as well as the conditions that make such a determination clouded.
Case Study
A 77-year-old woman is seen in the emergency department 5 hours after a mechanical fall down three steps. The patient’s Glasgow Coma Scale score is 15 per the emergency department. She is also noted to have suffered a right midshaft femur fracture and multiple cuts and bruises on her knees and elbows. Physical examination reveals an awake and alert patient with stable vital signs. Focused neurologic exam reveals the pertinent positive findings to be 3/5 strength of her bilateral deltoid, biceps, and brachioradialis muscles; however, the remaining distal musculature is flaccid. She has preserved pinprick sensation only from the lateral elbow and up, and spinal reflexes are absent, including abdominocutaneous, cremasteric, anocutaneous, and bulbocavernosus reflexes. While the patient is being interviewed she begins to display signs of respiratory distress, including decreased pulmonary excursion and difficulty answering questions. The patient’s blood pressure suddenly drops to 65 systolic and SPO2 (saturation of peripheral oxygen) declines to 78. Neuroimaging reveals a flexion-distraction-type fracture at C6.
See end of chapter for Case Management.
6.1 Introduction
When encountering a patient with spinal cord injury (SCI), special consideration is paid to the basic principles of trauma in order to optimize the patient’s outcome and survival, while also addressing the specific issues that are related to the spinal cord itself. Principles of treatment of spinal cord injury (SCI) patients include the following:
Preservation of life and prevention of complications.
Preservation of neurologic function.
Restoration of spinal stability and treatment of deformity.
Optimizing the potential for neurologic recovery and rehabilitation.
SCI may be emergently life threatening. SCI may acutely and adversely affect cardiopulmonary stability due to traumatic disruption of autonomic pathways in the spinal cord. Strict adherence to Advanced Trauma Life Support/Advanced Cardiovascular Life Support (ATLS/ACLS) protocols must be observed. Although radiographic findings and the neurologic exam are important in assessing SCI and spinal trauma, emergency measures are considered first. Emergent intubation, correction of blood pressure and volume, and similar emergency resuscitative measures may be indicated. A complete understanding of autonomic function and preservation of such is critical. Additionally, the physiology and consequences of cardiopulmonary events in SCI patients must be completely understood.
6.1.1 Effects of Spinal Cord Injury on Autonomic Function
Overview of the Autonomic Nervous System: Autonomic anatomy and physiology are complex and are only reviewed in brief detail here. The autonomic nervous system (ANS) is unique in that it requires a sequential two-neuron efferent pathway; the preganglionic neuron must first synapse onto a postganglionic neuron before innervating the target organ. The preganglionic, or first, neuron will begin at the “outflow” and will synapse at the postganglionic, or second, neuron’s cell body. The postganglionic neuron will then synapse at the target organ. The two divisions of the ANS are the sympathetic and the parasympathetic divisions. The sympathetic nervous system outflow is from the thoracolumbar region (T1–L2/3) of the spinal cord. The parasympathetic nervous system outflow is from craniosacral neurons that begin at cranial nerves III, VII, IX, and X, and from the S2–S4 sacral nerve roots.
In spinal cord injury, a phenomenon known as traumatic sympathectomy, leading to deafferentation, may occur. This phenomenon is essentially a traumatic disconnection of sympathetic outflow, which is responsible for the maintenance of blood pressure and therefore blood flow and oxygen delivery to tissues. Traumatic sympathectomy leads to uninhibited parasympathetic outflow leading to vasodilation, decreased heart rate, and decreased cardiac contractility. This phenomenon may rapidly lead to neurogenic shock, which must be clinically distinguished from spinal shock, 1 a distinct entity.
6.2 Neurogenic Shock
Neurogenic shock results from excessive vasodilation and impaired distribution of blood flow; it typically presents with hypotension and bradycardia (vs. hypotension and tachycardia in hypovolemic/hemorrhagic shock). Decreased systemic vascular resistance results in pooling of blood within the extremities. Hypotension can cause secondary damage to an already injured spinal cord, while also dramatically worsening outcomes for any associated closed head injury. Neurogenic shock can be a potentially devastating complication, leading to organ dysfunction and death, if not promptly recognized and treated.
6.2.1 Treatment of Neurogenic Shock
Volume resuscitation and hemodynamic stability are the mainstays of treatment of neurogenic shock. Because patients with SCI frequently have multisystem injury, it is critical to rule out hemorrhagic shock in these patients, though that is typically associated with hypotension and tachycardia versus neurogenic shock, which is typically associated with hypotension and bradycardia or eucardia. Volume resuscitation for patients with neurogenic shock can be done with fluids and/or blood and blood products (cryoprecipitate, fresh frozen plasma, and platelets). Inotropic and vasopressor agents are also used–it makes intuitive sense to use sympathomimetics in the face of “traumatic sympathectomy.” Sympathomimetics, such as epinephrine, noradrenaline hydrotartrate (norepinephrine), phenylephrine, dobutamine, and dopamine can be used. Most recommendations concerning vasopressor choice are based on class III evidence, and there are no prospective, randomized, placebo-controlled trials at this time. Most authors advocate the use of norepinephrine or dopamine. Dopamine is the precursor of norepinephrine, both of which act on alpha-1 and beta-1 receptors. In some studies dobutamine was used with good results. Vasopressin is not used because of the antidiuretic effects, which can lead to water retention and hyponatremia. Phenylephrine acts only on alpha-1 receptors and can theoretically cause worsened hypotension by a reflexive bradycardia, especially when not used in conjunction with another beta agonist.
The goal for mean arterial pressure (MAP) is generally regarded to be 85 mm Hg, although several studies have shown no mortality difference between a MAP of < 85 mm Hg and a MAP of < 90 mm Hg. The objective of higher MAPs than found in other forms of shock is to increase spinal perfusion.
6.3 Spinal Shock
Spinal shock is defined as the complete loss of all neurologic function, including reflexes and rectal tone, below the specific level of the SCI, which may also be associated with autonomic dysfunction. This kind of shock is a state of transient physiological, as opposed to anatomical, reflex depression of spinal cord function below the level of injury, with associated loss of all sensorimotor functions. 2 Spinal shock results in the release of catecholamines, causing an initial increase in blood pressure often followed by hypotension; flaccid paralysis, including of the bowel and bladder, and oftentimes sustained priapism are observed. Symptoms of spinal shock can last several hours to days until the reflex arcs below the level of the injury begin to function again; however, spinal shock typically starts to recede within 24 hours. The most reliable indicator of the return of spinal reflex arc function is the bulbocavernosus reflex (BCR), which is the first reflex to return as spinal shock begins to recede. 2 The last residue of spinal shock disappears weeks to months after an SCI as flaccid paralysis is replaced by muscle spasticity.
Key Clinical Point: Until there is return of the bulbocavernosus reflex (BCR), the physical examination is unreliable and the patient may still be in spinal shock (► Table 6.1).
6.4 Primary versus Secondary Spinal Cord Injury
SCI does not stop at the time of the ictus, or accident; it is a dynamic process in which the injury starts at the outset (“primary” SCI), and can progress with subsequent sequelae (“secondary” SCI). The key point is that, for SCI, the full extent of injury may not be initially apparent. Incomplete cord lesions may evolve into more complete lesions. Commonly, the level of injury may rise one or two spinal cord levels during the hours to days after the initial event, leading to devastating consequences. A complex cascade of pathophysiological events related to free radicals, vasogenic edema, and altered blood flow accounts for the clinical phenomena of secondary SCI. Normal oxygenation, blood perfusion, and acid–base balance are required to minimize secondary SCI.
Primary SCI arises from acute mechanical disruption, transection, or distraction of neural elements. It is usually, but not always, associated with fracture and/or dislocation of the spine. It may be caused by penetrating injuries from bullets, projectiles, stabbings, and the like, or it may be caused by displaced bony fragments. Primary SCI may be caused by extradural pathology due to direct cord compression (includes epidural hematomas, disk ruptures, bone fragments, and foreign bodies). Longitudinal distraction, with or without flexion and/or extension of the vertebral column, may result in primary SCI without spinal fracture or dislocation since the spinal cord is tethered more securely than the vertebral column. These injuries may not be apparent radiographically, resulting in the condition known as spinal cord injury without radiological abnormality (SCIWORA).
Secondary SCI occurs after the primary ictus, which serves as the nidus from which additional secondary mechanisms of injury extend. Secondary SCI mechanisms include, but are not limited to, ischemia, hemorrhage, thrombosis, edema, inflammation, free radical–induced cell injury and death, glutamate excitotoxicity, cytoskeletal degradation and induction of apoptosis, 3 fluid/electrolyte disturbances, mitochondrial dysfunction, immunologic injury, and other miscellaneous processes. 4 Anoxic or hypoxic effects compound the extent of SCI. Neurocritical care goals are to minimize secondary SCI, largely by assuring spinal cord perfusion and oxygenation.
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