Injuries associated with spinal trauma include spinal cord contusion, vertebral fracture or luxation, and traumatic intervertebral disc herniation (see Chapter 13). Common causes of spinal trauma in dogs and cats include motor vehicle accidents, animal–animal or human–animal interactions, falls, and projectile injuries. Patients with spinal trauma commonly have concurrent injuries to other major organ systems, necessitating rapid and thorough assessment and survey for evidence of other life-threatening injuries.
The pathophysiology of traumatic spinal cord injury can be divided into two main components: primary injury and secondary injury. Primary injury occurs as a direct result of the trauma, while secondary injury includes several biochemical processes that are triggered by the primary injury, and that perpetuates spinal cord damage in the hours to days after the traumatic event.
Primary spinal cord injury
Spinal luxation, vertebral fracture, traumatic intervertebral disc herniation, spinal cord contusion, and extra-axial hemorrhage are examples of primary spinal cord injuries that can occur secondary to trauma.
Concussion vs. compression—it is important to understand that not all injuries affect the spinal cord in the same way. Intervertebral disc extrusion is a form of spinal cord injury that is primarily compressive in nature. There is a concussive component, but this component is typically less significant. This explains the rapid recovery when the spinal cord is decompressed. Patients with external trauma, such as those hit by a car, have primarily a concussive spinal cord injury. They may also have compressive injuries caused by fractures or hematomas, but the concussive injury is the most relevant. Compression impacts spinal cord perfusion by limiting arterial supply and occluding venous drainage, and causes direct damage to myelin and axons. Concussion is a more severe form of spinal cord injury. It has been shown that the prognosis of dogs with severe spinal cord injury (plegic with absent nociception) caused by external trauma is significantly worse compared with those dogs with acute intervertebral disc extrusion.
Vertebral fracture and luxation—the stability of a spinal luxation or vertebral fracture is commonly determined using a three-compartment model of the vertebra (Fig. 15.1). The dorsal compartment incorporates the articular processes, laminae, pedicles and spinous processes; the middle compartment includes the dorsal longitudinal ligament, the dorsal aspect of the vertebral body and the dorsal portion of the annulus fibrosus; the ventral compartment contains the ventral longitudinal ligament, the lateral and ventral aspects of the annulus fibrosus, the nucleus pulposus, and the remaining portions of the vertebral body. When any two of the three compartments are compromised, the injury is considered unstable. The type of fracture or luxation that occurs is dependent upon the magnitude of force applied as well as the nature of that force with respect to the spinal column. Extension of the spine commonly results in vertebral lamina, facet, or pedicle fractures. These types of fractures often occur simultaneous with rupture of the annulus fibrosus. Therefore, these types of fractures are commonly unstable with extension of the spine, but remain stable in flexion. Shearing or compressive forces most commonly result in vertebral body fractures, and these types of fractures are generally unstable. Spinal cord compression can also result if fracture fragments are located within the vertebral canal. Pure compression forces of sufficient magnitude result in vertebral compression fractures. These fractures are rarely unstable due to preservation of the dorsal ligaments. Flexion of the vertebral column (with or without rotation) most commonly results in vertebral luxation, but often does so without vertebral fracture. Damage to both the dorsal and ventral stabilizing ligamentous structures is the cause of the resultant instability. Rotation of the vertebral column with or without flexion is the most common cause of vertebral fracture with concurrent spinal luxation. Similar to luxation without fracture, the instability of this type of injury is due to compromise of both dorsal and ventral ligamentous structures. The form of vertebral luxation seems to differ between dogs and cats. In dogs the caudal segment is displaced ventrally in the majority of cases, whereas in cats it tends to be displaced dorsally.
Figure 15.1 Schematic representation of the three-compartment model for evaluating stability of a vertebral fracture/luxation. (Shores, 1992.72 Reproduced with permission from Elsevier.)
Traumatic intervertebral disc herniation—this type of primary injury typically occurs in dogs with underlying intervertebral disc disease, most commonly chondroid degeneration of the dorsal aspect of the annulus fibrosus. This pathology predisposes the annulus to rupture with trauma, resulting in compression of the spinal cord due to herniation of the nucleus pulposus into the vertebral canal (see Chapter 13). In a recent study, less than one-third of dogs with traumatic disc extrusion had spinal cord compression. Most dogs had the so-called type III, noncompressive, high velocity/low volume, explosive disc herniations. These noncompressive traumatic herniations occur most commonly in older chondrodystrophic breeds, but can be seen in any dog. Although it is much less common, cats can also develop chondroid degeneration of the intervertebral disc, predisposing them to traumatic herniation.
Spinal cord contusion—reports of hemorrhage into the spinal cord parenchyma are rare in the veterinary literature; however, it is likely that contusions do occur secondary to vertebral fracture, spinal luxation, or traumatic intervertebral disc herniation. Contusions are the result of damage to blood vessels in the spinal cord parenchyma, and in addition to resulting from direct trauma to the cord, they may also develop secondary to traumatic motion of the spinal cord within the vertebral canal, resulting in coup and contrecoup lesions, similar to cerebral contusions that develop after head trauma.
Extra-axial hemorrhage—disruption of blood vessels serving the supportive structures surrounding the spinal cord can result in an accumulation of blood and hematoma formation. Subdural or epidural accumulations can cause neurologic dysfunction by compressing the spinal cord and compromising spinal cord blood flow. Although epidural and subdural spinal hematomas have been reported secondary to trauma in humans, they are rare. Several veterinary case reports describe the development of epidural hematomas secondary to spontaneous intervertebral disc herniation, but there are no published reports of these types of injuries secondary to trauma.
Secondary spinal cord injury
Many biochemical processes are set into motion by traumatic spinal cord injury and lead to continued spinal cord injury over the first 24–48 hrs after the primary injury. An understanding of these mechanisms of secondary injuries is essential when devising a therapeutic plan for a patient with spinal cord trauma.
Excitotoxicity—excitatory neurotransmitters such as glutamate and aspartate are present in increased concentrations in the spinal cord parenchyma due to leakage from damaged neurons as well as decreased clearance by ischemic astrocytes. Stimulation of neighboring neurons by these neurotransmitters leads to adenosine triphosphate (ATP) depletion as well as an influx of sodium and calcium. The result is cellular edema and spinal cord swelling. Compression of the swollen spinal cord contributes further to cellular ischemia.
Loss of autoregulation and ischemia—spinal cord blood flow remains constant despite changes in systemic blood pressure due to intrinsic autoregulatory mechanisms, causing vasoconstriction in response to increased blood pressure and vasodilation in response to decreased blood pressure. These autoregulatory mechanisms are commonly compromised after spinal cord trauma, and systemic hypotension, common in patients with trauma, leads to decreased spinal cord blood flow. If hypotension persists, spinal cord ischemia can result. The ischemia affects primarily the gray matter because its metabolic needs are higher and the blood supply to the gray matter is five times higher than the white matter.
Accumulation of intracellular calcium—excitotoxicity and activation of voltage-gated calcium channels result in activation of phospholipase A2, triggering the inflammatory cascade. In addition, ATP is depleted due to the binding of calcium to phosphates, mitochondrial dysfunction occurs, and cytotoxic edema develops. All of these processes triggered by increases in intracellular calcium concentration lead to continued neuronal cell death.
Oxidative injury—the presence of increased intracellular calcium, ischemia-reperfusion phenomena, the presence of iron and copper due to hemorrhage, and the high lipid content of spinal cord tissues all favor the production of reactive oxygen species. Neuronal cell membranes, rich in polyunsaturated fatty acids, provide an excellent medium for chain reactions that perpetuate this injury. This cycle of oxidative damage contributes to ongoing cellular injury and necrosis.
Inflammation—local spinal cord and systemic inflammation secondary to traumatic injury can be severe. Inflammatory mediators contribute to secondary injury by inducing nitric oxide (NO) production via inducible nitric oxide synthetase (iNOS), providing a chemotactic stimulus for influx of inflammatory cells, and activating the arachidonic acid cascade. Several of these inflammatory mediators are potent activators of coagulation, resulting in microvascular thrombosis and further spinal cord ischemia.
Apoptosis—following acute spinal cord injury, neurons, glial, and endothelial cells die by necrosis or apoptosis. Oligodendrocyte death caused by apoptosis is a prominent feature of the early phase of acute spinal cord injury and continues for extended periods after injury, contributing to demyelination and loss of function. Oligodendrocyte apoptosis occurs primarily through activation of the Fas receptors by microglial cells expressing the Fas ligand, and p75 neurotrophin receptor signaling. Activation of the Fas receptor triggers the caspase cascade, resulting in apoptosis.
Although the neurologic signs present in patients with spinal trauma can be severe, the clinician must take a global approach when initially evaluating the patient, and must take care to identify all imminently life-threatening injuries. The basic “ABC” approach—quickly evaluating the patency of the airway, the ability of the patient to breathe, and the effectiveness of circulation—will afford identification of most life-threatening injuries. Most patients with significant traumatic injuries will present in a state of hypovolemic shock due to inappropriate vasodilation, blood loss, or both. A minimum database—including packed cell volume (PCV), total solids (TS), Azostix (AZO), and blood glucose (BG)—is part of the initial patient assessment. Hypovolemia and hypoxemia can contribute to secondary spinal cord injury, and the rapid correction of perfusion deficits is of paramount importance.
Fluid therapy
A patient with a systolic blood pressure less than 90 mmHg or a mean arterial blood pressure less than 80 mmHg is hypotensive and at risk of secondary spinal cord injury. Aggressive fluid resuscitation is warranted in all hypovolemic trauma patients. If the patient is anemic, whole blood or packed red blood cell (pRBC) transfusion may assist in maintaining normovolemia as well as adequate tissue oxygenation by improving blood oxygen content, the major determinant of which is hemoglobin concentration. Fluid support may include one or more of the following choices:
Synthetic colloids: 10–20 mL/kg over 15–20 min to effect (up to 40 mL/kg in the initial hour) for hypovolemic shock. This can be given as a rapid bolus in dogs; give it in 5 mL/kg increments over 5–10 min in cats. In the euhydrated trauma patient, Hetastarch is an excellent choice for restoring normal blood pressure. Dextran-70 is an acceptable alternative. Dehydrated trauma victims should receive isotonic crystalloid resuscitation.
Hypertonic saline (7%): 4–5 mL/kg over 15–20 min for hypovolemic shock. Hypertonic saline is also available as a 23.4% solution, which cannot be administered undiluted, but may be mixed 1:3 with hetastarch or dextran-70 (e.g. 20 mL of 23.4% hypertonic saline + 40 mL hetastarch or dextran-70 in a 60 mL syringe) to produce a solution of synthetic colloid suspended in a 7% hypertonic saline solution. Hypertonic saline also has positive inotropic effects, immunomodulatory effects, and reduces endothelial swelling.
Isotonic crystalloids (e.g. Lactated Ringer’s solution, 0.9% saline): 20–30 mL/kg bolus over 15–20 min for hypovolemic shock. May be repeated as necessary after reassessment. Since overhydration is a concern with crystalloid administration, the “shock dose” (90 mL/kg in the dog, 60 mL/kg in the cat) of crystalloids should be given incrementally to effect as described above. If the entire volume is not necessary to restore euvolemia and normal blood pressure, fluid administration should be tapered when these physiologic goals are met.
Blood products: Administration of 1 mL/kg of packed red blood cells (pRBCs) or 2 mL/kg of whole blood will increase the PCV by 1%. The severity of anemia will dictate the total dose to be administered, but 10–15 mL/kg of pRBCs is a reasonable starting dose. Blood products are typically administered over 4 hrs, but may be given faster (to effect) if the patient is unstable. Boluses of blood products are acceptable in the severely anemic trauma patient. Goals of therapy with blood products are a packed cell volume (PCV) between 25 and 30%. Patients with demonstrated coagulopathy should also be treated with fresh frozen plasma (FFP) at a dose of 10–15 mL/kg 2–3 times per day until the coagulopathy has resolved.
Pressors
In patients unresponsive to fluid therapy, vasopressor agents should be used to maintain adequate systemic blood pressure. Patients with inappropriate vasodilation, which is common in traumatized animals, may benefit from dopamine (5–12 μg/kg/min) or norepinephrine infusion (1–10 μg/kg/min). Patients with decreased cardiac contractility due to underlying heart disease or traumatic myocardial injury may respond to dopamine or dobutamine (1–20 μg/kg/min) infusion.
Oxygenation and ventilation
Hyperoxygenation (but not hyperventilation) is recommended for most trauma patients. Initial assessment is based upon respiratory rate and effort, mucous membrane and tongue color, and thoracic auscultation. Pneumothorax and pulmonary contusions are common sequelae of trauma, and must be promptly addressed. In the face of increased respiratory rate and effort, lung sounds may not consistently be decreased on auscultation in patients with pleural space disease (e.g. pneumothorax or hemothorax). A rapid, shallow breathing pattern, pale oral mucous membranes, and evidence of respiratory distress are indications of pleural space disease, and thoracocentesis should be done in any trauma patient with these signs. Thoracocentesis should be considered a diagnostic test as well as a therapeutic intervention. If negative pressure cannot be obtained via thoracocentesis, a chest tube should be placed immediately. If arterial blood gas analysis is available, the partial pressure of oxygen in arterial blood (PaO2) should be maintained at or above 90 mmHg for dogs and 100 mmHg for cats. Pulse oximeters are extremely useful, and relatively accurate, estimators of oxygenation status. However, the reliability of pulse oximeters varies with model used, with the PaO2 level (pulse oximeters may overestimate oxygenation status at lower PaO2 levels), and with the patient’s hemodynamic status.
Patients who are conscious and not obviously deteriorating neurologically should be administered supplemental oxygen via facemask, nasal cannulae, nasal oxygen catheter, or transtracheal oxygen catheter. Facemasks tend to stress dogs and cats, and should only be used temporarily, until another form of oxygen (O2) delivery can be instituted (e.g. nasal O2). The use of an O2 cage is generally an ineffective method of administering supplemental O2 to patients with severe spinal injury, as most require frequent or constant monitoring. Oxygen cages do not allow for concomitant close patient observation (requires opening the cage door) and maintenance of a high-oxygen environment. With nasal and transtracheal O2 catheters, an inspired oxygen concentration of 40% is provided with flow rates of 100 mL/kg/min and 50 mL/kg/min, respectively. Oxygen concentrations as high as 95% can be delivered with proportionally higher flow rates. Nasal O2 catheters should not be placed farther than the level of the medial canthus.
Patients with airway trauma causing obstruction or spinal cord disease causing hypoventilation should be intubated and ventilated. If intubation is not possible due to airway obstruction, emergency tracheostomy is indicated. Arterial blood gas measurement is the best way to monitor ventilation, which is reflected in PaCO2 levels. End-tidal CO2 measurement is a useful monitoring tool, but tends to underestimate the true PaCO2 levels due to the likelihood of dead space ventilation. Venous CO2 levels (PvCO2) are also helpful, and are usually less than 5 mmHg greater than PaCO2. However, in patients with perfusion deficits, peripheral PvCO2 levels can be significantly higher than arterial values, and should be interpreted cautiously. Ventilatory rates of 10–15 breaths per minute should be sufficient to maintain PaCO2 levels between 35 and 45 mmHg in the absence of significant pulmonary parenchymal disease. Hyperventilation may be deleterious to the spinal trauma patient due to potential vasoconstriction, which reduces spinal cord blood flow. The goal should be normocapnia (PaCO2 of 35–45 mmHg).
The initial neurologic examination (Video 32)
Once immediately life-threatening extra-central nervous system problems have been identified and addressed, an initial brief neurologic exam should be done to localize any spinal cord lesions and to determine whether an unstable fracture is present. Nonambulatory animals should be minimally manipulated on presentation until the presence of an unstable injury has been ruled out. Initially, all patients should be treated as if an unstable injury is present. Taping patients to a rigid “backboard” (Fig. 15.2) can provide external coaptation sufficient to protect the spinal cord from significant additional trauma in the face of unstable spinal injuries.
Figure 15.2 Patient with spinal trauma taped to a backboard to prevent further spinal cord injury.
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