Acute, traumatic injury to the horse’s central nervous system is an occasional, and often devastating situation facing equine veterinarians, most often caused by a collision or fall. Injuries to the spinal cord and/or brain may result in a variety of different clinical presentations, however, the damage incurred by the tissues and cells of the nervous system are similar. Treatment of such injuries is based on rapid recognition and reduction of swelling and inflammation so as to help avoid secondary injury to the tissues. Even with prompt and appropriate treatment, it can be months before an injured horse can recover, assuming it does so at all. The ultimate prognosis for horses is somewhat out of the treating veterinarian’s hands and depends on the severity of the initial insult and location of the injury. Biomechanics of injury If a horse stands on his hind limbs, the head can be more than 10 ft above the ground. When it falls, the head accelerates downward. The force with which the head hits the ground is tremendous; force equals mass times accelerations (F = MA)—the mass of the horse is substantial. If the horse lands on a hard surface, the force on the tissues can be catastrophic. If a horse hits his head going up, the force is less; if the horse hits his head squarely, the force is more than if he hits his head obliquely. While the physics involved in traumatic injuries are completely out of the attending veterinarian’s control, they are directly relevant to the extent of the injury. Additional fractures/separations of supporting bones that can destabilize the fracture site and result in serious displacements can also occur at or after the time of impact. Pathophysiology of acute neurologic injury While a minority of head injuries also cause brain injury, when the latter occurs, the anatomical constraints dictated by its confinement in the skull can exacerbate the initial injury. Injury to any tissue causes swelling. When swelling occurs in a closed space, it impairs blood flow and the delivery of oxygen to tissues. Swelling can ultimately cause cell death. There is a small amount of space in the calvarium for the brain, blood, and cerebrospinal fluid (CSF). A change in the volume of any of these tissues or fluids affects the volume of the others. If brain tissue swells in response to traumatic injury, blood and CSF volumes are reduced and brain tissue may receive suboptimal levels of oxygen and nutrients. Complex molecular, cellular, and biochemical events may cause further cell injury and make treatment challenging. Since the damage from the initial injury is out of the attending veterinarian’s control, the goal of treatment is to keep secondary injury to the tissues unaffected by the initial injury to a minimum. Since there are so many factors involved, it’s unrealistic to think treatment with any single substance will be completely effective. Treatments There is much discussion as to the best ways to reduce secondary injuries to brain and spinal cord tissue after injury, as well as on methods to improve delivery of oxygen to injured tissues. Well known treatments include: 1) Fluid therapy, including blood, serum, albumin, hypertonic fluids, and isotonic fluids. 2) Nonsteroidal anti-inflammatory drugs (NSAIDs) 3) Dimethylsulfoxide (DMSO) 4) Corticosteroids Blood loss that occurs secondary to traumatic injury may result in a drop in blood pressure and, secondarily, reduce perfusion to tissues. Approaches to maintaining blood pressure include intravenous blood transfusions, serum, or hyper- or isotonic fluids. If there is significant blood loss, transfusion with whole blood is preferred. The use of vasopressors and/or inotropes (agents that alter the force or energy of muscular contractions) have also been advocated; however, the effects of these drugs on cerebral vascular tone are unpredictable. To help reduce swelling, administration of mannitol and/or hypertonic fluids have been advocated. The goal with these agents is to move fluid into the vascular space from the injured tissue by osmosis. Hypertonic saline has advantages of low cost and small volume and, in human medicine, has been shown to have an over 50 percent reduction effect on raised intracranial pressure, with minor side effects. Osmotic treatments should be combined with efforts to maintain normal blood pressure (120/70 mm Hg for the horse). Hyperbaric or normobaric oxygen therapy, while having shown promise in some human clinical trials, and while a rational consideration for therapy, has not yet been shown to be important. It is also not readily available. NSAIDs, DMSO, and/or corticosteroids are commonly used for the treatment of acute neurologic trauma based on reduction of inflammation and possible antioxidant properties. While readily available and fairly inexpensive, and while there is rationale for their use, whether these medications have positive effects on the outcome of cases of acute equine neurologic trauma is still unknown. In addition to allopurinol, Vitamins E and C are other antioxidant therapies that have been used; however, real effects remain to be demonstrated. If there are open wounds or fractures, antibiotics may be indicated. Finally, a single initial dose of intravenous magnesium sulfate can potentially inhibit some parts of the secondary injury cascade (doses such as 25 gm MgSO4 for a 500 kg horse, given in 5-10 ml fluid have been described). Surgery and ancillary treatments Any concurrent wounds or injuries should be addressed. Padded helmets may help reduce further injury to the head. Surgery for acute neurologic problems is not a routine practice, but it may be required in cases of fractures to orbital, facial, or jaw bones, for example. Decompressive cranial surgery is not feasible in the horse. A surgical treatment for temporohyoid osteopathy—ceratohyoidectomy—has been developed for the treatment of acute neurologic signs associated with this nontraumatic condition. Conclusions When a horse sustains neurologic trauma, a thorough examination is always warranted. Prompt treatment is often necessary; however, the ultimate outcome may be beyond the veterinarian’s control. As such, the prognosis for recovery is usually guarded. Repeat exams are warranted to check for signs of progression or recovery. Investigations into the optimum treatment for acute neurologic trauma are ongoing, and improvements in treatments will likely continue to be made. David W. Ramey, DVM, is a Southern California equine practitioner who specializes in the care and treatment of pleasure horses. Visit his website at doctorramey.com. Columnists’ opinions do not necessarily reflect those of Veterinary Practice News.
