BASICS
Trauma to the skull and/or associated soft tissues results in primary damage to the brain. Secondary brain injury results from the primary injury and causes physiologic changes in brain tissue. Secondary brain injury can be prevented or lessened, whereas primary injury cannot.
- Following a traumatic insult to the brain, a cycle of cellular events occurs, including membrane disruption, ischemia, hypoxia, edema, and hemorrhage. The severity of these abnormalities is dependent on the type and extent of the initial primary injury. The traumatic insult is also responsible for increased permeability of brain capillary endothelial cells, resulting in vasogenic edema. This is the most common type of edema found following head trauma, and white matter is especially prone to vasogenic edema. Vasogenic edema results in displacement of cerebral tissue and increased ICP. Ultimately, these changes may produce brain herniation
- Cytotoxic edema results from swelling of the cellular elements of the brain. This type of edema occurs in gray and white matter and often results in decreased cerebral function, with stupor and coma as signs. A cycle occurs when increased ICP leads to decreased cerebral blood flow, resulting in further ischemia and brain swelling
- The types of cranial trauma from least to most severe are concussion, contusion, laceration, and hemorrhage. Concussion is short-term loss of consciousness and is often reversible and occurs without anatomic lesions. Contusion is associated with vascular and neural tissue damage without major structural disruption. Laceration and hemorrhage result from penetrating wounds, fractures, or direct blunt trauma. Cerebral hemorrhage in horses may be subdural (rare), intracerebral, or subarachnoid (common)
- Fracture of the basisphenoid/basioccipital bones is not uncommon after poll trauma (falling over backward)
- Hematoma formation is potentially devastating as hemorrhage results in expansion within the rigid skull with herniation, pressure necrosis, and brainstem compression possible
- Behavioral—altered mentation
- Cardiovascular—arrhythmias/bradycardia due to dysfunction of central cardiovascular centers
- Musculoskeletal—skull fracture(s); postural/gait abnormalities due to disruption of central motor pathways; other lacerations/fractures from traumatic episode
- Nervous—disruption of neural pathways resulting in changes in behavior, heart rate and rhythm, respiratory rate and rhythm, and neurologic testing
- Ophthalmic—abnormal eye position, movements, and reflexes, and changes in vision
- Respiratory—apneustic and/or erratic breathing due to dysfunction of respiratory regulatory center in the caudal medulla oblongata
- Ascertain if any known episode of trauma or physical evidence of trauma to the horse or its environment
- Potentially abnormal behavior, gait changes, sudden blindness, or recumbency
- The initial evaluation should be directed toward identification and stabilization of life-threatening problems such as open skull fractures, airway obstruction, hemorrhage, cardiovascular collapse, pneumothorax, and other fractures
- Look for evidence of head trauma. Palpation of the skull may reveal fractures
- Blood from the ears, mouth, or nostrils suggests potential basisphenoid or basioccipital fractures
- Occasionally, CSF may be seen draining from the ears with basilar fractures
- Bradycardia and/or arrhythmias may be present with apneustic or erratic breathing
Neurologic deficits may range from inapparent to recumbency with profound depression, dementia, and tetraparesis. Injury to the:
- Cerebrum may manifest as behavior changes, obtundation, coma, circling or wandering, seizures, and blindness with normal pupillary reflexes
- Cerebellum may manifest as altered behavior, ataxia, hypermetria, intention tremor, hypertonicity, and lack of menace without blindness
- Diencephalons (thalamus) may manifest as depression to stupor, normal to mild tetraparesis, deviation of the head and eyes with circling toward the side of a unilateral lesion, and bilateral nonreactive pupils with blindness
- Midbrain may demonstrate stupor to coma with hemiparesis, tetraparesis or tetraplegia, and changes in pupils such as miosis, mydriasis (if mydriatic and unresponsive, sign of poor prognosis) or anisocoria
- Pons and rostral medulla oblongata (including the inner ear) often shows obtundation, ataxia with tetraparesis or tetraplegia, and head tilt, nystagmus, facial paralysis, and medial strabismus
- Caudal medulla oblongata may manifest as obtundation, ataxia with hemiparesis to tetraparesis, abnormal respiratory patterns, and dysphagia with a flaccid tongue
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS