EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014


523


Case Report Bilateral traumatic optic nerve avulsion in a Thoroughbred gelding


A. Kullmann*, J. V. Marteniuk, M. R. Williams, S. J. Holcombe, F. M. Mowat† and T. P. Mullaney‡


Department of Large Animal Clinical Sciences, †Department of Small Animal Clinical Sciences, Ophthalmology Service, and ‡Diagnostic Center for Population and Animal Health, College of Veterinary Medicine, Michigan State University, East Lansing, USA. *Corresponding author email: akullm@cvm.msu.edu


Keywords: horse; blindness; head trauma; optic nerve avulsion; basisphenoid fracture


Summary This report describes an unusual case of acute blindness following traumatic head injury in a mature horse. The horse fell over backwards and subsequently presented with bilateral blindness and epistaxis. Vision did not return following medical supportive therapy and euthanasia was elected. Post mortem findings revealed a basisphenoid fracture and bilateral optic nerve avulsion rostral to the optic chiasm, an uncommon presentation of traumatic blindness not previously reported in the horse.


Introduction


Traumatic head injury in horses is relatively common (Feary et al. 2007). Approximately half of all reported cases result from rearing and falling over backwards and subsequent poll trauma (Ragle 1993; Feary et al. 2007). Epistaxis is a consistently reported clinical sign in such injuries in conjunction with basilar bone fractures (Stick et al. 1980; Ragle 1993; Feary et al. 2007). Trauma to adjacent soft tissues occurs with basisphenoid fractures. Laceration of adjacent blood vessels such as occipital and basilar arteries causes bleeding into the retropharyngeal spaces or guttural pouches, resulting in epistaxis (MacKay 2004). Although the equine optic nerve, particularly the intracranial portion, is susceptible to injury during blunt head trauma, blindness following head trauma has rarely been reported (Martin et al. 1986; Blogg et al. 1990; Millichamp 1992; Reppas et al. 1995). A recent retrospective study found that only 4/34 (12%) horses with head trauma exhibited loss of vision (Feary et al. 2007). This report describes a case of bilateral traumatic optic nerve avulsion in the horse resulting in blindness.


Case history and clinical presentation


A 12-year-old Thoroughbred gelding was admitted for evaluation and treatment of suspected traumatic brain injury. After rearing while being worked in long lines the horse flipped over backwards and was briefly unconscious. The horse stood but was obtunded and mildly ataxic. The horse was admitted to the hospital approximately 3 h


after the injury. He was alert and responsive with a heart rate of 56 beats/min, respiration of 12 breaths/min and rectal temperature of 39.3°C. Mucous membranes were bright pink and moist with a capillary refill time of 2 s. Mild bilateral epistaxis was noted. Packed cell volume and estimated total protein measured 43% (reference range [rr] 30–45%) and 61 g/l (rr 59–75 g/l), respectively. The gelding reluctantly moved forward but was comfortable and coordinated backing up and circled


normally in both directions. No gait abnormalities were noted and postural reactions were normal. No neck pain or guttural pouch distension was noted. The horse had a soft tissue swelling caudal to the right mandibular ramus, which decreased during hospitalisation and probably resulted from trauma caused by the halter during the fall. A neurological examination revealed normal mentation,


tongue tone, facial symmetry and balance. Both pupils were symmetrically dilated and menace responses were absent. Direct and consensual pupillary light reflexes and dazzle reflexes were also absent bilaterally. The horse had a slight head tilt to the left and mild ventromedial strabismus bilaterally.


Diagnostics


Venous blood gas analysis and complete blood count were normal. No fractures were evident on skull radiographs that included right lateral, dorsoventral and both oblique views. Fluid lines were seen in the right and left maxillary sinuses. A focal soft tissue opacity was seen within the right caudal maxillary sinus, consistent with a haematoma (Fig 1). Upper airway endoscopy revealed mild compression of the lateral compartment of the right guttural pouch. The bilateral epistaxis was presumed to originate from the paranasal sinuses.


Fig 1: Right oblique (left 30° dorsal right ventral oblique view) view of skull showing a fluid line (solid arrow) and soft tissue opacity (open arrow) in the right caudal maxillary sinus.


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