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EQUINE VETERINARY EDUCATION / AE / OCTOBER 2014


Bilateral mydriasis, bilateral negative dazzle reflexes and


lack of menace responses were noted during the ophthalmic examination performed 24 h after hospital admission. Direct and consensual pupillary light reflexes were also absent bilaterally. A 3–4mm region of endothelial fibrosis was identified on the left cornea, at the ventronasal aspect near the limbus with corneal thinning, consistent with a healed corneal ulcer. Fluorescein stain uptake was negative in both eyes. Slit lamp biomicroscopy revealed a small (2 × 3 mm) incipient cataract affecting the mid posterior subcapsular lens cortex in the left eye. Indirect ophthalmoscopy revealed a normal optic disc, decreased pigment in the nontapetal fundus, which was considered normal variation. Intraocular pressure was measured at 17 mmHg and 22 mmHg in the right and left eye, respectively. Differential diagnoses for bilateral blindness in this horse,


included impairment of the visual pathway at the level of the optic chiasm, optic tracts or a bilateral optic nerve lesions. Trauma and/or pain from the contralateral throatlatch swelling or vestibular dysfunction may have induced the head tilt. There were no other clinical signs of vestibular disease. The medial strabismus may have been a consequence of the head trauma and injury to the abducent nerve (Reed and Andrews 2010). Advanced imaging techniques such as computed tomography or magnetic resonance imaging were discussed, but declined by the owners. Ultrasound examination of the eye and rostral optic tracts were not performed.


Treatment


Intravenous fluid therapy (1 l bolus of 7.2% saline solution followed by lactated Ringer’s solution supplemented with calcium borogluconate [25 ml/l of a 23% solution]) was administered (2 ml/kg bwt/h) to maintain adequate plasma volume and hydration. Hypertonic saline was administered as an osmotic agent to decrease potential brain swelling. Flunixin meglumine (Flunixiject1; 1.1 mg/kg bwt, i.v., q. 12 h) was administered for anti-inflammatory and analgesic effects. Broad-spectrum antimicrobials (potassium penicillin G [Pfizerpen]2 22,000 iu/kg bwt, i.v., q. 6 h and gentamicin [Gentafuse]1 6.6 mg/kg bwt, i.v., q. 24 h) were given prophylactically due to the presence of blood in the paranasal sinuses. The horse received omeprazole (GastroGard3; 2.2 mg/kg bwt, per os, q. 24 h) to prevent gastric ulceration. Vitamin E4 (10,000 iu per os q. 24 h) was administered as an antioxidant, to ameliorate oxidant damage, a recognised sequel in the secondary phase of brain injury (Mackay 2004). Eye lubrication (Paralube Vet ointment)5 was applied to both eyes q. 4 h to help to protect the corneas from trauma due to the blindness.


Case progression and outcome


Over the next 24 h of hospitalisation the gelding remained intermittently febrile with rectal temperatures ranging between 38.4 and 39.3°C. On Day 3 of hospitalisation the gelding developed mild to moderate colic signs, exhibited as pawing and lying down. A nasogastric tube was placed and enteral fluid therapy (6 l of alternating isotonic NaCl or KCl solutions q. 2 h via the indwelling nasogastric tube) administered for 8 h. The horse developed watery diarrhoea. Serum chemistry profile revealed hypoproteinaemia (52 g/l; rr 60–87 g/l) with mild hypoalbuminaemia (34 g/l; rr 36–48 g/l),


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Fig 2: Gross post mortem of ventral brain showing the traumatic bilateral optic nerve avulsion (solid arrows) rostral to the optic chiasm (open arrow).


hypoglobulinaemia (1.8 g/l; rr 24–51 g/l), total


hyperbillirubinaemia (46 mg/l; rr 1–21 mg/l), hyponatraemia (129 mmol/l; rr 132–141 mmol/l) and hypochloraemia (98 mmol/l; rr 101–110 mmol/l). These abnormalities in conjunction with diarrhoea indicated acute colitis. The gelding’s feet were placed into ice boots and the antimicrobial regime was changed to oxytetracycline HCl (Vetrimycin 1006; 6.6 mg/kg bwt, i.v., q. 24 h for 3 consecutive days), because Neorickettsia risticii (Potomac horse fever) is seasonally prevalent in Michigan. Faecal Salmonella spp. cultures as well as Clostridium difficile and Clostridium perfringens faecal enzyme-linked immunosorbent toxin assay and culture yielded negative results. The gelding was not tested for N. risticii. The horse remained blind and showed no improvement


during 5 days of hospitalisation. The owners elected humane euthanasia.


Post mortem findings


A post mortem examination was performed on the horse by a board-certified pathologist. Macroscopic examination of the skull revealed haemorrhage within the external canal of the right ear and blood clots within the right paranasal sinuses. The optic nerves were avulsed rostral to the optic chiasm with haemorrhage within the proximal segments (Fig 2). The distal segment of the left optic nerve was mildly haemorrhagic and there was a blood clot noted ventral to the nerve. The distal segment of the right optic nerve was haemorrhagic and there were 5 ml of extradural unclotted blood present on the right side of the sella turcica ventral to the pituitary gland. A complete sagittal nondisplaced fracture of the basisphenoid bone ventral to the ethmoid turbinates was found. The fracture was rostral to the synchondrosis of the basisphenoid and basioccipital bones and did not involve the optic canals (Fig 3).


Microscopic sections of the right and left optic nerve and


the optic chiasm were examined. The histopathological findings were consistent with a traumatic avulsion of both optic nerves.


Sections of both the right and left optic nerves (nearest the avulsion sites) were characterised by locally extensive regions


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