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Traumatic Brain Injury with Loss of Eye and Traumatic Optic Neuropathy (TON) in Fellow
Eye following Cannon Blast
Catherine Tran OD, Sally Dang OD, and Edward Chu OD
Long Beach VA Medical Center
5901 E. 7th Street, Long Beach, CA 90822
Abstract: A 19 year old male suffers from a ruptured globe OD and TON OS due to a direct
cannon blast to the left side of his face during pre-deployment with the US Marine Corps.
I. Case History
A. Patient demographics: 19 year old Hispanic male
B. Chief complaint: Photosensitivity, blurred vision, functional vision loss
C. Ocular, medical history:
1. Cannon blast at close range resulted in direct impact to skull, and patient was
unconscious for 3 weeks
2. Extensive craniofacial reconstructive surgery was performed to his head and
face after the TBI incident
a. Intraparenchymal hematoma
b. Elbow fracture operation
c. Bilateral frontal craniotomy
d. Left mandible, maxilla, and zygomatic bones facial repair
e. Anterior cranial fossa floor of skull repair
f. Cerebrospinal fluid leakage sealed
3. Following the injury, the right eye was replaced with a prosthesis
4. History of seizures following accident
D. Medications: Anticonvulsive medication
E. Other salient information: Moderate risk for falls based on Morse fall scale
II. Pertinent Findings
A. Clinical:
1. Right eye is prosthesis
2. Left eye:
a. Vision is hand motion at 2 feet, and 10/300 with eccentric viewing
b. Pupil is round and reactive to light, limited abduction, pannus present
nasally on cornea, normal intraocular pressure of 10 mm Hg
c. Cup-to-disc ratio 0.30 round with optic nerve pallor diffusely
d. Dense atrophic chorioretinal scarring and fibrosis in the posterior pole
secondary to multiple choroidal ruptures
e. The scarring envelops the macula and traverses superiorly and
inferiorly into the periphery
B. Physical:
1. Left eye slightly sunken into eye socket, lids not fully opposed to globe
2. Linear scarring traversing coronal axis of patient’s head, more abundant
scarring on left side of face, and flatter bone structure.
C. Radiology/MRI Findings:
1. Extensive chronic changes to the skull base and bilateral orbits with
deformities greater on the right than left
2. Wire mesh reconstruction on floor of anterior fossa
3. Chronic rightward deviation of the nasal septum and nasal cavity
4. Bifrontal encephalomalacia with gliosis
5. Small arachnoid cyst in the middle cranial fossa
D. Laboratory testing: Osteomyletis due to Staphylococcus aureus (patient is on
treatment and currently recovering)
III. Differential Diagnosis
A. Primary: Traumatic optic neuropathy secondary to traumatic head injury
B. Secondary: Intracranial trauma with damage to optic chiasm and severe retinal
trauma
C. Optic neuropathy secondary to:
1. Compression from orbital hemorrhage
2. Compression from orbital foreign body
3. Bony impingement from a skull base fracture into the cavernous sinus
4. Optic nerve sheath hematoma from direct or indirect injury to the globe
5. Deceleration injury from shearing of blood vessels and optic nerve tissue
IV. Diagnosis and Discussion
A. TON: Whether through direct or indirect contracoup injuries, extreme trauma to the
brain and eye region can result in legal blindness, total blindness, or loss of one or both
eyes completely
1. Indirect causes:
a. The most common cause of TON is from indirect injury to the optic
nerve from a blunt force to the forehead, e.g. car accidents and falls
2. Direct causes:
a. Optic nerve transection: One cause of TON includes endoscopic sinus
surgery leading to damage of the optic nerve
b. Orbital hemorrhage: TON can also be caused by hemorrhaging within
the orbit, likely to be caused by retrobulbar injections during ophthalmic
procedures
c. Optic nerve avulsion
d. Optic nerve sheath hemorrhage
B. Unique features:
1. Most TBIs do not incur severe outcomes such as this specific case
2. Most TBIs are considered mild to moderate, with symptoms of intermittent
blur, inefficient ability to read, eyestrain, double vision, spatial deficits, and
extreme photosensitivity
3. Due to the severity of this patient’s case with loss of an eye and near total
visual impairment in the fellow eye, the patient requires more low vision needs
V. Treatment and Management
A. Treatment and response to treatment
1. The patient is currently participating in the Blind Rehabilitation Center at VA
Long Beach for incorporation of low vision devices to aid in participation in
normal life activities, such as being a full time student
2. Devices: 4x13 Monocular Microlux for distance spotting, 4x Galilean
Focusable spectacle mounted telescope for sustained distance viewing or TV
watching, and customized sunglasses for protection and alleviation of glare
3. Patient receives orientation and mobility training, optical devices mentioned
above, zoom and text-to-speech software for computer use
4. Follow-up visit: 1 year later, the patient has completed 25 credits for general
education at a local community college
B. Research
1. Experimental investigations have shown that large amounts of corticosteroids
are beneficial immediately after brain and spinal cord injuries; however, for
immediate care following TON, the beneficial outcomes for this treatment does
not translate to damage to the optic nerve
2. In animal studies, it has shown that glutamate receptor inhibitors have
increased visual outcome by noncompetitively blocking glutamate released from
apoptotic cells from inducing death of adjacent cells
3. Treatment for TON varies based on each patient’s case - considerations
include risks of side effects versus benefits of treatments
C. Bibliography
1. Boughton, B. (2009). Traumatic optic neuropathy: Previous therapies now
questioned or shelved. Eyenet, 27-28.
2. Kapoor, N & Ciuffreda, KJ. (2002) Visual disturbances following traumatic
brain injury. Current Treatment Options in Neurology, 4(4), 271-280.
3. Sarkies, N. (2004). Traumatic optic neuropathy. Eye, 18, 1122–1125.
doi:10.1038/sj.eye.6701571
4. Steinsapir, K.D. (1999). Traumatic optic neuropathy. Current Opinion in
Ophthalmology, 10, 340–342.
VI. Conclusion
A. Cases of TON are already devastating when patients still have their fellow eye;
however, in the case of our patient who suffered a ruptured globe and prosthesis
replacement, the eye with TON was his only remaining source of any vision
B. Clinical Pearls:
1. Patients with TON should be treated and managed as a patient with low vision
if both eyes are affected
2. In a low vision evaluation, a patient can be introduced to devices that can
maximize his remaining vision and increase quality of life