|Year : 1986 | Volume
| Issue : 3 | Page : 154-7
Trans-ethmoid decompression of the optic nerve in head injuries (a report of 7 cases).
SR Nayak, SP Wagh, SS Joshi
S R Nayak
|How to cite this article:|
Nayak S R, Wagh S P, Joshi S S. Trans-ethmoid decompression of the optic nerve in head injuries (a report of 7 cases). J Postgrad Med 1986;32:154-7
|How to cite this URL:|
Nayak S R, Wagh S P, Joshi S S. Trans-ethmoid decompression of the optic nerve in head injuries (a report of 7 cases). J Postgrad Med [serial online] 1986 [cited 2022 Jun 27 ];32:154-7
Available from: https://www.jpgmonline.com/text.asp?1986/32/3/154/5337
Approximately 2 per cent of all closed head injuries affect some portion of the visual system, the commonest being injury to the canalicular portion of the optic nerve. It is accepted that spontaneous recovery of vision in such cases is generally not known. In the past, the usual method of exploration of the optic nerve was by a frontotemporal craniotomy, an operation often accompanied by complications and morbidity. Decompression of the optic nerve by the transethmoid route is relatively free from such problems and the results have been reported to be satisfactory. We had, under our care, 7 patients admitted at the R. N. Cooper Hospital, Bombay, with loss of vision following head injury. Transethmoid approach was used for decompression in these cases. Our experience forms the basis of this paper.
MATERIAL AND METHODS
In a 15 month period from January 1985 to March 1986, 7 patients with loss of vision following head injury were operated upon by us. All the patients were males, their ages being in the range of 12-45 years. Five of the patients gave history of vehicular accident while one suffered the injury after a fall from a tree. One patient gave history of trauma over the right eye with a cricket bat. History of epistaxis was available in 5 cases.
A detailed ophthalmological examination revealed an absent direct light reflex on the side of the lesion but a normal consensual reaction (Marcus Gunn pupil). Evaluation of the visual acuity revealed finger counting at 2 feet in one case, finger counting at 3 feet only in the nasal quadrant in one case, perception of light in one case and absent perception of light in 4 cases. The optic nerve damages was unilateral in all the cases. Two patients had an associated fracture of the frontal bone on the side of the optic nerve injury.
Radiographic demonstration of the optic canal fracture was possible only in 1 case. All the above patients were subjected to a transethmoid decompression of the optic nerve, under general anaesthesia, the operative procedure being performed as described by Fukado and Karnik et al.
The commonest finding at surgery was fracture of the ethmoidal labyrinth with haematoma [Table 1]. Only one patient had a fracture of the optic canal.
It was indeed gratifying to see that 4 of the 7 patients operated (57%) had improvement of vision. One of the patients who regained a vision of 6/24 post-operatively suffered from loss of colour vision in the operated eye.
A.R., a 45 year old male, was referred to us for rapidly deteriorating vision in the right eye following a vehicular accident. Ophthalmic examination revealed an absent direct light reflex with the consensual reflex present. An associated history of epistaxis from the right nostril was available. There were multiple abrasions and contused lacerated wounds in the right frontotemporal region. There was no radiographic evidence of fracture of the optic foramen. At surgery, which was performed 8 hours after injury, a haematoma was found in the ethmoid air cells and around the optic foramen, and it was drained. The optic nerve appeared normal. Forty eight hours after surgery the patient's vision had improved from perception of light to finger counting at 1 meter which further improved to 6/18 when tested 7 days after surgery.
A man aged 30 years presented 3 days after a vehicular accident, his loss of vision being immediate and total. The direct pupillary reflex was absent while the consensual response was present. A history of epistaxis with a fracture of the frontal bone on the affected side was present. His X-rays revealed a fracture of the optic foramen. Transethmoid exploration of the optic nerve revealed a fracture with haematoma in the ethmoidal labyrinth and a fracture of the optic canal itself. The fractured fragments were removed to decompress the nerve in the optic canal. However, there was no post-operative recovery of vision.
A.S., a male aged 22 years was seen by us 6 days after injury over the right eye with a cricket bat. His vision had progressively worsened to finger counting at 3 feet present only in the nasal quadrant and he gave a history of epistaxis. At surgery, there was a fracture in the ethmoidal labyrinth with haematoma but the optic nerve was intact. The ethmoid was decompressed and within 48 hours the patient showed some recovery of vision. When seen 7 days post-operatively, his vision was found to be 6/60.
A lesion of the optic nerve following head injury was first postulated by Nuhn in 1845. (as quoted by Osguthorpe). Pringle published the first report of optic nerve decompression by an orbital approach in 1922. The transethmoid approach to the optic nerve was introduced by Niho et al.
Fukado reported 400 cases of transethmoid decompression of the optic nerve with a high incidence of recovery of vision. The transethmoid approach has obviated the risks associated with a frontotemporal craniotomy.
The characteristic clinical presentation of optic nerve compression includes a history of blunt trauma to the head, usually a frontal or a frontotemporal injury, diminished vision and inconsistent or absent direct light reaction of the ipsilateral pupil with a normal consensual response. An associated history of epistaxis is a common feature. A fracture of the frontal bone on the side of the lesion was present in 28.5% of our cases.
Radiographic demonstration of the optic canal fracture is not considered mandatory for exploration of the optic nerve. Reported incidence of radiologically identifiable fractures of the optic canal varies from 0-100% in various series. In fact, the patients with improvement of vision showed no fracture of the optic canal on exploration.
All the patients with post-operative improvement of vision were those who had rapid deterioration of vision following head injury indicating a progressively increasing compression while the patients who showed an immediate and total loss of vision following head injury had no postoperative improvement of vision.
Three of the 4 successful cases in our study were operated within 8 hours of injury which stresses the fact that early surgical intervention is necessary for better results. This is in agreement with the findings of others.,, However, one of our cases has shown improvement in vision even when operated 6 days after injury, thereby showing that decompression is mandatory even if delayed. Presence of a haematoma producing compression of the optic nerve carries better prognosis while a fracture of the optic canal may generally cause direct laceration of the nerve and hence indicates a poor prognosis.
In conclusion, we would like to stress that since the loss of vision due to traumatic optic nerve compression does not generally recover spontaneously, surgical intervention is mandatory. Such surgery should be performed as early as possible to obtain the best results. The approach of choice is the transethmoidal route as it is relatively free of complications and morbidity, and the results are satisfactory.
Thanks are due to Dr. S. Pershad, Medical Superintendent, Dr. R. N. Cooper Municipal General Hospital, Juhu, Bombay, for permitting us to publish the hospital data.
|1||Fukado, Y.: Proceedings of the Second International Symposium on Orbital Disorders. Vol. 14, Amsterdam, 1973, pp. 474-484. Quoted by Karnik et al (1981). |
|2||Harrison, D. F. N.: Surgical approach to the medial orbital wall. Ann. Otol., 90: 415-419, 1981.|
|3||Karnik, P. P., Maskati, B. T., Kirtane, M. V. and Tonsekar, K. S.: Optic nerve decompression in head injuries. J. Laryngol. and Otol., 95: 1135-1140, 1981. |
|4||Niho, S., Niho; M, and Niho, K.: Decompression of the optic canal by the transethmoidal route and decompression of the superior orbital fissure. Can. J. Ophthalmol., 5: 22-40, 1970.|
|5||Osguthorpe, J. D.: Transethmoid decompression of the optic nerve. Otolaryngol. Clin. North Amer., 18: 125-137, 1985.|
|6||Pringle, J. H.: Atrophy of optic nerve following diffused violence to the skull. Brit. Med. J., 2: 1156-1157, 1922.|
|7||Ramsay, J. H.: Optic nerve injury in fracture of the canal. Brit. J. Ophthalmol., 63: 607-610, 1979.|