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ORIGINAL ARTICLE |
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Year : 2016 | Volume
: 8
| Issue : 2 | Page : 46-50 |
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Ocular manifestations of head injury: A clinical study
Anu Malik1, Alka Gupta2, Neha Luthra2, Vivek Gupta3
1 Department of Ophthalmology, Postgraduate Diploma in Clinical Research, LLRM Medical College, Meerut, Uttar Pradesh, India 2 Department of Ophthalmology, LLRM Medical College, Meerut, Uttar Pradesh, India 3 Department of Plastic Surgery, IPGMER and SSKM Hospital, Kolkata, West Bengal, India
Date of Web Publication | 17-Jan-2017 |
Correspondence Address: Anu Malik H. No. 584, Sri Nagar, Panchsheel Nagar, Hapur - 245 101, Uttar Pradesh India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1858-540X.198536
Purpose: To clinically correlate the various ocular findings with the neurological status in cases of closed head injury and between ocular involvement and mortality rate. Study Design: Prospective study. Methods: In 189 patients with closed head injury, the Glasgow Coma Scale (GCS) and Revised Trauma Score (RTS) were applied to grade the severity. A detailed ophthalmological examination was carried out within 12 h of sustaining injury. Ocular neurological signs, GCS and RTS were then used to prognosticate the outcome. Apart from suturing of laceration, patients were managed by a multidisciplinary approach. Conclusion: Ocular complications occurred in 129 of 189 (68.3%) head-injured individuals with 172 cases, (91%) male and 17 cases (9%) female in the age range 3-75 years with a mean of 28.68 years. Young adult males (16-30 years) were more vulnerable to head injury. Road traffic accident was the most common cause of head injury in 130 cases (68.8%) leading to soft-tissue injuries to the globe and adnexae in maximum no. of patients. The most frequently encountered neuro-ophthalmic manifestation was pupillary involvement, followed by papilloedema and optic nerve trauma. The association between ocular signs and the outcome was significant (P = 0.003). All the patients that died had ocular signs of neurological significance. There was a significant co-relation of the GCS, neurodeficit and the ocular signs with the outcome. Pupillary abnormalities, papilloedema and lateral rectus palsy pointed towards a poorer outcome. The GCS, neurodeficit and ocular signs contribute significantly to the prediction of outcome. Keywords: Closed head injury, Glasgow Coma Scale, ocular signs of neurological origin, Revised Trauma Score
How to cite this article: Malik A, Gupta A, Luthra N, Gupta V. Ocular manifestations of head injury: A clinical study. Sudanese J Ophthalmol 2016;8:46-50 |
Introduction | |  |
Head injuries are a cause of hospitalization of 200-300 persons per 100,000 population per year [1] and about 25% of these are associated with ocular and visual defects. Ocular trauma is the cause of blindness in more than half a million people worldwide and of partial loss of sight in many more and it is often the leading cause of unilateral loss of vision, particularly in developing countries. [2] Hence, the role of ocular injuries secondary to head trauma in the causation of blindness and overall prognosis of patients has become a subject of immense importance. [3]
Head injuries are frequently associated with ophthalmic manifestations and consequent morbidity, but many of the ophthalmic findings are often ignored and present much later to specialist neuro-ophthalmic clinics. [4] Hence, clinical correlation of the ophthalmic findings is important in early localization of the site of injury, ongoing assessment, better management, and prognosis of the patient with head injury. [5],[6]
The aim of this study was to evaluate the pattern and clinical profiles of ocular and visual complications in patients hospitalized and managed for head injuries at our center and then prognosticate the outcome based on these findings.
Materials and Methods | |  |
The study comprised a prospective analysis of 189 patients diagnosed as having closed head injury by the neurosurgical team. They were hospitalized for varying periods between June 2013 and June 2014 at the emergency services of a tertiary care hospital. The Glasgow Coma Scale (GCS) and the Revised Trauma Score (RTS) were applied to grade the severity of the head injury and to assess the prognosis in all cases. Ophthalmic assessment of all the patients was carried out within 12 h irrespective of the presence or absence of ocular involvement. All the cases were reviewed daily by the same ophthalmic team until the patients were discharged from the hospital.
The study included closed head injury patients. In bilateral ocular involvement, the more severely damaged eye was studied. Patients with open head injury, direct orbital trauma or with head injury, older than 12 h were excluded from the study.
Diagnostic investigations carried out included skull and spine rent genograms, computed tomographic brain scanning (when indicated), gonioscopy, perimetry, diplopia charting, and measurement of intraocular pressure (wherever possible). Visual acuity in adults was assessed using the Snellen's chart, but in children, crudely by grading visual fixation and tracking to familiar objects. The findings were transferred into a questionnaire format, which included patient's sociodemographic data, mode of head trauma, and findings in neurological and ophthalmic evaluations.
Ocular and visual complications were grouped into three main classes of abnormalities of the visual system: soft tissue injuries to the globe and adnexa, neuro-ophthalmic abnormalities, and injuries to the bony orbit. Apart from suturing of lacerations, patients were managed according to their respective diagnosis by the neurological and ophthalmologic units. Those who presented with multiple organ involvement were referred to the appropriate specialties in the same hospital.
Results | |  |
Out of 189 cases of head injury, 172 cases (91%) were male and 17 cases (9 % ) were female. Age of the patients ranged from 3 to 75 years with a mean of 28.68 years (±8.78 years). Young adult males (16-30 years) were the major group who sustained head injury, i.e., 124 of the 189 of head injury cases. The incidence of head injury was less during childhood, peaked in the third decades of life, and thereafter declined [Figure 1]. | Figure 1: Ocular manifestations in the form of periorbital ecchymosis and lid laceration
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Road traffic accident (RTA) was the most common cause of head injury in 130 cases (68.8%) followed by assaults in 34 cases (18.0%). In remaining 25 patients (13.2%), causes of head injury included falls, pedestrians hit by motor vehicles, or cattle.
In 23 patients (12.2%), head and ocular injuries were associated with injuries to other organs such as chest, abdomen, and long bones. Ocular and visual complications occurred in 129 of 189 (68.3%) head injury patients managed during the period under consideration. The right, left, and both eyes combined were injured in an approximate ratio of 1:1:2, respectively.
[Table 1] shows the ocular and visual complications observed in 129 cases. They included soft tissue injuries to the globe and adnexa in 86 patients (45.5%), neuro-ophthalmic abnormalities in 27 patients (14.3%), and fracture of the orbit with rupture of the eye in 16 patients (8.5%). The most frequent soft tissue injuries were periorbital ecchymosis (39 patients - 20.63%), subconjunctival hemorrhage (20 patients - 10.58%), lid laceration (6 patients - 3.17%), corneoscleral laceration requiring surgery (6 patients - 3.17%), and macular edema (4 patients - 2.12%). The most frequently encountered neuro-ophthalmic manifestation was pupillary involvement (in the form of abnormalities of pupillary size and reaction in one/both eyes) in 15 patients (7.95%) followed by papilledema and optic nerve trauma. In all, 94 (49.7%) patients had a combination of two or more ocular findings such as ecchymosis, subconjunctival hemorrhage, orbital fracture, hyphema, and scleral tears. The more severe injury was taken as the main ocular finding for assessing prognosis in head injury.
The association between ocular signs and the outcome was significant. All the patients that died had ocular involvement of neurological significance, i.e., pupillary abnormalities, papilledema, sixth nerve palsy, neurogenic ptosis, and optic neuropathy [Table 2]. Twenty-one (11.1%) patients with ocular involvement in head injury died. Four died early (within 4 h) while six died within 24 h. A total of eleven patients died after 48 h.
A correlation of ocular findings with the GCS and RTS in the first few hours following head injury was attempted [Table 3]. In all, 139 patients (73.5%) had a mild head injury (GCS of 13-15 and RTS of 10-12) of which 86 (61.8%) patients had eye involvement of no neurological significance. None of the mild head injury cases died, and only four had minimal residual neurodeficit. A total of 29 patients (15.4%) was graded as having incurred moderate head injury (GCS 11-12), of which 24 patients (82.8%) had ocular involvement. Signs of neurological significance were seen in 22 patients, of which 11 died. There were 21 cases (11.1%) of severe head injury, of which 10 patients that had ocular neurological signs died.
There was a significant correlation of the GCS, neurodeficit, and the ocular signs with outcome [Table 4]. Pupillary abnormalities, papilledema, and lateral rectus palsy pointed toward a poorer outcome. All the patients that died had ocular involvement of neurological significance. The outcome is worse in patients with GCS 6-8 with ocular involvement and neurodeficit (P < 0.001, Fisher's exact test) and those with GCS 11-12 and ocular signs (P = 0.04, Fisher's exact test). The GCS, neurodeficit, and ocular signs contribute significantly to the prediction of outcome. | Table 4: Association of Glasgow Coma Scale, neurodeficit, and ocular signs with outcome
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Discussion | |  |
Age of the patients ranged from 3 to 75 years with a mean of 28.68 years (±8.78 years). Young adult males (16-30 years) were the major group who sustained head injury, i.e., 124 of the 189 of head injury cases. This finding is similar to the findings in other studies, for example, Kulkarni et al. [6] showed that the young adult males (21-30 years) were more vulnerable. Odebode et al. [7] showed a peak during third decades (21-30 years) of life. Sharma et al. showed a peak during 21-40 years. [8] This vulnerability of the young is due to the increased association with outdoor activities.
RTAs were the most common cause of head injury due to high-velocity impact. Other studies also showed almost similar observations. [6],[7] Raju reported 47.5% of cases because of RTA and 32.5% of cases due to fall from height. [9]
Emem and Uwemedimbuk conducted a retrospective study between January 2008 and December 2009 at University of Uyo Teaching Hospital, Uyo, Nigeria, where 5416 patients were examined, out of which 226 had ocular injury giving a prevalence of 4.06%. [10]
The proportion of head injuries - 68.8% resulting from RTA is higher than 44% quoted by Rowbotham et al., [11] other studies were it can be as high as 84.2%. [15]
Head injuries can be defined as those in which there is evidence of the involvement of the brain, including concussion, loss of consciousness, posttraumatic amnesia neurological signs of brain injury, or skull fractures. [12]
The GCS (includes eye opening response, best verbal response, and best motor response) and the RTSs (including the GCS, systolic blood pressure, and the respiratory rate) are commonly used in grading the severity of head injury. Where RTS is a physiological scoring system designed for use on the initial vital signs, lower scale indicates the higher severity of injury. The RTS is heavily weighted toward the GCS to compensate for major head injury without multisystem injury or major physiological changes in parameters with resuscitation of patients. [13] The data were derived from the vital signs and levels of consciousness mathematically culminates into a single variable that correlates with mortality. [14] Even if the ocular involvement is not present, poor GCS and RTS patients have poorer survival probability, however, we tried to correlate that probability with the ophthalmic signs of neurological significance.
The eyes are often involved in head injury (directly and indirectly) with neuro-ophthalmic deficits. [2],[4],[7],[11],[15],[16] Most ophthalmologists when faced with injured patients tend to focus on obvious ocular manifestations such as contusions and laceration. Subtle manifestations may be equally important and may go unrecognized. Neuro-ophthalmic evaluation is challenging in head injury patients with reduced consciousness or coexisting injuries.
None of the patients had diplopia, proptosis, or nystagmus in our study. Diplopia is a finding frequently encountered in head injury patients. [16] The eye and its adnexa are innervated by one-half of the cranial nerves, and 38% of all fibers in the central nervous system are concerned with visual function, so clinical findings of neuro-ophthalmological interest are frequently noted with head injury. [14] Pupillary signs (size, reaction to light) are of grave importance in indicating the site and severity of injury and in the prognosis of head injury. We compared our study to other retrospective studies by Madavi and Vasana, [5] Kulkarni et al., [6] and Odebode et al. [7]
Periorbital ecchymosis occurred in 20.63% in our study, which was comparable to 22%-27% in other studies. [5],[6],[7] The incidence of subconjunctival hemorrhage was 10.58% as compared to 36.8% in a study. [7] Pupillary abnormalities were found in 7.95% as in other studies. [6]
Only patients with closed head injury were included with head injury within 12 h. Accurate ocular motility assessment within the first few hours of head injury is not possible with patients in coma. Many signs and symptoms like third nerve misdirection arise a few months after trauma. This could account for a different spectrum of ocular findings in our study as compared to other studies. [17],[18] Specific tests of optic nerve function such as contrast sensitivity, color vision, optic nerve head morphology, field testing, and visually evoked potential could not be carried out in the acute setting of this study; hence, subtle optic neuropathy, especially in cases with normal or near normal Snellen acuity, could have been missed. [16]
Kulkarni et al. found a higher prevalence of ocular involvement of 83.5% in closed head injury patients. [6] Studies show that higher incidences of ocular findings are found when ophthalmologists participate in the examination of head injury patients. [17]
In our study, there were 3 (1.59%) patients with lateral rectus palsy. In a study by Kowal, 10 patients had exotropia, and three had esotropia. [17] Esophoria and exotropia are common sequelae of head trauma. Binocular single vision may be lost after a head injury, with the breakdown of a latent phoria or loss of the normal physiological fusion of the image presented to each eye. [19] Strabismus occurs in head injury due to ocular motor cranial nerve palsies or injury to extraocular muscles, for example, muscle entrapment in orbital fractures. Ciuffreda et al. [20] found strabismus in 25%.
In a study by Masila et al., a positive correlation was seen between severe head injury (GCS < 8) and occurrence of ocular signs. [21]
Rehabilitation of the head injury patient is much more difficult if the visual system is not efficient. Head injury patients may be difficult to examine because of cognitive and communication disorders. A complete assessment may include evaluation of the eye, refraction, and examination of ocular motility, accommodation, vergence, stereopsis, visual perception, and visual fields. [22]
Visual field testing was not possible in acute head trauma where the stabilization of the patient was more important. Surprisingly, none of the patients complained of double vision while admitted in hospital, however, seven patients did seek the ophthalmic opinion for diplopia within a month of being discharged after their head injury. We faced some problems during patient assessment because GCS is heavily weighted toward speech and eye opening. Some patients were unable to speak due to facial injury, and eye-opening was hindered by severe periorbital trauma/edema. Another limitation to the study was that any other major injury to the body was not considered as a cause of mortality. Kendall's test and Fisher's exact test were used to find the association of GCS, neurodeficit, and ocular signs.
This study highlights the importance of a detailed early ophthalmological assessment in correlation with GCS in head injury patients to prognosticating outcomes. This should be repeated at regular intervals to monitor the signs of progress and deterioration as well. The GCS, neurodeficit, and ocular signs contribute significantly to the prediction of outcome. This emphasizes the importance of integrating ophthalmic assessment into the routine head injury assessment. This aids in follow-up, prognosis, and further management of neurologic deficits, thus reducing the incidence of late/missed diagnosis.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | WHO. Strategies for the Prevention of Blindness in NationalProgrammes. A Primary Health Care Approach. 2 nd ed. Geneva, England: WHO Library Cataloguing; 1997. p. 74-6. |
2. | Baker RS, Epstein AD. Ocular motor abnormalities from head trauma. Surv Ophthalmol 1991;35:245-67. |
3. | Chaudhuri Z, Pandey PK, Gupta R, Chauhan D. Profile of Ocular Morbidity Associated with Head Injury. [AIOC Proceedings] MISCELLANEOUS; 2002. p. 609. |
4. | Van Stavern GP, Biousse V, Lynn MJ, Simon DJ, Newman NJ. Neuroophthalmic manifestations of head trauma. J Neuroophthalmol 2001;21:112-7. |
5. | Madavi BS, Vasana IG. Ocular manifestations of head injury in trauma patients. Glob Res Anal 2013;2:184-5. |
6. | Kulkarni AR, Aggarwal SP, Kulkarni RR, Deshpande MD, Walimbe PB, Labhsetwar AS. Ocular manifestations of head injury: A clinical study. Eye (Lond) 2005;19:1257-63. |
7. | Odebode TO, Ademola-Popoola DS, Ojo TA, Ayanniyi AA. Ocular and visual complications of head injury. Eye (Lond) 2005;19:561-6. |
8. | Sharma R, Gupta R, Anand R, Ingle R .Ocular manifestations of head injury and incidence of post-traumatic ocular motor nerve involvement in cases of head injury: A clinical review. Int Ophthalmol 2014;34:893-900. doi: 10.1007/s10792-014-9898-8. |
9. | Raju N. Ocular manifestations in head injuries. Indian J Ophthalmology 1983;31:789-92. |
10. | Emem A, Uwemedimbuk E. Prevalence of traumatic ocular injuries in a teaching hospital south- south Nigeria- a 2 year study. Advance Tropical Medicine and Public Health International 2012;2:102-8. |
11. | Rowbotham GF, Maciver IN, Dickson J, Bousfield ME. Analysis of 1,400 cases of acute injury to the head. Br Med J 1954;1:726-30. |
12. | Annegers JF, Grabow JD, Kurland LT, Laws ER Jr. The incidence, causes, and secular trends of head trauma in Olmsted County, Minnesota, 1935-1974. Neurology 1980;30:912-9. |
13. | Champion HR, Sacco WJ. WS Copes. "A Revision of the Trauma Score". J Trauma 1989;29:623-9. |
14. | ACS Committee on Trauma. Advanced Trauma Life Support Course for Physicians. 3 rd ed. Chicago: American College of Surgeons; 1993. |
15. | Sabates NR, Gonce MA, Farris BK. Neuro-ophthalmological findings in closed head trauma. J Clin Neuroophthalmol 1991;11:273-7. |
16. | Smith JL. Some neuro-ophthalmological aspects of head trauma. Clin Neurosurg 1966;13:181-96. |
17. | Kowal L. Ophthalmic manifestations of head injury. Aust N Z J Ophthalmol 1992;20:35-40. |
18. | Mariak Z, Mariak Z, Stankiewicz A. Cranial nerve II-VII injuries in fatal closed head trauma. Eur J Ophthalmol 1997;7:68-72. |
19. | Yanoff M, Duker JS. Ophthalmology. 3 rd ed. Expert Consult: Online and Print; 2012. |
20. | Ciuffreda KJ, Kapoor N, Rutner D, Suchoff IB, Han ME, Craig S. Occurrence of oculomotor dysfunctions in acquired brain injury: A retrospective analysis. Optometry 2007;78:155-61. |
21. | Masila F, Kiboi J, Marco S, Njuguna M. Ocular findings in patients with head injury. J Ophthalmol East Cent S Afr 2014;18(2):83-9. |
22. | Falk NS, Aksionoff EB. The primary care optometric evaluation of the traumatic brain injury patient. J Am Optom Assoc 1992;63(8):547-53. |
[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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