|Home | About | Journals | Submit | Contact Us | Français|
Orbital emphysema and associated pneumocephalus usually result from trauma to orbital bones or due to sinus disease, allowing air to travel from paranasal sinus into orbit and brain. However, it is extremely rare to have orbital emphysema and pneumocephalus in the absence of orbital wall fracture. In our case, a young male was admitted with severe eye pain, diminution of vision due to sudden exposure of compressed air gun. Examination revealed proptosed, emphysematous right eye with conjunctival laceration. Computed tomography scan of the head and orbit revealed multiple radiolucencies with air in the right orbit and brain extending up to the spinal canal without any evidence of orbital sinus or cranial bone fracture. Visual acuity recovered completely on follow–up; however, 2 weeks following injury, the patient developed disabling flashes of light which the patient perceived as central in location and resolved finally over a period of 3 months. Flashes of light, in our case, could be attributable to unnoticed damage to cerebral vasculature or connective tissue surrounding the optic nerve due to pneumocephalus.
Fracture of orbit or cranial bones can cause pneumocephalus, but it is extremely rare (only 4 reported cases) to have pneumocephalus with compressed air gun injury, especially when there is no orbital or cranial bone fracture.
Till now, the association between pneumocephalus, resulting from compressed air gun injury and flashes of light, was not mentioned anywhere. We found a case presenting with disabling flashes of light following compressed air gun injury. This case is unique in the sense that flashes of light could be directly attributable to pneumocephalus and air travelled upto spinal canal.
A young healthy male had accidentally been exposed to compressed air gun while working. He was admitted with complaints of severe pain, diminution of vision, lid swelling, and proptosis. The compressed air gun had a high-pressure air stream at around 80–120 psi.
Ophthalmological examination revealed a visual acuity of 20/40 in the right eye (with pinhole) and 20/20 in the left eye. There was no refractive error. No history of any previous eye or head injury was noted. Extensive crepitation and edema involving both upper and lower lids, severe proptosis, subconjunctival hemorrhage, emphysema, and large nasal conjunctival laceration were found in the right eye. The ocular movements were restricted in all direction of gaze in the right eye. Cornea shows fluorescein stain positive, multiple corneal erosions. Pupil – normally reacting. Lens – clear. Dilated fundus examination of the right eye did not show any evidence of any retinal break/tear/vitreous hemorrhage. There was no evidence of conjunctival or corneal injury on left side. Intraocular pressure with applanation tonometry - 14 mmHg BE.
An emergency computed tomography (CT) scan of orbits and head showed proptosis of right eye with extensive air inside the right orbital bony cavity and extending intracranially to suprasellar, parasellar region involving anterior and right of pons [Figures [Figures11–3]. Tiny air focus was seen at the upper part of spinal canal at the level of C1 [Figure 4]. Surgical emphysema was extended up to right temporoparietal region and neck. Both optic nerves showed no evidence of any injury or any retro-orbital hematoma. Extraocular muscles were grossly normal. There was no any obvious bony orbital fracture or any fresh blood or midline shift with normal brain parenchyma and ventricular system.
General physical examination including neurological evaluation was within normal limits (Glasgow coma scale = E4V5M6). The patient was given systemic and topical antibiotics. Although most of the lid emphysema, proptosis, and conjunctival chemosis resolved after 2 days, the patient started complaining of diplopia in all gazes which had slowly improved over a period of 3 months. Visual acuity improved to 20/20 without correction and conjunctival laceration healed on follow-up. However, 2 weeks following compressed air gun injury, the patient developed visually disabling flashes of light in right eye which was perceived as central in location. The symptom improved slowly over the period of 3–4 months.
Pneumocephalus usually results from orbital wall or cranial bone fractures. According to the existing literature, there were few reported cases of pneumocephalus which stemmed from compressed air gun injury where no fracture of orbital bones was noticed.[1,2,3,4]
Different modes of compressed air injury usually ascribed to an exploding automobile tire or an external hose. In our case, at 80–120 psi pressure, it may be possible for the air to travel intracranially up to the spinal canal.
Dissimilar mechanisms of air entry into the intracranial location have been postulated by different authors.[1,2,3,4,6] Yuksel et al. found air at multiple locations filled with cerebrospinal fluid (CSF) in the subarachnoid space, such as prepontine cistern, cerebellar folia, and superior cerebellar cistern, confirmed through CT scan. Most likely explanation of air entry to the cranial cavity seems to be due to dissection through Tenon's capsule, around optic nerve, and through optic canal into the subarachnoid space. Same mechanism of air entry has been assumed by Williams and Frankel in their case as well. Lubniewski and Feibel described that at 75 psi, it is possible for air to pass intracranially (extradurally) through superior orbital fissure. CT scan showed location of air adjacent to superior orbital fissure and sella.
In our case, extensive air was seen inside the right orbital bony cavity and extending further intracranially to the suprasellar, parasellar region, and anterior to right pons with tiny air focus at upper part of spinal canal at the level of C1. There was surgical emphysema extending from right temporoparietal region and neck. Serial CT, done after 10 days, established that pneumocephalus was present in the subarachnoid space (spinal canal and anterior to right pons). Mechanism of air entry in our case may be through dissection of Tenon's capsule and followed by air traveling around optic nerve into the subarachnoid space through CSF pathway. Although CT scan shows localization of air at superior orbital fissure, exact reason behind extradural entry of air could not be established at our case.
Complications that have been noted at many literature after compressed air injury include “traumatic optic neuropathy, the injection of foreign body through the conjunctiva with risk of infection and inflammation, proptosis, corneal exposure, blowout fracture, glaucoma, uveitis, central retinal artery occlusion, and tearing of ophthalmic vein with fatal air embolism.”[7,8,9] Gross and Doxanas and Lubniewski and Feibel mentioned about optic atrophy and poor vision following compressed air injury due to injury of the pial and arachnoid blood supply. Our case had good visual outcome till 1 year of follow-up. It is assumed that air did not damage the blood supply of the optic nerve in our case as supported by Yuksel et al. in their case.
Sequel of traumatic brain injury includes headache, dizziness, anxiety, apathy, depression, aggression, cognitive impairments, personality changes, mania, and psychosis. Flashes are caused by improper stimulation of the retina, optic nerve, or visual pathway, which brain interprets as light. As per as available literature and books, causes of flashes could be related to retinal tear, posterior vitreous detachment, retinal artery occlusion, uveitis, optic nerve injury, blow to head, diabetic retinopathy, multiple sclerosis, melanoma, acute posterior multifocal placoid pigment epitheliopathy, occipital lobe lesions, etc. In our case, pathology related to ophthalmic or neurological causes of flashes of light was ruled out by careful general physical and ophthalmological examination including diagnostic test like +90D examination, I/O, Amsler grid, color vision, fundus fluorescein angiography, optical coherence tomography, ultrasonography, autoperimetry, color Doppler, and CT scan and magnetic resonance imaging scan. Possible explanation behind the flashes in our case may be related to unnoticed damage to cerebral vasculature or connective tissue surrounding the optic nerve due to passage of air. Further long-term study and diagnostic test including visual-evoked potential and cerebral angiography are warranted to find out the causes and localization of flashes.
Our case could be only one of its reported cases where causation of flashes might be related to pneumocephalus or attendant microvascular damage to visual pathway secondary to compressed air gun injury. Pneumocephalus could be considered as a differential for flashes of light when the patient exposed to compressed air gun injury.
There are no conflicts of interest.