Discussion
Orbital emphysema is extremely rare in the absence of preceding trauma. A review of the literature identifies only a handful of cases in the absence of periorbital injury, and even fewer cases secondary to pneumothorax or iatrogenic factors such as chest tube thoracostomy [8-11]. Retrospective studies suggest that approximately 1 in 5 chest tube insertions for pneumothorax result in subcutaneous emphysema, but the phenomenon in which the subcutaneous air infiltrates soft tissue compartments of the neck and spreads to the face and eyes is comparatively scarce [12-14]. Nonetheless, orbital emphysema can pose significant morbidity in severe cases and urgent ophthalmic consultation is warranted to reduce the risk for vision loss.
To the authors’ knowledge, most cases of orbital emphysema in the setting of pneumothorax [8-10] are associated with the presence of bronchopleural fistulas, which are indicated by air leak from a chest tube [8, 9]. It is thought that air travels via a fistulous tract into the mediastinum or the adjacent subcutaneous tissues and ascends via the vascular sheaths into the thoracic and cervical subcutaneous tissues, from which it can then ascend into the inferior orbital fissure, resulting in emphysema of the eyelids and orbit [7, 9]. Furthermore, as air drains from the pleural space via the chest tube, additional air may escape into the subcutaneous tissue at the chest tube site. This air can also ascend via cervical and thoracic fascial planes into the orbit. Thus, proper chest tube functioning and positioning should be checked if orbital or subcutaneous emphysema is present [9].
Treatment is aimed at preventing orbital compartment syndrome, a sight-threatening condition that can occur due to progressive orbital emphysema, leading to increased intra-orbital pressure. This increased pressure can compress the optic nerve or its vasculature, which can impede perfusion of the central retinal artery, resulting in loss of vision [2, 7, 11]. Management for orbital emphysema depends on close observation for orbital signs. Initial assessment includes visual acuity, degree of proptosis, extraocular muscle restriction, pain with eye movement, and intra-orbital pressure, for which intraocular pressure can be used as an index [7, 11]. However, it should be noted that normal intraocular pressures do not exclude orbital compartment syndrome [11]. Imaging is useful for confirming orbital emphysema. Though radiographs and ultrasound can be used, CT has proven to be the gold standard [15, 16]. Regarding treatment, patients with good visual acuity do not need interventions, as the condition typically resolves within 7 to 10 days [7, 17]. Careful monitoring for worsening signs of orbital involvement as well as prompt intervention are required to prevent permanent vision loss. Needle decompression or lateral canthotomy with or without cantholysis can be performed [7, 17, 11]. In addition, the use of “fish gill” incisions for the placement of corrugated drains has been described as a novel surgical technique for treating progressive orbital emphysema [18].
In the case presented here, immediate intervention for the patient’s orbital emphysema was not warranted. Per the four-stage clinical classification of orbital emphysema proposed by Hunts et al., our case would be categorized as stage I orbital emphysema with standard protocol consisting of observation only [2]. The patient’s reported symptoms included blurry vision and minimal eyelid swelling, with gradual improvement in vision since onset. An absence of proptosis, dystopia, significant visual compromise, rise in intraocular pressure, or central retinal artery occlusion meant that a conservative approach without escalation in management was indicated.