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.