[1][9] It is most commonly result from forceful sneezing, nose blowing, or coughing among patients with a history of periorbital trauma or orbital fractures that happened several hours-days in advance.

[10] Rare occasions have also been reported in relation to individuals with no traumatic past events that include: infection, esophageal rupture, postoperative complications, pulmonary barotrauma, with the same predisposing factors (sneezing, nose blowing, or coughing).

[1][16][17] Any object with force and/or speed, typically a ball, fist or vehicle accidents, can result in orbital floor and/or medial wall fractures.

[3][13][28] These surgical procedures may possibly introduce staphylococci, streptococci, and anaerobic bacteria via a compromised bony wall that can cause periorbital infection.

[25] The corresponding weakened or degenerated tissues cannot withstand the sudden increase in intraocular pressure and impaired ocular perfusion, driven by severe coughing or sneezing.

It subsequently results in air trapped in the periorbital subcutaneous tissue and the development of orbital emphysema, which is often mistaken as allergic reactions.

[3] The signs and symptoms of orbital emphysema vary depending on the original cause, but it is preliminary associated with swelling, bruising, and tenderness around the impacted eye.

[1][23] The entrapped air may cause an acute increase in the intraocular pressure or vascular compromise that restrict ocular motility, prohibit the closure of eyelids, and the loss of sensation over the upper cheek areas.

[30] Server entrapment in the soft tissues tends to stimulate oculocardiac reflex, which is likely to generate significant vagal responses including nausea, dizziness, vomiting, bradycardia, syncope and heart block.

[1][7][33][34] Orbital emphysema is typically a harmless disorder because air escapes as quickly as it enters the fracture site, and the increase in intraorbital pressure is usually transient, lasting for as long as the sneeze or nose blowing.

[33] However, when orbital soft tissues, such as fat,[1] falls back on the sino-orbital communication,[1][3][4][33] a one-way ball valve will be created, leading to the entrapment of air.

[6][3][36] The air usually enters the orbit when the pressure within the upper respiratory tract is increased due to expiratory efforts, nose blowing or sneezing.

[1][15] Stage II orbital emphysema develops as the intraorbital air volume increases, causing the eyeball to displace horizontally or vertically (globe dystopia) or to protrude anteriorly (proptosis).

[1][15] Stage IV orbital emphysema develops when the intraorbital air mass results in an intraocular pressure of more than 60 to 70 mmHg.

The significantly elevated intraocular pressure will lead to central retinal artery occlusion, which may result in permanent and irreversible damage to the retina.

The findings of the examination are supported with the medical history of the patient and confirmed with orbital CT.[6] Computed tomography is effective and sensitive in the diagnosis of orbital emphysema,[3][37] as it can confirm the anatomical location and size of air, bony defects, indentation of the eyeball, and the condition of the optic nerve, as well as the presence of any extraocular muscle entrapment and herniation of preorbital fat into the sinus cavities.