A 46-year-old moderately myopic man (−6 D) with a past history of Graves’ disease, preseptal cellulitis and a left-sided peri-orbital haematoma arising from injury 7 years ago presented with another episode of orbital floor fracture, mild orbital emphysema (Fig. 1A) and microhyphaema in the left eye. On the day of presentation, the visual acuity (VA) remained unaffected (6/6) in both eyes. However, on day 2, the VA of his left eye was reduced to hand movement. The left eye was proptotic, Hertel measurements were 23/30–110, motility was reduced and a relative afferent pupillary defect was present (Fig. 1B). Orbital haemorrhage or emphysema was suspected, and an emergency lateral canthotomy with severing of the lateral canthal ligament was performed. A computer tomography (CT) scanning revealed a large amount of air in the orbit (Fig. 1C), and punctures with an 18-gauge venous cannula through the upper (Fig. 1D) and lower lids were performed under local infiltration anaesthesia with the use of the CT scanning as a guide. During this procedure, audible escape of air was noted. On day 3, the patient was discharged with a VA of 6/24.
On day 4, the patient presented again with left-sided proptosis and a VA of hand movements. A CT scanning revealed air in the orbit, and orbital punctures were repeated. On day 5, he was discharged with a VA of 6/24. Unfortunately, on day 7 at 1.30 am, the patient presented again with proptosis, and the VA was reduced to counting fingers at 0.5 m. The orbital punctures were thus repeated and later that day, he was discharged with a VA better than 6/9. The patient explained that he had blown his nose each time he presented a reduced VA. Although he was aware of the risk involved with nose blowing, he admitted to have been drinking large quantities of red wine, which made him unaware of this risk.
Six weeks after the presentation (Fig. 1E), the best corrected VA was 6/6 in both eyes. Hertel measurements were 25/23–100. The only complaint was discomfort in the right eye that now appeared bigger than the left and continued to have symptoms of exposure.
Traumatic orbital compartment syndrome is caused by accumulation of blood or air or a fracture reducing the orbital volume (Lima et al. 2009). It is most commonly caused by orbital haemorrhage, but a traumatic communication between the paranasal sinuses and the orbit may result in accumulation of air in the orbit if the patient blows his nose forcefully. This is rarely complicated by an orbital compartment syndrome, but orbital emphysema may result in visual loss caused by central retinal artery occlusion, compressive optic neuropathy or, more commonly, ischaemic optic neuropathy (Zimmer-Galler & Bartley 1994). Such cases present as an ophthalmological emergency requiring immediate action. Urgent repair of the causative blow-out fracture (Hunts et al. 1994) and orbital puncture (Linberg 1982) have been described as first-line therapy.
Several factors possibly contributed to the fact that our patient developed an orbital compartment syndrome and not only emphysema, which is commonly seen after blow-out fractures. These factors include:
- • A history of Graves’ disease.
- • Myopia, which makes the eye occupy a larger part of the obit and leave less space for accumulated air.
- • Male gender making nose blowing more forceful.
- • A large consumption of wine, making the patient forget the advice of refraining from nose blowing.
Our case demonstrates that orbital punctures are efficient in treating an orbital compartment syndrome resulting from emphysema.