Mechanism and Emergency Management of Blast Eye/Orbital Injuries

Sabri T Shuker


Expert Rev Ophthalmol. 2008;3(2):229-246. 

In This Article

Tension Pneumo-orbitus (Orbital Emphysema)

It is common for blast injury casualties to sustain pulmonary injuries with spontaneous pneumomediastinum, which presents with various manifestations. However, it is extremely rare for head and neck signs to be the sole presenting feature due to civilian chest trauma with facial subcutaneous emphysema. Air from the mediastinum can easily ascend along fascial planes and into the subcutaneous spaces of the head and neck.[45,46]

Orbital emphysema due to orbital trauma is a well-known occurrence. Visual loss due to orbital emphysema, however, is an uncommon phenomenon.

An overpressurized blast wave front impact leads to implosion of the paranasal air cells; these can allow the passage of air into the orbit space and orbital soft tissues, particularly of the medial orbital wall. The orbital emphysema does not last as it deflates through the fractured orbital walls.

The compartmentalized orbital space holds the compressed air and occasionally creates a one-way valve effect that entraps this air within, as in civilian conditions, or the pressurized air dissected from oropharynx or upper part of pulmonary system. This situation can precipitate proptosis of the globe, elevation of the intraorbital and intraocular pressure, and vascular insufficiency of the optic nerve and retina. The orbit, therefore, follows pressure–volume dynamics, with a pathophysiology, in which increased tissue pressures in an enclosed space are associated with decreased blood perfusion. When the pressure within the orbit exceeds central retinal artery pressure, ischemia results from insufficient blood supply. It is more serious in retrobulbar hematoma, as the pressure effect of fluid is higher than more diffusible air pressure in tissue anatomical spaces, hematoma can cause a substantial rise in pressure if not treated and may result in blindness if not decompressed by drainage.

Irreversible optic nerve pathology may occur within 90–120 min of ischemia. Front-line surgeons should be familiar with retro-bulbar emergent decompression by lateral canthotomy and inferior cantholysis.[110] Medial and lateral canthal tendons limit the forward movement of the globe. Canthotomy may compensate for small increases in orbital volume by forward movement of the globe.[47–49]

Facial emphysema and orbital emphysema due to blast is mostly due to the rupture of the upper part of trachea, or marginal pulmonary alveoli. The air ascends along the mediastinum toward the subcutaneous space of the neck, causing cervico-facial subcutaneous emphysema in 70–90% of cases.[50–53]

Shuker et al. (1989) reported pneumomediastinum and cervical emphysema subsequent to mandibular injury associated with a flare pistol shot blast injury.[54]

Suspected globe rupture is a contraindication to lateral orbital canthotomy (Liu [2006][108]). Signs of globe rupture include hyphema; a peaked, teardrop-shaped, or otherwise irregularly shaped pupil; exposed uveal tissue, which appears reddish-brown; and extra ocular movement; a restriction that is greatest in the direction of the rupture. Subtle signs of globe rupture include subconjunctival hemorrhage, enophthalmos or a conjunctival laceration.


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