Orbital Compartment Syndrome

A rapid rise in pressure within the closed orbital space that compromises perfusion of the optic nerve, retina and extraocular muscles. The orbit is a rigid cone with a relatively fixed volume, and only the anterior septum and eyelids give way, so a small increase in volume produces a large rise in pressure.

• Causes:
  • Haemorrhage (trauma, surgery, retrobulbar or peribulbar block, anticoagulation, coagulopathy).
  • Infection (orbital cellulitis and abscess).
  • Orbital emphysema (sinus fracture with positive pressure from nose blowing, ventilation or air travel).
  • Thyroid eye disease with massive muscle swelling.
  • Aggressive fluid resuscitation, burns, prolonged prone positioning, massive transfusion, sepsis, snake bite, and inflammatory disease.
  • Tumour haemorrhage and rapid expansion, and venous obstruction.
• When intraorbital pressure exceeds ophthalmic artery perfusion pressure, central retinal artery occlusion and optic nerve ischaemia occur within 60 to 120 minutes. Irreversible injury is likely beyond about 2 hours.

• Severe orbital pain, nausea and vomiting, rapid onset or progressive tense proptosis, tight swollen lids, subconjunctival haemorrhage and chemosis, restricted ocular motility, and decreasing vision.
• Relative afferent pupillary defect, dilated or sluggish pupil, intraocular pressure above 30 to 40 mmHg, pulsation of retinal arteries or retinal artery occlusion, disc pallor or swelling, choroidal folds, and a hard orbit that cannot be retropulsed.
• In sedated or intubated patients: new proptosis, tense lids, pupil changes and loss of the red reflex are the only clues.
• Infection: fever, systemic signs and sinus disease.

• Clinical emergency diagnosis based on the triad of proptosis, elevated intraocular pressure and reduced vision or pupil defect. Do not wait for imaging when vision is threatened.
• Measure intraocular pressure with a handheld tonometer; assess acuity, colour vision, pupils, motility, and retinal circulation by ophthalmoscopy.
• CT orbits after decompression (or before it only when stable and delay will not harm): haematoma, abscess, air, tenting of the posterior globe, enlarged muscles, fractures.
• Coagulation screen, full count, group and save, CRP, blood cultures; arterial blood gas and glucose.

• Decompress immediately by lateral canthotomy and cantholysis:
  • Local anaesthesia: 2 percent lidocaine with adrenaline, 3 to 5 mL into the lateral canthus; cleanse with povidone iodine.
  • Clamp the lateral canthus for 1 to 2 minutes, cut a 1 to 2 cm incision through the clamped tissue to the orbital rim (canthotomy).
  • Retract the lower lid, strum the inferior limb of the lateral canthal tendon with the scissor tips and cut it (inferior cantholysis) until the lid is free and mobile; add superior cantholysis if the orbit remains tense and pressure stays high.
  • Success: reduced proptosis, a soft orbit, intraocular pressure below 30 mmHg, improved pupils and vision.
• Medical adjuncts: acetazolamide 500 mg IV, mannitol 20 percent 1 to 2 g/kg IV, topical timolol 0.5 percent twice daily, head elevation 30 degrees, analgesia, antiemetics.
• Treat the cause: drain haematoma or abscess, stop and reverse anticoagulation (vitamin K, prothrombin complex concentrate), antibiotics for infection, high dose steroids for thyroid eye disease (methylprednisolone 500 mg to 1 g IV daily for 3 days), reduce ventilatory pressure for emphysema.
• If no response: surgical orbital decompression (medial wall and floor, or lateral wall) urgently.
• Serial monitoring every 15 to 30 minutes at first, then hourly, for acuity, pupils, pressure and orbital tension.
• Prognosis depends on speed of decompression; late treatment results in permanent visual loss, optic atrophy and ocular motility deficits.