Keywords

FormalPara Learning Objectives

  • At present, there is no treatment for traumatic optic neuropathy. However, spontaneous improvement is often seen.

  • Treatment of a tight orbit due to raised intraorbital pressure as a result of fast increase of the intraorbital volume by, for instance, retrobulbar hemorrhage consists of immediate lateral canthotomy and cantholysis.

Introduction

Loss of vision is the most dramatic outcome of disorders of the eye and of orbital trauma and orbital diseases. One of the most common causes of loss of vision is trauma or disease of the eyeball itself, such as perforation of the cornea or globe, inflammation of the globe (endophthalmitis) or massive intraocular hemorrhage, but these conditions are beyond the scope of this book. Brain trauma or diseases may also result in blindness. Here, we will focus on situations that may cause blindness, which are located outside the globe itself and are due to changes of the optic nerve. The optic nerve is sensitive for shock and compression. Blunt trauma of the orbit can cause blindness due to contusion of the optic nerve. A number of intraorbital changes, that give an increase in intraocular tension may cause optic neuropathy, eventually leading to loss of visual functions.

Traumatic Optic Neuropathy

Even rather mild contusion of the orbit can cause optic neuropathy, which is thought to be the result of a transmitted shock to the optic canal resulting in edema of the intracanalicular part of the optic nerve, compression, ischemia and loss of axons. This condition is called indirect traumatic optic neuropathy (TON) and can stand alone or present in combination with orbital fractures. The term direct TON is reserved for situations in which after trauma, orbital bony fragments have injured the optic nerve. The majority of patients with TON are young males [1].

Patients with TON complain of blurred vision, and/or decreased color vision, and/or decreased visual field. On inspection, the pupil on the affected side is wide and not responding to light or a RAPD (Chap. 7) is present. After some weeks to months, the optic nerve head can become pale as a sign of atrophy.

In order to decease optic nerve edema, patients with TON have been treated with high doses of prednisone or with optic canal decompression, but neither appeared to result in a better outcome than no treatment at all (e.g., observation) [2, 3]. Moreover, the Corticosteroid Randomization for Acute Head Trauma (CRASH) trial found an increased rate of death among patients with acute head trauma treated with high-dose corticosteroids compared to placebo-treated patients [1]. Hence, no treatment exists at this time for patients with TON. However, some spontaneous improvement is to be expected in up to 57% [2].

Retrobulbar Hemorrhage

A so-called retrobulbar hemorrhage (RH) in fact is a bleeding that can occur at any place in the orbit and not just posterior to the globe. Because the orbit is surrounded by bony walls at the medial, lateral, superior and inferior side and by the orbital septum in the front, a compartment syndrome with increasing intraorbital pressure develops if the intraorbital volume increases. Typical causes of increasing intraorbital volume are enlargement of the extraocular muscles and fat increase as seen in patients with Graves’ orbitopathy (Chap. 14), subperiosteal empyema and orbital abscess in retroseptal orbital cellulitis (Chap. 17) and hemorrhages due to orbital varices or venous malformations and to orbital trauma. RH after retrobulbar nerve blocks for intraocular surgery have been reported in 55 out of 12,500 patients, e.g., in 0.44% [4]. RH causing blindness has been described after elective surgery, such as, orbital decompression, blepharoplasty and even after fine-needle aspiration [5,6,7,8].

Patients with RH complain about extreme pain and blurred vision. On inspection, there is swelling of the eyelids, increasing exophthalmos, impaired motility, a RAPD that turns into a wide pupil not responding to light and finally a tight orbit with no light perception.

The best option for treatment is a lateral canthotomy and inferior cantholysis of the lateral ligament. The upper and lower lid are cut in a skin fold with sharp scissors in the lateral angle, where the eyelids fuse (Fig. 13.1).

Fig. 13.1
An illustration of the eye exhibits sharp scissors cutting the skin folds in the canthus region at a lateral angle.

Lateral cantholysis

Full size image

One blade of scissors is then placed under the lower arm of the lateral canthal ligament and cut. Immediately, the lower lid gives way and the intraorbital tension decreases followed by a narrowing of the dilated pupil. Local anesthesia is not necessarily used. Infiltration with anesthetic fluid takes time and would increase the pressure even more. In addition, the pain caused by the cut is quickly compensated as the pain caused by the high pressure decreases [9, 10]. This wound usually heals beautifully even without stitches. Cantholysis for RH should be done as soon as possible if a tight orbit is found. RH can occur together with other manifestations of orbital trauma such as orbital fractures. Further clinical and radiological evaluation of the patient, however, should be postponed until a cantholysis has been performed.

Cantholysis is generally advised to do within 24 hours after the onset of the proptosis, but we have seen patients with a complete recovery of visual functions, who had been operated after more than 24 hours. So, it is worth the effort to do a cantholysis in any patient with a tight orbit [11]. The significance of a cantholysis in a tight orbit is comparable to a tracheotomy in obstructed airways. Tracheotomy saves lives; cantholysis saves eyes.

An alternative for a cantholysis is a horizontal incision through the eyelid halfway the lid margin and the eyebrow. The cut should have a length of 1–2 cm and be deep enough to pass through the orbital septum (Chap. 22), which will be apparent from a prolapse of pre-aponeurotic fat through the wound. Steroids or tension lowering eyedrops are of little use. If no or insufficient response is seen after cantholysis or incision of the orbital septum, other causes of optic injury have to be excluded and orbital decompression can be considered.

Conclusion

It must be clear that the clinician should be alert on signs and symptoms of trauma or compression of the optic nerve which often warrants immediate intervention. Depending on the cause of the optic nerve damage, decompression and or steroid therapy can be considered.