Ischaemic optic neuropathy (ION) refers to ischaemic damage to the optic nerve itself. ION is subclassified into arteritic or non-arteritic ION. Arteritic ION is secondary to inflammation of blood vessels chiefly associated with giant cell/temporal arteritis and responds to steroid therapy. In contrast, non-arteritic ION is secondary to occlusive disease or other noninflammatory disorders. In the general population, non-arteritic ION is the leading cause of sudden visual loss in patients above 50 years of age with an annual incidence in the United States of 82 per 100,000 persons [21]. Non-arteritic ION is the overwhelming cause of POVL. It has been reported after a wide spectrum of surgical procedures, most commonly cardiothoracic surgery [18], instrumented spinal fusion [22] and head and neck surgery [23, 24]. Multiple cases following gynaecological, urological and general surgical procedures have also been reported [25].

ION is further classified by the location of the nerve ischaemia into anterior ischaemic optical neuropathy (AION) and posterior ischaemic optic neuropathy (PION) . This classification is of importance due to the difference in incidences, proposed aetiologies and clinical presentations of each group. Postoperative AION predominately occurs following cardiothoracic surgeries. All reported cases of POVL secondary to ION related to robotic pelvic surgery have been PION injuries [1, 25]. Similarly the vast majority of reported ION following spinal surgery have been posterior injuries.

The exact mechanism of PION and AION is contentious and likely multifactorial. Posterior ischaemia occurs behind the globe and is probably not related to predictable increases in intraocular pressure; it may well be related to disruption of blood supply to the optic nerve from a network of very small perforating pial arteries (Fig. 14.3). In contrast AION proposed to be caused by disruption of blood supply through the posterior ciliary arteries feeding the head of the optic nerve, and this condition may be related to impaired autoregulation of flow (perfusion pressure vs intraocular pressure).

AION and PION have been reported in the setting of massive fluid replacement especially in prone-positioned patients. Excessive fluid administration could result in increased IOP or accumulation of fluid in the optic nerve or both. As the retinal vein exits out of the optic nerve, the oedematous nerve may inhibit venous outflow resulting in an internal ‘compartment syndrome ’ [4]. Patients on the ASA Postoperative Visual Loss Registry received on average 9.7 L of crystalloids intraoperatively, suggesting that fluid replacement may play a role [26].

Key surgical factors linked to perioperative ION are prolonged prone or steep Trendelenburg positioning, prolonged overall surgical duration and massive blood loss. Possible intraoperative haemodynamic factors include decreased systemic blood pressure, anaemia or haemodilution, a high ratio of crystalloid to colloid fluid replacement and venous congestion. Characteristics of the optic nerve and disc may predispose to ION such as reduced flow of cerebrospinal fluid, abnormal auto regulation, anatomic variants in blood supply and small cup-to-disc ratio. Potential systemic risk factors include hypertension, diabetes, atherosclerosis, hyperlipidaemia, smoking history and hypercoagulability [4, 14, 18, 26, 27]. Minimization of these potential risk factors where possible is the basis of ION prevention.

Typically PION results in complete visual loss within 24 h postoperatively compared to AION where two thirds of cases were not evident until more than 24 h following surgery and initial symptoms more likely to be incomplete visual loss. Bilateral visual loss is more common with PION (63%) compared with AION (52%). Nearly all patients with AION have disc oedema, pallor or both on initial assessment (Fig. 14.4). In comparison PION is associated with a normal optic disc on initial fundoscopic evaluation in 92% of patients [4, 14].

No effective treatment for ION has been proven. Only approximately 30% of patients with either AION or PION will have any improvement. The focus of management is therefore on prevention.

Cortical blindness is the result of decreased perfusion to the occipital cortex by tributaries of the posterior cerebral artery. The cause is either hypoperfusion or embolic phenomenon. Cortical blindness is a very rare cause of POVL that is usually associated with cardiac surgery [4, 28].