Postoperative visual loss after non-ocular surgery can result from an insult to the retina, anterior visual pathway (optic nerve), or posterior visual pathway (occipital cortex). A complete neuro-ophthalmic examination with formal visual field testing will aid in determining the location of injury. Ancillary testing such as IV fluorescein angiography, computed tomography, and MRI may be required to evaluate and confirm the suspected site of injury. Once visual loss has occurred, curative treatment is often not possible; therefore, the major goal of treatment is the prevention of complications by promptly recognizing, avoiding, and correcting preoperative and intraoperative risk factors. In some cases, predisposing risk factors may not be amenable to modification or there may be multiple risk factors involved. Furthermore, controlling one risk factor may potentiate the affect of another, i.e., avoiding intraoperative hypotension to better facilitate intraoperative visualization may result in larger surgical blood loss.
Ophthalmic complications, in particular postoperative visual loss, have been reported to occur after a wide variety of non-ocular surgical procedures including spine surgery, general surgical procedures, cardiac surgery, neurosurgical procedures, head and neck surgery, liposuction, paranasal sinus surgery, dental procedures, epidural puncture, obstetric surgery, and transurethral prostatectomy (1). Based on several retrospective studies, the incidence of postoperative visual loss has ranged from 0.0009%–16.3%(5,8–10). A national registry was established in an attempt to determine and assess the risks of postoperative visual loss from non-ocular surgery. Twenty-three cases have been collected, with prone position spine surgery (57%) and cardiopulmonary bypass (22%) the most common surgeries associated with postoperative visual loss (11).
Our patient presented with concomitant visual loss and ophthalmoplegia, suggesting a carotid artery dissection, lesion at the orbital apex, or pituitary apoplexy. None of these possibilities were supported by the MRI or MRA. Despite the limitation of eye movements in all directions of gaze, there was no associated ptosis or pupil involvement, arguing against a neuropathic mechanism as the cause of the ocular motility disturbance but possibly for an orbital or extraocular muscle ischemic process. In addition to the right optic neuropathy, our patient also had an asymptomatic superior temporal defect in the fellow eye detected by formal visual field testing (Fig. 2). This pattern of visual field loss is often seen from a lesion at the anterior chiasm, disrupting the ipsilateral optic nerve fibers and contralateral decussating axons (Wilbrand knee) (12). Therefore, it seems that multiple anatomical sites may have been involved in explaining our patient’s eye findings, suggesting a multifocal process that can occur with the scattering of emboli and multiple vascular occlusions.
Preoperative (patient) systemic factors may have played a role in our patient’s clinical findings. He was a tobacco user and before surgery, was noted to be hypertensive. Peripheral vascular disease, diabetes mellitus, hypertension, and tobacco smoking are characteristics more frequently found in patients with postoperative visual loss (4–6,13,14). Patients with these systemic conditions may be predisposed to ischemia because of increased arterial resistance secondary to atherosclerotic disease.
There is an association between intraoperative hypotension and postoperative visual loss (1,14). Other risk factors, such as anemia or cardiopulmonary bypass, seem to be required in combination with hypotension for the development of ischemic optic neuropathy (4,14). Our patient had a preoperative hemoglobin of 15.3 g/dL with minimal intraoperative blood loss. Although there were no hypotensive episodes recorded during surgery, the sphygmomanometer cuff was placed on the distal lower extremity, a dependent limb in the beach-chair position, which may have overlooked an extreme hypotensive situation. In addition, at the request of the surgeon, the systolic blood pressure was maintained at 100 mm Hg. The concern over deliberate hypotension, in particular during spinal surgery, precipitating postoperative visual loss has been raised, (6,13) yet the optimal blood pressure range has not been determined (4).
It is difficult to establish the contribution of the ISB, patient positioning, and the surgical procedure on the development of our patient’s ophthalmic findings. Although ISB is a relatively safe procedure, neurological complications reported during ISB include Horner syndrome, brachial plexus injury, phrenic nerve injury, recurrent laryngeal nerve trauma, central neuraxis (epidural, subdural, subarachnoid, and parenchymal) penetration, and intravascular injection (15–17). Based on case reports from other regional anesthesia procedures, we can only theorize on the possible mechanisms of injury to our patient from the ISB. Several authors have described visual loss, external ophthalmoplegia, or both after inadvertent intravascular (arterial or venous), lymphatic, neural, or direct orbital anesthetic injection during dental procedures (18–23). Intravascular or neuraxial injection does not seem plausible in our case because contralateral motor deficits, hypotension, and seizure activity were not present.
Despite an unusual case of transient hypoglossal nerve palsy attributed to poor head positioning, the beach-chair position is safe for shoulder surgery (24). However, we do not know the effect that sitting our patient up to 90 degrees (modified beach-chair position) had on the ophthalmic manifestations. Prone position surgery or inadvertent direct compression on the eye may lead to extreme increase of the intraocular pressure and subsequent optic nerve ischemia or central retinal artery occlusion (4). A protective foam rest was placed over the patient’s face before surgery, which could have displaced during surgery resulting in direct ocular pressure. This is an unlikely scenario in our case because there was no clinical evidence of external pressure on the orbit.
Stroke because of cardiogenic emboli is a well-recognized adverse outcome after cardiac surgery (1). Emboli can arise from a variety of sources including cardiac disease, atherosclerotic disease, thromboembolic disease, air, fat, or platelet aggregation.
Our patient underwent a closed shoulder procedure with little bone manipulation, making the likelihood of a fat embolism small. Theoretically, an embolus could have dislodged at some point during the ISB or shoulder procedure, but no clear embolus was seen clinically during the retinal examination after surgery. Vascular or local spread of the epinephrine used during the ISB could have compromised blood flow to the optic nerve and extraocular muscles; however, an overall small concentration was injected, and there were no hemodynamic signs of a catecholamine surge during the ISB or shoulder procedure (1,9).
This is the first reported case of an ophthalmic complication after shoulder surgery. Our patient presented with the curious combination of visual loss and unilateral external ophthalmoplegia. The clinical findings improved spontaneously over an extended period of time. The exact etiopathogenesis of the clinical findings remains unexplained. Ophthalmic complications after non-ocular surgery are often a diagnostic and therapeutic challenge for physicians, and it seems that many factors can contribute to postoperative visual loss.
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