Secondary Logo

Journal Logo

Visual Loss and Ophthalmoplegia After Shoulder Surgery

Bhatti, M. Tariq MD*; Enneking, F. Kayser MD

doi: 10.1213/01.ANE.0000047272.31849.F9

Departments of *Ophthalmology, Neurology, and Neurological Surgery and

†Anesthesiology, Orthopedics, and Rehabilitative Medicine, University of Florida College of Medicine, Gainesville

Supported, in part, by an unrestricted departmental grant from Research to Prevent Blindness, Inc (New York, NY).

October 29, 2002.

Address correspondence and reprint requests to M. Tariq Bhatti, MD, University of Florida College of Medicine, Department of Ophthalmology, PO Box 100284, Gainesville, FL 32610-0284. Address e-mail to

Ophthalmic complications after non-ocular surgery are well documented in the ophthalmic, surgical, and anesthesia literature (1) and have serious medical-legal implications (2). Studies on the incidence of perioperative ocular complications vary widely, ranging from 0%–100% depending on the patient population, method of study, and observational end-points (1). Ophthalmic complications during non-ocular surgery are diverse, the most common and benign being a simple corneal abrasion (3). In comparison, a devastating complication may be complete and irreversible blindness. The incidence of postoperative blindness is 0.1%–1.0%(4). Despite the apparent increasing incidence of perioperative ocular complications in recent years, (5,6) in many cases, the pathomechanism of injury is enigmatic (7). We present a unique case of concomitant unilateral visual loss and external ophthalmoplegia after shoulder surgery under regional and general anesthesia. The case highlights the challenges physicians may encounter when evaluating a patient with perioperative ophthalmic complications and the various potential contributing risk factors for injury.

Back to Top | Article Outline

Case Report

A 64-yr-old man underwent right arthroscopic shoulder surgery for a rotator cuff injury and superior labral anterior posterior lesion. He was a licensed pilot in excellent ocular health. His medical history was significant for cigar smoking, 20-pack/yr history of smoking cigarettes, and mild obesity. He specifically did not report hypertension despite a preoperative blood pressure of 165/104 1 day before surgery. One hour before surgery, his arterial blood pressure measured 173/98 for which he received labetalol and hydralazine. He received 2 mg of midazolam and 100 μg of fentanyl before initiation of a right interscalene-brachial (ISB) plexus nerve block, which resulted in minimal sedation. ISB was performed for postoperative analgesia with a 21-gauge Stimuplex-stimulating needle (B Braun, Gauteng, South Africa). The landmarks for the ISB were the lateral border of the sternocleidomastoid muscle and the interscalene groove. The latter was palpated with some difficulty because of the patient’s redundant neck tissue. Contraction of the biceps and deltoid muscles occurred at 0.6 mA as the needle approached the brachial plexus, and a total of 50 mL of 1.5% mepivacaine with 1:400,000 epinephrine, NaHCO3, and 100 μg of clonidine were injected without complications. Anesthesia of the shoulder girdle developed over the next 15 min. The patient was awake, alert, hemodynamically stable, and without complaints during the 30-min interval between receiving the ISB and entering the operating room.

Despite the initial therapy with antihypertensive and anxiolytic medications, arterial blood pressure on arrival to the operating room was 195/95, and heart rate was 78 bpm. Anesthesia was induced with propofol, and a laryngeal mask airway (Laryngeal Mask Company, Henley-on-Thames, United Kingdom) #5 was placed. Ventilation with the laryngeal mask airway was considered suboptimal, therefore an endotracheal tube was placed using a Macintosh #4 blade after administration of 120 mg of succinylcholine. Anesthesia was maintained throughout the procedure with oxygen, nitrous oxide, and isoflurane (end tidal concentration 1.0–0.14). Arterial blood pressure decreased to 118/78 after the induction of anesthesia.

In preparation for surgery, the patient was placed in a 90 degree upright sitting position (modified beach-chair position). The eyes were covered with clear adhesive (Tegaderm, 3M, St Paul, MN), and a foam rest was placed over the face. An Ace wrap secured the foam rest to the head and backrest, holding the head in a neutral position without pressure on the eyes or orbital rim. Arterial blood pressure monitoring was performed with a noninvasive cuff placed above the ankle on the right leg. At the request of the surgeon, the blood pressure was maintained at 100 mm Hg systolic throughout the 98-min procedure. The surgeon reported no intraoperative complications with minimal blood loss. The patient emerged from anesthesia, and the trachea was extubated without difficulties. The analgesia from the ISB resolved approximately 8 h after placement of the block, consistent with our experience using mepivacaine with clonidine in ISB.

In the postanesthesia care unit, the patient complained of having no vision in the right eye. He did not report eye pain or headache. An immediate ophthalmology consultation was obtained. Visual acuity was light perception only in the right eye and 20/25 in the left eye. Eye movements in the right eye were significantly limited in all directions of gaze. The conjunctiva and orbit were normal. Intraocular pressures were 17 mm Hg in both eyes. A dilated fundus examination was normal in both eyes. Cranial and orbital magnetic resonance imaging (MRI) with contrast was normal. Magnetic resonance angiography (MRA) from the aortic arch to the circle of Willis was also normal. A transthoracic echocardiogram was unremarkable. The patient was admitted to the hospital for observation. The next morning, his vision spontaneously improved to 20/200. Pupils were equal with a right relative afferent pupillary defect. Eye movements remained limited in the right eye, but were improved from the previous night (Fig. 1). The ocular adnexa and retinal examination remained normal. Kinetic perimetry using the Goldmann perimeter confirmed a large central scotoma in the right eye and an asymptomatic superior temporal defect in the left eye (Fig. 2). An IV fluorescein angiogram showed normal transit time and vascular filling. The next day, the vision continued to spontaneously improve and measured 20/80. Six days after surgery, the vision was 20/50, and motility of the right eye was much improved. Two weeks after surgery, vision improved to 20/25 with only mild limitation of abduction and adduction of the right eye (Fig. 3). Six months later, eye movements were normal, and despite 20/20 vision, the patient had a residual right optic neuropathy as demonstrated by a relative afferent pupillary defect, color desaturation, and temporal optic nerve pallor (Fig. 4).

Figure 1

Figure 1

Figure 2

Figure 2

Figure 3

Figure 3

Figure 4

Figure 4

Back to Top | Article Outline


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.

Back to Top | Article Outline


1. Roth S, Gillesberg I. Injuries to the visual system and other sense organs. In: Benumof JL, Saidman LJ, eds. Anesthesia and perioperative complications. 2nd ed. St Louis, MO: Mosby, 1999: 377–408.
2. Gild WM, Posner KL, Caplan RA, Cheney FW. Eye injuries associated with anesthesia: a closed claims analysis. Anesthesiology 1992; 76: 204–8.
3. White E, Crosse MM. The aetiology and prevention of peri-operative corneal abrasions. Anaesthesia 1998; 53: 157–161.
4. Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80: 1018–29.
5. Nuttall GA, Garrity JA, Dearani JA, et al. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg 2001; 93: 1410–6.
6. Cheng MA, Sigurdson W, Tempelhoff R, Lauryssen C. Visual loss after spine surgery: a survey. Neurosurgery 2000; 46: 625–30; Discussion 630–1.
7. Roth S, Thisted RA, Erickson JP, et al. Eye injuries after nonocular surgery: a study of 60,965 anesthetics from 1988 to 1992. Anesthesiology 1996; 85: 1020–7.
8. Shaw PJ, Bates D, Cartlidge NE, et al. Neuro-ophthalmological complications of coronary artery bypass graft surgery. Acta Neurol Scand 1987; 76: 1–7.
9. Shapira OM, Kimmel WA, Lindsey PS, Shahian DM. Anterior ischemic optic neuropathy after open heart operations. Ann Thorac Surg 1996; 61: 660–6.
10. Sweeney PJ, Breuer AC, Selhorst JB, et al. Ischemic optic neuropathy: a complication of cardiopulmonary bypass surgery. Neurology 1982; 32: 560–2.
11. Lee LA. Postoperative visual loss data gathered and analyzed. ASA Newsl 2000; 64: 25–7.
12. Karanjia N, Jacobson DM. Compression of the prechiasmatic optic nerve produces a junctional scotoma. Am J Ophthalmol 1999; 128: 256–8.
13. Myers MA, Hamilton SR, Bogosian AJ, et al. Visual loss as a complication of spine surgery: a review of 37 cases. Spine 1997; 22: 1325–9.
14. Brown RH, Schauble JF, Miller NR. Anemia and hypotension as contributors to perioperative loss of vision. Anesthesiology 1994; 80: 222–6.
15. Ekatodramis G, Macaire P, Borgeat A. Prolonged Horner syndrome due to neck hematoma after continuous interscalene block. Anesthesiology 2001; 95: 801–3.
16. Borgeat A, Ekatodramis G, Kalberer F, Benz C. Acute and nonacute complications associated with interscalene block and shoulder surgery: a prospective study. Anesthesiology 2001; 95: 875–80.
17. Benumof JL. Permanent loss of cervical spinal cord function associated with interscalene block performed under general anesthesia. Anesthesiology 2000; 93: 1541–4.
18. Wilkie GJ. Temporary uniocular blindness and ophthalmoplegia associated with a mandibular block injection: a case report. Aust Dent J 2000; 45: 131–3.
19. van der Bijl P, Meyer D. Ocular complications of dental local anaesthesia. SADJ 1998; 53: 235–8.
20. van der Bijl P, Lamb TL. Prolonged diplopia following a mandibular block injection. Anesth Prog 1996; 43: 116–7.
21. Penarrocha-Diago M, Sanchis-Bielsa JM. Ophthalmologic complications after intraoral local anesthesia with articaine. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 90: 21–4.
22. Cole JK. Ocular complications resulting from intra-arterial injection during inferior alveolar nerve anesthesia. Anesth Prog 1982; 29: 9–10.
23. Hyams SW. Oculomotor palsy following dental anesthesia. Arch Ophthalmol 1976; 94: 1281–2.
24. Mullins RC, Drez D Jr, Cooper J. Hypoglossal nerve palsy after arthroscopy of the shoulder and open operation with the patient in the beach-chair position: a case report. J Bone Joint Surg Am 1992; 74: 137–9.
© 2003 International Anesthesia Research Society