Abstract

To the Editor: I (REW) recently performed cataract surgery on an 84-year-old woman who experienced transient contralateral visual loss after a retrobulbar block, presumably from ipsilateral optic nerve sheath penetration. Preoperatively, visual acuity was best-corrected to 20/60 OD, 20/30 OS, entirely attributable to cataract. After intravenous sedation, 3.5 mL of 2% lidocaine was injected into the right retrobulbar space. Fifteen minutes later, before commencing the surgery, the patient stated that she could not see. This was interpreted as visual loss on the injected side, and the patient was reassured. On completion of the case 25 minutes later (40 min after the retrobulbar injection), it became apparent that the patient could not see in either eye. Visual acuity was hand movements in the operated eye and no light perception in the unoperated eye. Motility was very limited in the operated eye and was normal except for a marked deficit of adduction in the unoperated eye. The pupil in the operated eye measured 6 mm in dim light and was minimally reactive to direct light; the pupil in the unoperated eye measured 7 mm and was unreactive to direct light. Indirect ophthalmoscopy of both eyes was normal. No intervention or treatment occurred. Over the next two hours, the visual acuity in the unoperated OS gradually recovered to its 20/30 baseline and the visual acuity in the operated OD ultimately improved to 20/25. Contralateral transient visual loss after retrobulbar anesthetic injection is a rare but well-recognized complication (1–6) (Table 1). Antoszyk and Buckley (3) reported the largest case series: three patients. In all three, there was evidence of contralateral visual loss and contralateral third nerve palsy, similar to the present case. They theorized that the anesthetic was injected into the subdural space of the optic nerve sheath and tracked along the ipsilateral optic nerve sheath to the orbital apex. As the anesthetic tracked posteriorly within the subdural space to the area of the chiasm, it interfered with conduction within the contralateral optic nerve and third cranial nerve.TABLE 1: Contralateral transient visual loss after retrobulbar anesthetic injectionBrod (4) reported a case of ipsilateral central retinal artery occlusion and contralateral transient visual loss after a retrobulbar anesthetic injection in which computed tomography performed 90 minutes after the injection demonstrated an air bubble within the ipsilateral optic nerve sheath, consistent with intra-nerve sheath injection. The proposed mechanism of intra-optic nerve sheath injection and subsequent tracking of anesthetic into the intracranial subdural space is consistent with that observed in contrast orbitography (7–10), a technique used in the pre-modern imaging era to delineate orbital anatomy and tumors. Local anesthetic and contrast material are injected into the retrobulbar space and plain film x-rays are taken. Reed (7) reported a patient with temporary vertical nystagmus and contralateral sixth cranial nerve palsy, and x-rays confirmed the presence of radiopaque material within the optic nerve sheath and the intracranial subdural space. Kaufer and Augustin (8) reported the presence of radiopaque material along the optic nerve and within the subdural space of the midbrain in a patient who remained asymptomatic during a three-hour observation period. Lombardi (9) reported contrast material in the intracranial subdural space in 3 (2%) of 150 orbitographies. All three patients experienced pain, nausea, and vomiting but no focal neurologic deficits. Although a 2% incidence of subdural penetration with retrobulbar injections in contrast orbitography may seem high relative to the number reported for retrobulbar anesthetic injections, orbitography allows visualization of the injected material; with retrobulbar anesthetic injections, nerve sheath injections and subdural penetrations may be asymptomatic and go unrecognized. Cardiovascular instability and apnea after retrobulbar blocks have been attributed to “brain stem anesthesia” (11–13). In these cases, the anesthetic is thought to enter the cerebrospinal fluid through the subarachnoid space of the optic nerve sheath. Why some injections enter the subdural and others the subarachnoid space is unknown. Perhaps the depth of needle penetration, the force and volume of injection, or individual anatomic variations are explanations. We know of no reports of permanent contralateral visual loss or systemic neurologic sequelae after intra-optic nerve sheath injections of anesthetic agents. With the growing popularity of topical ocular anesthesia, complications related to retrobulbar injections will likely decrease. However, retrobulbar alcohol injections for blind, painful eyes are still used. Although we are not aware of any reports of intra-optic nerve sheath injection of alcohol, the effect on the contralateral nerve and/or the central nervous system could be devastating. Ronald E. Warwar, MD Eric K. Romriell, DO Eric A. Pennock, MD

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