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Patient has visual loss 1 day after cataract surgery
On fundus exam, the right eye showed diffuse nerve fiber hemorrhages, intraretinal and subretinal hemorrhages, retinal vasculature segmentation and diffuse superficial retinal whitening.
 Jeffrey Chang |  Vivek Chaturvedi | ||
A 69-year-old woman was referred to the New England Eye Center for decreased vision on postoperative day 1 after uncomplicated cataract extraction in the right eye.
The patient’s ocular history was unremarkable other than uncomplicated cataract surgery in the left eye 2 months earlier. Medical history was significant for hyperlipidemia, gastroesophageal reflux disease, osteoporosis, and breast cancer status post lumpectomy and radiation therapy. Medications included atorvastatin, omeprazole, risedronate and exemestane. Allergies included penicillin, sulfas, iodine and intravenous dye. Family history, social history and review of systems were unremarkable.
Examination
The patient’s best corrected preoperative vision in the right eye was 20/200. After the patch was removed on postoperative day 1, she was counting fingers at 2 feet in the postoperative eye. Vision measured 20/20 in the left eye. The right pupil was pharmacologically dilated with a new right relative afferent pupillary defect noted. Extraocular movements were full bilaterally, and IOPs were within normal limits.
The eyelids and orbits demonstrated no ptosis or proptosis. The conjunctiva of the right eye contained mild scant subconjunctival hemorrhage. Slit lamp examination of the right eye showed minimal corneal stromal edema near the main incision with 1+ anterior chamber cell. The lens was centered within the capsular bag. Examination of the left eye revealed a well-centered IOL.
Fundus examination of the right eye demonstrated diffuse flame-shaped nerve fiber hemorrhages, diffuse intraretinal and subretinal hemorrhages concentrated in the macular region, segmentation of the retinal vasculature and diffuse superficial retinal whitening (Figure 1a). Fundus exam of the left eye was normal (Figure 1b). Fluorescein angiogram showed a marked delay in the central retinal artery filling, with incomplete filling even in the last frames of the angiogram (Figure 2). Optical coherence tomography demonstrated subretinal fluid and nerve fiber layer swelling of the right eye.
 Fundus exam of the right eye (1a) and left eye (1b) demonstrates diffuse nerve fiber layer, intraretinal and subretinal hemorrhages, segmentation of the retinal vasculature and diffuse superficial retinal whitening. Images: Yoon SJ, Wiegand TW  Fluorescein angiogram shows a marked delay in the central retinal artery filling at 0:39 (2a) with incomplete filling in the last frames of the angiogram at 5:16 (2b). |
What is your diagnosis?
Vision loss after surgery
The differential diagnosis of visual loss on the first postoperative day after cataract surgery is sizeable, but may include diffuse corneal edema, toxic anterior segment syndrome, lens dislocation, incorrect lens placement, retinal detachment, central retinal artery occlusion, central retinal vein occlusion, ischemic optic neuropathy, giant cell arteritis, hypotony or a traumatic ocular injury.
 MRI of the brain and orbits demonstrated significant enhancement of the right optic nerve and nerve sheath on axial (3a) and coronal (3b) views. |
The anterior segment in this case was unrevealing; however, the fundus examination demonstrated a combined central retinal artery and central retinal vein occlusion pattern. MRI of the brain and orbits was performed per request of the referring physician and demonstrated significant enhancement of the right optic nerve and nerve sheath (Figure 3). Additional labs were performed and ruled out a coagulation abnormality.
Diagnosis
The operative report from the surgeon was reviewed, and it was noted to be an uncomplicated procedure. A retrobulbar block was performed by the ophthalmologist in the preoperative area. The presumed diagnosis was a traumatic optic neuropathy related to the retrobulbar injection of anesthetic, causing a combined central retinal artery and vein occlusion.
Discussion
Retrobulbar anesthesia was first described by Knapp in 1884 and regained popularity in 1936 by Atkinson. In a retrobulbar block, the needle tip is introduced into the muscle cone and is aimed at blocking the ciliary ganglion, ciliary nerves and oculomotor nerves. The superior oblique may retain activity because of its extraconal course. It is a low-volume block of approximately 4 mL of anesthetic and has a relatively rapid onset within 3 minutes to 5 minutes.
Variations of performing the block exist; however, a widely accepted method is to start along the inferior orbital rim between the lateral limbus and lateral canthus with the needle tip pointing perpendicular to the orbital floor. Once a pop is felt through the septum, the needle is slightly directed upward and medial to approach the midsagittal plane of the globe. The needle is gently aspirated to ensure the tip is not in a vessel, and then the anesthetic is injected slowly. After withdrawing the needle, firm pressure is applied to the globe, and a Honan balloon can be used to spread the anesthetic and soften the eye.
Retrobulbar anesthesia is a reliable block producing excellent anesthesia and akinesia and has been the standard for intraocular surgery for many years. Complications, although rare, can be devastating and theoretically higher than other types of regional anesthesia for cataract surgery.
Retrobulbar hemorrhage is the most common ocular complication with retrobulbar anesthesia, occurring at a rate of 0.1% to 1.7%. Predisposing factors include systemic anticoagulants, hemostatic disorders, vascular disease, diabetes and carotid insufficiency. A significant retrobulbar hemorrhage may require an urgent bedside canthotomy and cantholysis to relieve elevated ocular and orbital pressure. However, most retrobulbar hemorrhages are of little clinical consequence, and definitive surgery may be postponed to a later date without sequelae.
Globe perforation can be a devastating complication of retrobulbar anesthesia. The reported risk of perforation is 0.075%, and risk factors include myopia, posterior or inferior staphyloma, enophthalmos, prior scleral buckling or repeated injections. Pathologic myopia with an axial length greater than 26 mm poses a 30-fold increased risk of globe perforation. Signs and symptoms may not be recognized immediately and have been reported to be unsuspected in 50% of cases during block administration. Vitreous hemorrhage, retinal detachment and proliferative vitreoretinopathy may occur after perforation, and visual outcomes are related to the presence or absence of a retinal detachment.
Traumatic optic neuropathies related to retrobulbar anesthesia may occur by direct injury to the optic nerve, by hemorrhage in the optic nerve sheath or by compressive ischemia. The Atkinson method of performing the injection, initially described by Atkinson in 1936, directed the patient to look upward and inward during the procedure. However, this has fallen out of favor because it causes the downward and outward displacement of the optic nerve, potentially into the pathway of the needle. The accepted position for orbital blocks is to have the patient look in primary gaze to keep the nerve out of the pathway of the needle tip. Central retinal artery occlusion may result from direct trauma to the central retinal artery or compression from an optic nerve sheath or retrobulbar hemorrhage. A combined central retinal artery occlusion and central retinal vein occlusion may occur if injection occurs into the optic nerve sheath, causing an increased pressure in the neural sheath that first compromises venous outflow and then arterial inflow.
Central nervous system toxicity may occur with retrobulbar anesthesia, reported at a rate of 0.09% to 1.5% of blocks. Arterial injection with retrograde flow from the ophthalmic artery to the internal carotid to midbrain may cause seizure activity within seconds and precipitate cardiopulmonary arrest. Injection into the optic nerve sheath with flow to the brainstem may cause a retrobulbar apnea syndrome, with an average onset within 8 minutes to 10 minutes, with drowsiness, agitation and confusion followed by respiratory depression. Usually supportive treatment with resuscitation allows rapid recovery without sequelae.
Other complications related to retrobulbar injections include ptosis and extraocular muscle paresis. Ptosis may be transient or persistent, related to postoperative edema, inflammation or damage to the levator aponeurosis. Direct trauma or myotoxicity of the anesthetic may occur to an extraocular muscle, most commonly the inferior rectus, but usually resolves spontaneously.
In our patient, a combined central retinal artery occlusion and central retinal vein occlusion presumably occurred due to retrobulbar injection into the optic nerve sheath. This caused an increased pressure in the neural sheath that first compromised venous outflow and then arterial inflow. This is a rare but devastating complication of retrobulbar anesthesia. Currently there are many highly effective approaches to anesthesia management for cataract surgery available to the surgeon. Options for regional anesthesia include retrobulbar, peribulbar, sub-Tenon’s and topical blocks. It is the responsibility of the surgeon and anesthesiologist to disclose all potential complications during the consent and to decide which method is most appropriate for each patient.
For more information:
- Steven J. Yoon, MD, and Torsten W. Wiegand, MD, PhD, can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.
- Edited by Jeffrey Chang, MD, and Vivek Chaturvedi, MD. Drs. Chang and Chaturvedi can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com. Drs. Chang and Chaturvedi have no direct financial interest in the products mentioned in this article, nor are they paid consultants for any companies mentioned.
References:
- Aldrete JA, Romo-Salas F. et al. Reverse arterial blood flow as a pathway for central nervous system toxic responses following injection of local anesthetics. Anesth Analg. 1978;57:428-433.
- Atkinson WS. Local anesthesia in ophthalmology. Trans Am Ophthalmol Soc. 1934:32;399-451.
- Duker JS, Belmont JB, et al. Inadvertent globe perforation during retrobulbar and peribulbar anesthesia. Ophthalmology. 1991;98:519-526.
- Hamilton RC. A discourse on the complications of retrobulbar and peribulbar blockade. Can J Ophthalmol. 2000;35:363-372.
- Hamilton RC, Gimbel HV, Strunin L. Regional anesthesia for 12,000 cataract extraction and intraocular lens implantation procedures. Can J Anaesth. 1988:35:615-623.
- Nicoll JM, Acharya PA, et al. Central nervous system complications after 6000 retrobulbar blocks. Anesth Analg. 1987;66:1298-1302.
- Ramsay RC, Knobloch W. Ocular perforation following retrobulbar anesthesia for retinal detachment surgery. Am J Ophthalmol. 1978;86:61-64.