Bilateral Angle Closure Glaucoma After General Anesthesia

Gayat, Etienne MD, MSc*; Gabison, Eric MD; Devys, Jean-Michel MD*

Anesthesia & Analgesia:
doi: 10.1213/ANE.0b013e3182009ad6
Patient Safety: Case Report

Acute angle closure glaucoma is a rare complication of general anesthesia. However, in case of delayed diagnosis, it may lead to blindness. We present a case of bilateral acute angle closure glaucoma after cervical spine surgery under general anesthesia in a hypermetropic patient. In this case, the most likely trigger was the use of ephedrine, but nefopam administration and the prone surgical position are discussed as additional potential factors.

In Brief

Published ahead of print November 16, 2010

Author Information

From the *Department of Anesthesia and Intensive Care, and Department of Ophthalmology, Fondation Ophtalmologique Adolphe de Rothschild, Paris, France.

The authors declare no conflicts of interest.

Address correspondence and reprint requests to Jean-Michel Devys, MD, Departement d'Anesthésie-Réanimation-Urgences, Fondation Ophtalmologique Adolphe de Rothschild, 25-29 rue Manin, 75019 Paris, France. Address e-mail to

Accepted September 26, 2010

Published ahead of print November 16, 2010

Article Outline

Acute angle closure glaucoma (AACG) is a rare complication of general anesthesia. Eldor and Admoni1 reported only 2 cases among approximately 25,000 non-ophthalmic operations during the 1986 to 1989 period. However, general anesthesia and the perioperative period may predispose patients with a previous tendency to the development of AACG. We describe a case of bilateral AACG after cervical spine surgery under general anesthesia in a hypermetropic patient. The authors sought, and received, written permission from the patient to report the case.

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A 72-year-old woman (ASA physical status II, body weight 72 kg) with arthrosis of the cervical spine with myelopathy was scheduled for a cervical arthrodesis under general anesthesia in the prone position. Her medical history was significant for systemic hypertension, treated with β-blockers and angiotensin II receptor antagonists. Her hypermetropia was corrected with lenses (+6.0 diopters). General anesthesia was induced with IV propofol (2.5 mg · kg−1), sufentanil (0.2 μg · kg−1), and cisatracurium (0.15 mg · kg−1) to facilitate tracheal intubation (size 7.5 oral cuffed tracheal tube). Anesthesia was maintained with a mixture of nitrous oxide and oxygen (50%:50%) supplemented with isoflurane 1 to 1.5 minimum alveolar concentration and sufentanil boluses as needed. Anesthesia lasted almost 3.5 hours with a period of 1.5 hours in the prone position. A headrest was used for support intraoperatively, and her eyes were protected by application of pressure-free eye patches. The patient received 10 mL · kg−1 · h−1 crystalloid infusion during the surgery. An episode of intraoperative hypotension (systolic blood pressure <80 mm Hg), which lasted <10 minutes, was successfully treated with 24 mg IV ephedrine (4 boluses of 6 mg) and a 500-mL infusion of hydroxymethyl starch solution. IV paracetamol (1 g) and IV nefopam (20 mg) were administered 30 minutes before the end of the surgery and every 6 hours thereafter for postoperative pain relief. No additional drug was administered. Subcutaneous morphine sulfate was administered in the surgical ward according to the patient's pain level.

On the second postoperative day, the patient complained of bilateral reduced visual acuity associated with periorbital pain and nausea. Slit lamp examination revealed lid edema, conjunctival hyperemia, and circumcorneal injection. The iris showed fixed, mid-dilated pupils. Gonioscopic examination showed bilateral narrow angles. Intraocular pressures were 36 mm Hg and 26 mm Hg in the left and right eye, respectively (normal intraocular pressure is 12–20 mm Hg). Medical treatment included IV mannitol 20% (250 mL), IV acetazolamide (500 mg), and pilocarpine 2%, 1 drop in each eye every half hour. Unfortunately, intraocular pressure remained as high as 40 mm Hg and 45 mm Hg in the left and right eye, respectively, after 24 hours of medical treatment. Because of the persistent high intraocular pressures, surgical peripheral bilateral iridectomy was performed. One week postoperatively, intraocular pressure was normalized, and the patient recovered normal vision.

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This case illustrates bilateral AACG most likely related to general anesthesia. Bilateral AACG is a rare complication of general anesthesia. In AACG, the iris obstructs the trabecular meshwork in the angle of the eye. Indeed, the development of AACG requires the coexistence of both a predisposed eye (i.e., eye with a narrow anterior chamber angle) and a pupillary block. A pupillary block may appear in different circumstances such as the use of mydriatic agents or a mydriatic situation.

Usual risk factors for postoperative AACG are a genetic predisposition, female gender, shallow anterior chamber depth or hypermetropia, increased lens thickness, small corneal diameter, and increased age.2 Additionally, precipitating factors have been described. These are pharmacologic manipulations of the pupil, producing a partially or fully dilated pupil, and emotional factors. These 2 conditions are frequent in the context of general anesthesia.3,4 Thirty-one cases of AACG related to anesthesia have been published.1,515 The key findings of these cases are summarized in Table 1. The gender distribution is 1 male:3 females, with a mean age of 63 years (58–64 interquartile range), of which there were 23 unilateral and 8 bilateral cases. The main identified precipitating factors for the development of AACG were stress and the use of atropine or scopolamine. Eight cases (26%) were related to ephedrine use. Ephedrine was the sole trigger factor in only 2 cases of unilateral glaucoma and none in the cases of bilateral glaucoma. Nefopam, which is a centrally acting, non-opioid analgesic that inhibits reuptake of serotonin, norepinephrine, and dopamine,16 was not mentioned, although this product is contraindicated in patients with known angle closure glaucoma because of its parasympatholytic effects.

In the present case, 1 possible triggering factor could have been the use of a relatively high dose of ephedrine (a total of 24 mg in 4 serial doses of 6 mg). Ephedrine is a synthetic indirectly acting α-1-adrenergic catecholamine, which stimulates norepinephrine secretion and is contraindicated in cases of known and untreated AACG. Of note, unlike the short vasoactive effect of ephedrine, its mydriatic effect may last for 3 to 6 hours. The use of a powerful analgesic therapy in the postoperative period could have attenuated the usual symptoms of AACG, thus explaining the delay between surgery and the diagnosis of AACG. Indeed, different drugs can cause AACG, including adrenergic drugs administered locally (phenylephrine drops, nasal ephedrine, or nebulized salbutamol) or systemically; drugs with anticholinergic effects and atropine drops; tri- and tetracyclic antidepressants; and cholinergic drugs. The use of periocular botulinum toxin may result in diffusion back to the ciliary ganglion, thus inhibiting the pupillary sphincter and causing AACG.17

In the present case, surgery required prone positioning. The prone position increases the intraocular pressure.18 Indeed, Hyams et al.19 showed that prone position in awake patients with a known narrow angle yielded an intraocular pressure increase of at least 8 mm Hg, significantly higher than in patients with normal angle. Moreover, several studies reported that intraocular pressure may reach 40 mm Hg during prone position under general anesthesia.18,20,21 Such high intraocular pressure during prone position, irrespective of the presence of accompanying hypotension or anemia, may enhance ischemic optic neuropathy, which is a much more frequent cause of postoperative vision loss than AACG, but in contrast with AACG, its prognosis is often poor.22,23 In the present case, we cannot exclude that the prone position may have contributed to the occurrence or severity of the AACG. Indeed, closure may occur when the peripheral iris moves into direct contact with the corneal surface, mechanically obstructing outflow of aqueous humor. This can occur with agents that cause mydriasis, but, in a patient at risk because of baseline narrow angles, one may also argue that the effect of gravity while in the prone position facilitated anterior dislocation of the lens/iris apparatus, precipitating the angle closure.

In conclusion, AACG is an exceptionally rare cause of postoperative vision loss. Physicians should be aware of its risk factors such as hypermetropia, particularly when mydriatic drugs such as atropine or ephedrine are administered. AACG prognosis is better than anterior ischemic optic neuropathy if early diagnosis and medical or surgical treatment are rapidly initiated.

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Name: Etienne Gayat, MD, MSc

Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.

Attestation: This author approved the final manuscript.

Name: Eric Gabison, MD

Contribution: This author helped analyze the data and write the manuscript.

Attestation: This author approved the final manuscript.

Name: Jean-Michel Devys, MD

Contribution: This author helped design the study, conduct the study, analyze the data, and write the manuscript.

Attestation: This author approved the final manuscript.

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