Anesth Analg 2002;94:1034-1035
© 2002 International Anesthesia Research Society
GENERAL ARTICLES
Acute Postoperative Glaucoma After Nonocular Surgery Remains a Diagnostic Challenge
Claude Lentschener, MD*,
Abdelmalek Ghimouz, MD*,
Philippe Bonnichon, MD
,
Christine Parc, MD
, and
Yves Ozier, MD*
Departments of *Anesthesia and Critical Care, Surgery, and Ophthalmology, Hôpital Cochin, Paris, France
Address correspondence and reprint requests to Claude Lentschener, MD, Department of Anesthesia and Critical Care, Hôpital Cochin, 27 Rue du Faubourg Saint Jacques, 75679 Paris Cedex 14, France. Address e-mail to claude.lentschener{at}cch.ap-hop-paris.fr
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Abstract
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IMPLICATIONS: Anesthesia may acutely reveal angle-closure glaucoma. This complication is an ophthalmologic emergency. However, symptoms of acute glaucoma may be overlooked or misinterpreted in a sedated or comatose patient, and this may result in delayed treatment. Immediate diagnosis and appropriate treatment should be done to prevent visual loss.
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Introduction
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Anesthesia may acutely reveal angle-closure glaucoma (1). Acute angle-closure glaucoma can lead to optic nerve and cornea damage (1–4). Immediate diagnosis and appropriate treatment should be done to prevent visual loss (4). Symptoms of acute postoperative glaucoma may be overlooked or misinterpreted in a sedated or comatose patient (1).
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Case Report
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A 66-yr-old woman underwent thyroidectomy. Preoperative assessment was unremarkable. The patient used corrective lenses as a consequence of hyperopia. Ophthalmological assessment had been performed 1 yr before surgery.
General anesthesia was conducted with sufentanil- and propofol-based total IV anesthesia. Cisatracurium was given to facilitate tracheal intubation. Mechanical ventilation was used. An intraoperative decrease in arterial blood pressure was treated with 15 mg of IV ephedrine. Propacetamol 2.0 mg and ketoprophen 100 mg were administered IV for analgesia. Extubation of the trachea was possible 10 min after the last skin suture. No additional drugs were given. The patient was discharged from the postanesthesia care unit 2 h after the end of surgery.
Four hours after returning to the ward, the patient complained of a right eye visual loss together with a bilateral frontal headache. Both the anesthesiologist and the surgeon on call described a right eye slightly red and no additional clinical abnormalities. Particularly, cranial nerves appeared normal, and extraocular movements were full. Practitioners on call mainly hypothesized that an anesthesia-related corneal injury probably accounted for this eye discomfort. Morphine 10 mg subcutaneously was given. The next morning (16th postoperative hour), ocular redness and pain had worsened. In addition, the patient had become very anxious and agitated. At the 24th postoperative hour, the ophthalmologist did not notice any sign of eye trauma. On the right eye examination, visual acuity was blurred, and the lids were swollen. Biomicroscopic examination showed conjunctiva hyperemia and circumcorneal injection. The cornea was edematous, the anterior chamber was shallow, and the pupil was middilated. The right eye intraocular pressure was 60 mm Hg. The left eye examination was normal except for a shallow anterior chamber. The left eye intraocular pressure was 18 mm Hg. A right eye acute angle-closure glaucoma was diagnosed and treated with IV acetazolamide and timolol, apraclonidine, pilocarpine, and dexamethasone eyedrops. After a 15-h treatment, the right eye intraocular pressure had decreased to 18 mm Hg, but the blurred vision was still present. Oral acetazolamide and eyedrops of pilocarpine and betaxolol were administered for the next 24 h. Two days after this acute attack, the right eye intraocular pressure remained normal, and visual acuity had completely recovered. A right eye laser iridotomy was then performed, and a prophylactic left eye laser iridotomy was performed 1 wk later. The patient denied ever having experienced any previous ocular symptoms suggesting subacute glaucoma.
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Discussion
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Aqueous humor is produced in the ciliary body, in the posterior chamber of the eye. It circulates around the lens through the pupil and flows out of the anterior chamber, primarily through the trabecular meshwork (4,5). In primary angle-closure glaucoma, the posterior surface of the dilated iris is apposed to the anterior surface of the lens, leading to a pupillary block. It impedes aqueous humor flow from the posterior to the anterior chamber through the pupil (4,5). If the pupillary block becomes absolute, the pressure in the posterior chamber increases, pushes the peripheral iris further to cover the trabecular meshwork, and results in closure of the angle, with an ensuing increase in intraocular pressure (4,5). Middilated pupils are causative factors of this sudden condition in susceptible people (4,5). As a consequence of a shallow anterior chamber, the peripheral iris and the anterior lens surface bow forward and obstruct aqueous humor egress through the trabecular meshwork (4,5).
Hyperopia is often associated with a shallow anterior chamber when the lens becomes thicker and consequently with angle-closure glaucoma (5). In case of acute glaucoma, clinical examination shows swollen lids, conjunctiva hyperemia, and circumcorneal injection (4,5). Corneal edema results in blurred vision and intense pain (4,5). The pupil is middilated and sometimes vertically oval as a consequence of iris ischemia (4,5). Intraocular pressure is very high (4,5).
The incidence of acute angle-closure glaucoma increases to its maximum between the ages of 55 and 65 years (4). Women are affected three times as often as men (4). Most attacks occur in the evening (4). Precipitating events reported in predisposed individuals include emotional upsets, darkness, and pharmacological dilation of the pupil (4–7). Topical parasympatholytic substances such as cyclopentolate or sympathomimetics such as phenylephrine can cause acute angle-closure glaucoma through pupillary dilation (4,5). However, systemic drugs caused 25% of the angle-closure acute attacks (6). Indeed, many routinely used drugs have sympathomimetic or parasympatholytic properties. These drugs include antiemetics, inhibitors of histamine, psychoactive drugs, therapeutic drugs for Parkinson’s disease, laxatives, antidiarrheics, and antispasmodics (6). Treatment of acute glaucoma begins with topical drugs, including mainly 1) ß-adrenergic antagonists (the exact mechanism by which they lower intraocular pressure is not known); 2) 
-adrenergic agonists, mainly apraclonidine and brimonidine, selective 2-adrenergic agonists that decrease the production of aqueous humor by constricting the vessels supplying the ciliary body; 3) carbonic anhydrase inhibitors, which decrease bicarbonate production within the ciliary body, and therefore the flow of water after sodium to form the aqueous humor into the posterior chamber; 4) cholinergic agonists, which produce the contraction of the longitudinal muscle of the ciliary body, open the trabecular meshwork, and thereby increase aqueous outflow from the eye; and 5) corticosteroids, which decrease edema associated with acute glaucoma (2).
Differential diagnosis of a painful postoperative eye must be made rapidly (8). Corneal abrasion is the most frequent intraoperative complication of general anesthesia after nonocular surgery (8). It results mainly from exposure of an unprotected eye to the atmosphere or spillage of antiseptic solutions running into the eyes during skin preparation (8). A red eye with sensation of a foreign body is highly suggestive of corneal abrasion (8). Orbital compression may occlude retinal artery blood flow and may result in postoperative blindness (8). Supraorbital nerve compression may cause local numbness (8). Acute angle-closure glaucoma after nonocular surgery is a rare complication of anesthesia (1,8–12). This clinical event is not reported in two review articles sampling 1112 claims in ophthalmology (11,12). A MEDLINE survey disclosed 10 anecdotal clinical reports published in national anesthesiology journals, and only one review article was specifically dedicated to this event in an international journal (1,9,10). This review article reports nine cases of acute angle-closure glaucoma after nonocular surgery. They were identified among 913 clinical records of glaucoma treated from 1955 to 1980 (1). Postoperative acute angle-closure glaucoma after nonocular surgery was reported after abdominal, orthopedic, facial, and endoscopic surgery and in patients with or without a previous history of eye disease (1,8–10). Age older than 50 years, a red, painful eye, a visual impairment, and a headache were common features of these reports (1,8–10). The acute attack was exceptionally bilateral (1). It is important to note that the time interval between the first symptoms and the correct diagnosis ranged from several hours to five days (1,8–10). Indeed, general anesthesia and postoperative events often mask the first symptoms (1,8). Most drugs used for general anesthesia decrease intraocular pressure and are not likely to be associated with glaucoma worsening (13). However, several factors are likely to induce postoperative acute angle-closure glaucoma in predisposed individuals. Parasympatholytic or sympathomimetic drugs, such as atropine, scopolamine, ephedrine, or epinephrine, routinely administered during anesthesia, dilate the pupil and may acutely reveal angle-closure glaucoma in susceptible individuals (13). Moreover, the perioperative period carries the risk of psychological stress.
In this case report, intraoperative ephedrine administration combined with surgery, a stressful situation, in a 66-year-old woman may have precipitated this acute event.
In conclusion, even postoperatively, any patient who has a red eye and a subjective vision loss should be referred to an ophthalmologist the same day.
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References
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Fazio DT, Bateman JB, Christensen RE. Acute angle-closure glaucoma associated with surgical anesthesia. Arch Ophthalmol 1985; 103: 360–2.[Abstract]
-
Alward WLM. Drug therapy: medical management of glaucoma. N Engl J Med 1998; 339: 1298–307.[Free Full Text]
-
Cashwell LF. Laser iridotomy for management of angle-closure glaucoma. South Med J 1985; 78: 288–91.[Medline]
-
Mapstone R. The syndrome of closed-angle glaucoma. Br J Ophthalmol 1976; 60: 120–3.[Abstract/Free Full Text]
-
Lowe RF. Aetiology of the anatomical basis for primary angle-closure glaucoma: biometrical comparisons between normal eyes and eyes with primary angle-closure glaucoma. Br J Ophthalmol 1970; 54: 161–9.[Free Full Text]
-
Denis P, Charpentier D, Berros P, Touameur S. Bilateral angle closure glaucoma after dexfenfluramine treatment. Ophthalmologica 1995; 209: 223–4.[Medline]
-
Singh J, O’Brien C, Wright M. Nebulized bronchodilator therapy causes acute angle-closure glaucoma in predisposed individuals. Respir Med 1993; 87: 559–61.
-
Rosenberg M. Ocular injuries during general anesthesia. J Oral Surg 1981; 39: 945–7.[Medline]
-
Ujino H, Morimoto O, Yukioka H, Fujimori M. Acute angle-closure glaucoma after total hip replacement surgery. Masui 1997; 46: 823–6.[Medline]
-
Eldor J, Admoni M. Acute glaucoma following nonophthalmic surgery. Isr J Med Sci 1989; 25: 652–4.[Medline]
-
Bettman JW. Seven hundred medicolegal cases in ophthalmology. Ophthalmology 1990; 97: 1379–84.[ISI][Medline]
-
Bettman JW. A review of 412 claims in ophthalmology. Int Ophthalmol Clin 1980; 11: 131–42.
-
Murphy DF. Anesthesia and intraocular pressure. Anesth Analg 1985; 64: 520–30.[Free Full Text]
Accepted for publication November 30, 2001.
This article has been cited by other articles:
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M. B. Sosis, B. Cohen, C. Lentschener, A. Ghimouz, P. Bonnichon, C. Parc, and Y. Ozier
Diagnosis of Acute Glaucoma in the Postoperative Period * Response
Anesth. Analg.,
November 1, 2002;
95(5):
1462 - 1463.
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Abstract
Introduction
