Misdiagnosis of angle closure glaucoma (original) (raw)
Angle closure glaucoma is a sight threatening ophthalmic emergency. Patients classically present with an acutely painful red eye and periocular headache, loss of vision, nausea, and vomiting, but sometimes the presentation is less dramatic or more systemic than ocular. The diagnosis may be missed in such cases, leading to unnecessary investigations, delayed treatment, and blindness. We describe three cases of angle closure glaucoma in which initial diagnostic uncertainty led to a delay in treatment and which highlight the need for a wider awareness of this condition. Case reports Case 1 A 66 year old woman was admitted to the orthopaedic ward for elective spinal canal decompression for spinal stenosis. She was otherwise healthy and was taking oral diclofenac, morphine, and amitriptyline. During the operation, she was placed prone for spinal laminectomy. Postoperatively, she received regular opiate analgesia. On the third postoperative day the patient developed severe headache, photophobia, and neck stiffness without focal neurological deficit. An urgent computed tomography scan of the head was normal. On the fourth postoperative day she complained of visual loss, a red eye was noted, and an ophthalmology referral was made. Her visual acuity was counting fingers for both eyes. Slit lamp examination was hampered by her immobility, but both eyes were red with cloudy corneas; shallow anterior chambers; fixed, middilated pupils; and high intraocular pressures of 45 mm Hg in the right eye and 33 mm Hg in the left eye (normal < 21 mm Hg). A diagnosis of bilateral angle closure glaucoma was made. She was treated immediately with the standard medical regimen (using eye drops to constrict the pupil and systemic acetazolamide to lower the intraocular pressure). Her amitriptyline was stopped, as it was a potential precipitating factor. Her response to medical treatment was partial, and, as she had coexistent cataracts, bilateral lens extraction, lens implantation, and surgical peripheral iridotomies were done. The anterior chambers deepened immediately, and the intraocular pressures normalised postoperatively. Two months later, intraocular pressures were normal without treatment. The best corrected Snellen visual acuity was only 6/12 in either eye, with bilateral visual field constriction and reduced colour vision associated with glaucomatous optic atrophy (fig 1).