Acute glaucoma classically presents with severe pain, redness, and reduced vision in the affected eye. Systemic symptoms such as headache, nausea, and vomiting may be associated in variable severity. The typical presentation is thus dramatic. In spite of this, especially in the elderly, there can be a delay or misdiagnosis of this condition. We report three cases to re-emphasise this and to draw attention to this condition.

CASE REPORTS

Case 1

A 77 year old woman was referred to the acute general medicine department by her general practitioner following a general deterioration in her condition. Her past medical history included Parkinson’s disease, recent weight loss, and 2 days of vomiting.

On referral, her medications were sodium picosulphate 10 ml once daily, and thrice daily doses of betahistine 8 mg, bromocriptine 5 mg, domperidone 10 mg, levodopa 125 mg, and orphenadrine 50 mg. Family and personal history was inconclusive. On clinical examination, she was drowsy but oriented. All vital signs were normal. Systemic examination was within normal limits. Haematological and biochemical investigations, ECG, and chest x ray were normal. Malnutrition, malignancy, or chest infection was suspected as the likely causes of her condition.

Swollen lids and conjunctival injection were also noted. The systemic problem was thought to be with parkinsonism related generalised deterioration and cachexia, worsened by gastrointestinal upset and its treatment. Chloramphenicol eye ointment was started for the eyes. After 6 days, the patient was referred to the ophthalmologists with a persistent red eye.

Ophthalmic examination showed conjunctival injection and a semi-dilated, fixed pupil in both eyes. Fundus examination showed glaucomatous optic disc changes. Intraocular pressure (IOP) was 50 mm Hg in the right eye and 38 mm Hg in the left, suggesting acute angle closure glaucoma (AACG). She was given intravenous acetazolamide 500 mg immediately, sustained release acetazolamide capsules 250 mg twice daily; ocusert pilocarpine twice daily, levobunolol eyedrops twice daily, latanoprost eyedrops nightly, and prednisolone acetate ophthalmic suspension 1% (Pred Forte) eyedrops four times daily in both eyes. After 1 day, she was more comfortable, and IOP dropped to 25 mm Hg in the right eye, and 10 mm Hg in the left. YAG laser peripheral iridotomies were made in both eyes. Subsequently, the IOP was 22 mm Hg in the right eye and 25 mm Hg in the left.

Case 2

A 71 year old Indian woman was referred to the physicians by her general practitioner for sudden onset, right sided temporal headache, vomiting, and a red, sore right eye. The vision was poor from longstanding cataract and had not worsened. There had been similar "minor" episodes previously. On examination, there was scalp tenderness, and the right eye was red with advanced cataract. Erythrocyte sedimentation rate was 24 mm. A diagnosis of temporal arteritis was made. She was started on prednisolone tablets 60 mg once daily and referred to the ophthalmologists for temporal artery biopsy.

On ophthalmic examination, her vision was light perception in te right eye and 6/12 in the left. The right eye showed circum corneal congestion, corneal oedema, a shallow anterior chamber, semi-dilated fixed pupil, mature cataract, and IOP of 52 mmHg. The left eye showed a shallow anterior chamber and a pressure of 16 mmHg. A diagnosis of acute (?phacomorphic) glaucoma right eye was made. The patient was treated as for case 1. IOP dropped to 8 mm Hg in 2 hours.

Bilateral YAG laser peripheral iridotomies were performed. Subsequently she underwent cataract surgery with intra cular lens implantation separately for both eyes, and improved to 6/18 with correction in the right eye and 6/12 in the left.

Case 3

An 84 year old female with past medical history of Alzheimer’s disease presented following a fall at home. She sustained a lacerated wound temporal to the left eye, which was sutured. There was no loss of consciousness or head injury.

Five days later, she developed increasing drowsiness with lucid interval, new and progressive headache and increasing confusion. Examination revealed left periocular bruising, mild subconjunctival haemorrhage and a red eye. The pupil was dilated and fixed. She was not oriented in time and space. There was no focal neurological deficit. A CT scan excluded subdural or intracranial bleed and showed fractures of the anterior and lateral walls of the left maxilla and displacement of the zygomatic arch. A fracture of the optic canal was suspected and the patient thus referred to the ophthalmologists.

On ophthalmic review, vision in the left eye was down to detection of hand movements. There was ecchymosis, chemosis, severe corneal oedema with pigment deposit, a very shallow anterior chamber, a semi-dilated and fixed pupil, and some lenticular opacity in the left eye. Right eye vision and examination was normal except for a shallow anterior chamber. IOP was 24 mmHg in the right eye and 55 mmHg in the left. Gonioscopy revealed a narrow angle. An ophthalmic diagnosis of angle closure glaucoma in the left eye was thus made.

The patient was treated as for case 1. After 2 hours, the pressure was 35 mmHg, the headache had subsided, and the cornea had cleared. The lens was swollen. YAG peripheral iridotomies were performed the following day.

Ten days later, the patient underwent complicated cataract extraction with anterior vitrectomy and anterior chamber intraocular lens implantation. Three months later, vision was 6/60 and pressure 16 mmHg in the left eye, and the optic disc was pale and cupped.

DISCUSSION

In the UK, the incidence of AACG in people over the age of 40 years is about 1 in 1000, with a female to male ratio of 4:1.¹ In AACG, there is a build up of aqueous fluid in the anterior chamber of the eye leading to pain, reduced vision due to corneal oedema and optic nerve compromise, and redness due to circumcorneal congestion. Small, usually hypermetropic eyes that have a shallow anterior chamber and narrow iridocorneal angle are at a higher risk.² The initiating factor is the development of pupillary block, which is caused by contact between the iris in a semi-dilated pupil and the lens, resulting in blockage of the flow of aqueous humour from its site of production in the ciliary body, through the pupil, into the anterior chamber. This leads to a build up of aqueous humour in the posterior chamber. This in turn results in forward bowing of the iris, which then closes the already narrow iridocorneal drainage angle, producing a rise in intraocular pressure.^1,3 A persistent increase in the intraocular pressure results in a progressive and irreversible loss of vision and even blindness.

Physiological pupillary semi-dilation, such as occurs in the evening or when watching television in a darkened room, can precipitate an acute angle closure in an anatomically predisposed eye. Pharmacological dilation with 1% tropicamide, used routinely in ophthalmoscopy for diabetic retinopathy screening, rarely results in pupil block, but in diabetes the iris may spontaneously semi-dilate rather than fully dilate owing to autonomic neuropathy. This probably explains the increased risk of angle closure glaucoma in diabetic patients.⁴ Various drugs, most commonly those with anticholinergic properties, such as the tricyclic antidepressants,⁵ nebulised ipratropium bromide,^6,7 and nebulised atropine⁸, have also been reported to precipitate angle closure glaucoma. In case 1, drugs such as levodopa and bromocriptine, which are dopaminergic, and orphenadrine, which is antimuscarinic, may have contributed to the acute angle closure.

Complete angle closure may be preceded by intermittent episodes of partial or temporary closure of the angle.³ These are terminated by pupil constriction induced by bright light or sleep. Between episodes, however, the eye looks perfectly healthy, and the diagnosis must be based on a history of evening headaches associated with blurred vision and haloes around lights (due to the presence of corneal oedema), coupled with the presence of a shallow anterior chamber on slit lamp biomicroscopic examination. Patients with such symptoms should have a careful review of their drug treatment and be referred for an early ophthalmological opinion, as they will require laser peripheral iridotomy to prevent the development of AACG. Such a history of intermittent preceding symptoms is, however, present in only half of patients presenting with AACG.¹

Systemic symptoms such as headache, malaise, and vomiting may be the presenting complaints apart from reduced visual acuity, pain, and redness of the affected eye in acute, prolonged closure of the iridocorneal angle. In some cases, and particularly in elderly people, the systemic disturbance may be so severe that the ocular symptoms are initially overlooked, as in our cases, and the patient may be misdiagnosed as having an acute medical or surgical condition. On examination, the visual acuity will be reduced in a red eye, which may feel hard to touch, with a cloudy cornea and a fixed, semi-dilated pupil. These patients require urgent ophthalmological referral for immediate medical treatment to lower the intraocular pressure, followed by definitive bilateral laser or surgical procedures. After iridotomy, iridectomy, or trabeculectomy, it is safe to dilate these patients’ pupils and to re-start treatment with anticholinergic drugs.

CONCLUSION

The diagnosis of acute glaucoma in a patient who presents with sudden onset of a painful, red eye with reduced visual acuity, a hazy cornea, and a fixed, semi-dilated pupil is comparatively straightforward. However, any patient with headache, malaise, or gastrointestinal disturbance, especially with clinical signs of an acute red eye and reduced vision, should alert doctors to the possibility of acute glaucoma. This is especially important in elderly people, who may not volunteer any specific ocular symptoms. An awareness of the same should help in seeking early ophthalmological opinion.