Acute metabolic cataract in patients with newly diagnosed Type 1 diabetes mellitus is a rare complication, which may develop within a few weeks or months after starting treatment.1, 2 It can affect visual acuity from slight visual impairment to complete blindness.1 We report a case of acute bilateral irreversible metabolic cataract in a patient with recently diagnosed Type 1 diabetes mellitus.

Case report

An 18-year-old Caucasian female presented with a 4-week history of feeling unwell; a 2-month history of thirst and polyuria; and a 1-year history of weight loss. There was no significant past medical history. Her body mass index was 24.3. Urinalysis revealed moderate ketones and glucose but she was not acidotic. Her fasting plasma glucose level was 22.3 mmol/l (normal range: 3.3–5.5 mmol/l) and HbA1C was 10.5% (normal range: 4–6%). Urea, electrolytes and arterial blood gases were within normal limits. She was diagnosed as having Type 1 diabetes mellitus, and started on Novomix™ 30–26 U in the morning and 28 U in the evening.

After 1 week of treatment, she noticed blurring of vision in both eyes, which gradually worsened. She was referred to the Ophthalmology Department. There was no history of previous eye problems and visual acuity was 6/6 in both eyes at the start of treatment. On presentation visual acuity was only perception of light in both eyes. Slit-lamp biomicroscopy revealed dense intumescent cortical cataracts bilaterally (Figures 1 and 2). No fundal details were visible in either eye. She was diagnosed as having bilateral acute irreversible metabolic cataract and cataract surgery was planned. She underwent right phacoemulsification with an acrylic posterior chamber intraocular lens (PCIOL) implantation (Sensar® OptiEdge) under general anaesthesia (GA) and her visual acuity improved to 6/5 without glasses. After 2 months, left phacoemulsification and PCIOL implantation (Sensar® OptiEdge) under GA was performed and her visual acuity improved to 6/6 without glasses, although she required +2.5 for near vision. There were no changes of diabetic retinopathy seen.

Figure 1
figure 1

Anterior segment photograph of right eye showing dense cortical cataract. There is no fundal glow visible due to density of cataract.

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Figure 2
figure 2

Anterior segment photograph of left eye showing dense cortical cataract and no view of fundus.

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After 3 months, left posterior capsular opacification developed and her visual acuity reduced to 6/9. Left YAG posterior capsulotomy was performed to improve visual acuity.

On her last visit the visual acuity in both eyes is 6/5 and there is no diabetic retinopathy.

Comments

The exact mechanism of diabetic cataract is not known although it is thought to be related to poor glycaemic control and abnormalities in the polyol pathway.3 Reduction of glucose to sorbitol by aldose reductase (AR) leads to accumulation of sorbitol, which produces osmotic stress. It also produces oxidative stress by depleting cofactor NADPH that is an important cofactor for regeneration of reduced glutathione (GSH).3 Some authors also mention the probable importance of genetic factors in their case studies but the mechanism is still poorly understood.4

Our patient was started on insulin and just after a week, noticed blurring of vision. It deteriorated very quickly to perception of light within 4 weeks. Her blood glucose level was 22.3 mmol/l and it came down rapidly to 10 mmol/l with insulin treatment. The rapid change in blood glucose following initiation of insulin may be responsible for the development of metabolic cataract.5 The cataract was of cortical snowflakes type and the whole lens was swollen in both eyes. Acute metabolic cataract can either be transient resolving spontaneously with improved glycaemic control or irreversible.

Phacoemulsification cataract surgery with intraocular lens implantation has a good visual outcome but is challenging in intumescent cataracts, especially there is a high risk of peripheral radiation of capsulorhexis or capsulotomy because of swollen lens. We used Sensar® OptiEdge IOL, which has sharp posterior edge and it is well known to reduce posterior capsular opacification.6 In our patient, left posterior capsular opacification developed earlier as early posterior capsular opacification is a well-known postoperative complication in diabetic patients.7

Young patients with diabetes mellitus can present with eye problems during the early course of the disease and treatment.8 These cataracts once developed can be irreversible in spite of good metabolic control and require surgical intervention.