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Refractive stability in diabetes.

The discussion on the ocular changes arising as a consequence of diabetes is often confined to the changes which appear at a retinal level. This article considers the short-term changes that can occur in refractive error as a result of acute fluctuations in blood glucose levels in patients with diabetes.

Course code: C-37466 | Deadline: October 3, 2014

Learning objectives

To be able to ask appropriate questions relating to blood glucose control in patients with diabetes (Group 1.1.1)

To be able to identify the significance of atypical refractive changes by interpreting existing records (Group 2.2.5)

To be able to recognise the ocular manifestations of diabetes and manage the patient accordingly (Group 6.1.10)

To be able to recognise the refractive anomalies that may arise in patients with diabetes (Group 7.1.1)

Learning objectives

To be able to explain to the patient about the implications of diabetes on refractive status (Group 1.2.4)

To be able to understand the refractive changes that may arise in patients with diabetes (Group 8.1.5)

Learning objectives

To be able to understand the natural progress of refractive status in patients with diabetes before and after treatment (Group 1.1.1)

To be able to ask appropriate questions relating to blood glucose control in patients with diabetes (Group 2.1.1)


With approximately two million patients with diabetes mellitus above 12 years of age in England, it is expected that 10% of sight tests conducted are likely to involve people with the condition. (1) Although NICE guidelines are clear about the management of diabetic retinopathy, eye care practitioners may encounter additional ocular problems as part of diabetes. This article focuses on acute fluctuations in blood glucose levels, and the effect this may have on refractive error in patients with diabetes.

Classification of diabetes

Diabetes is one of the most common systemic diseases in the world. (2) It is defined as a chronic disorder of carbohydrate metabolism characterised by increased blood glucose concentration and the presence of glucose in the patient's urine. (3) This occurs when the pancreas does not produce enough insulin and/or when the body cannot effectively use the insulin it produces. The main types of diabetes are Type 1 and Type 2. Type 1 diabetics are often diagnosed during their childhood, and represent approximately 10% of all cases.3 They are insulin dependent due to the destruction of pancreatic beta cells in the islets of Langerhans, leading to deficiencies in insulin production and/or secretion. Type 1 diabetes most commonly results from an immune mediated disorder, although in some instances this cannot be proven.

Prevalence of diabetes

The prevalence of Type 2 diabetes increases with age, and may result from a cellular or receptor resistance to insulin action, which may be exacerbated by inadequate compensation in insulin secretion to reduced insulin action. (4) Type 2 diabetes is by far the most prevalent form accounting for 85 to 95% of all patients with the condition and may be present at an asymptomatic level for long periods before diagnosis. (3) Obesity and strong family histories for Type 2 diabetes are important risk factors for the disease. (5) Type 2 diabetes was formerly known as adult or maturity-onset diabetes. However, an increasing prevalence in youngsters has been reported, some as young as eight years of age. (6-7) In 2004, a UK survey reported that 25 out of 112 diabetic children (from birth to under 16 years of age) were found to have Type 2 diabetes (median age 12.8) of which the majority were female, obese or overweight and of ethnic minority origin. (8) Until recently, the gender distribution for diabetes has been slightly skewed, with a female predominance compared to males. This is primarily caused by the incidence of gestational diabetes, the development of any glucose intolerance with its onset or first recognition during pregnancy. Older maternal age, the epidemic of obesity and diabetes, and the decrease in physical activity may all contribute to an increase in the prevalence of gestational diabetes. (9) Interestingly, more men than women are now diagnosed with Type 2 diabetes caused by a more inactive lifestyle among men, resulting in increased obesity. (10)


The number of patients diagnosed with diabetes has increased significantly over the past decades. Today, the total number of people in the UK with diabetes is almost three million, representing 6.7% of the population between 20 and 79 years of age. (11) According to the statistics of the International Diabetes Federation, there were 382 million diabetics worldwide in 2013 (global prevalence of 5.4%), and this is estimated to increase to 592 million by 2035 (prevalence of 6.8%; see Figure 1). This is mainly attributed to poor nutrition, obesity, lack of exercise, and urbanisation. (12,13)

An individual's ethnicity can either increase or decrease their risk of developing diabetes. While in some cases this can be explained by access to healthcare and other socioeconomic factors, (15,16) studies have proved that even with equal access, prevalence of diabetes differs between people of different ethnicity. (17,18)

The incidence of diabetes is higher in south Asian and to a lesser extent Afro-Caribbean subjects compared to white Caucasians. (19) The risk of diabetes in women has also found to be significantly higher among Asians, Hispanics, and Afro-Caribbeans than among white Caucasians. (18)

Hypo- and hyperglycaemia

In an optometric practice, it is important to recognise the acute complications of diabetes known as hypo- and hyperglycaemia. Hyperglycaemia occurs when the blood glucose levels are above 10mmol/l, which can be measured with a finger prick test. Normal blood glucose levels in non-diabetics are between 4 and 6mmol/l. These marginally elevated levels of blood sugar are fairly benign and asymptomatic, but if the levels stay above 15-20mmol/l for a prolonged period of time, a phenomenon called ketoacidosis may occur. When there is not enough insulin to move glucose into the cells, the body then uses fat as a fuel source instead. As these fats are broken down, acids called ketones will start to build up in the blood and urine. The signs of severe hyperglycaemia will be a flushed face, dry skin/mouth, feeling nausea/vomiting, and rapid and deep breathing with fruity odour. It is important to lower the blood sugar levels with insulin and/or exercise and send these patients straight to hospital for a urine test.

In healthy patients, glucagon is produced when blood glucose levels are low, causing them to rise. In diabetic patients, hypoglycaemia is caused by an insufficient production of glucagon, which in turn does not stimulate the release of glucose from the liver in case the blood glucose levels are low or there is too much insulin. In this case, adrenalin is released instead, which is responsible for the warning signs of a 'hypo'. It occurs when the blood sugar levels are below 4mmol/l. It is important to recognise hypoglycaemia although symptoms vary greatly between hunger, trembling, sweating, being aggressive, looking pale or grey, blurry vision, difficulty concentrating and being confused or irrational. In some cases the patient could lose consciousness and even fall into a coma. The treatment of a mild hypoglycaemia is to offer the patient quick carbohydrates (fruit juice, glucose tablets) and long-acting carbohydrates (sandwich, fruit). If the patient has a severe hypo and is unable to swallow, it may be necessary to rub about two to three teaspoons of honey or jam on their gums, prior to offering carbohydrates. If the patient is unconscious, a trained person can give them glucagon or intravenous glucose.

Episodes of acute hyperglycaemia are a regular occurrence in patients with diabetes, especially after a meal. Blood glucose levels tend to peak two hours after a meal, and return to baseline approximately two to three hours later. In subjects without diabetes, blood glucose levels tends to peak at 7.8mmol/l after a meal. In patients with diabetes this may occur much faster, resulting in greater diurnal blood glucose levels. An example of diurnal variations from baseline blood glucose levels comparing subjects with Type 1 and Type 2 diabetes with those without diabetes are shown in Figure 2 (see page 52). Early morning (8.00am) baseline blood glucose levels were 11.1 [+ or -] 5.0 mmol/l for Type 1 subjects; 8.3 [+ or -] 3.0 mmol/l for Type 2 subjects; and 4.6 [+ or -] 0.5 mmol/l for subjects without diabetes. (20) Considering that these measurements were taken after a night of sleep, it is perhaps surprising to see the high levels of blood glucose in patients with diabetes so early in the morning. However, these patients may lower their long-acting insulin or increase their carbohydrate intake at night to ensure they do not to slip into a hypoglycaemic state overnight.

Diabetic retinopathy screening

Until recently, diabetic retinopathy and maculopathy were the leading cause of certifiable blindness among working age adults in England and Wales. However, a recent report shows that this has been overtaken by inherited retinal disorders. (21) This is mainly due to the introduction of public health measures such as diabetic retinopathy screening. The NHS Diabetic Eye Screening Programme was set up with the aim to reduce the risk of sight loss among people with diabetes by the early detection and treatment of sight-threatening retinopathy. (22) This created opportunities for optometrists to become involved in their local diabetic retinopathy screening service, which provides screening for diabetic retinopathy at the time of diagnosis and at least annually thereafter as recommended by NICE guidelines. (23) Diabetic retinopathy screening involves dilated digital retinal photography and visual acuity testing.

Refractive changes

Eye care practitioners in clinical practice often encounter patients with diabetes complaining of blurred vision and problems with reading and/or driving. In fact, a study from 2009 reported that approximately 10% of these individuals complained of blurred vision during hyperglycemia. (24)

Since blood glucose levels in patients with diabetes fluctuate significantly during the day, optometrists may expect to find short-term daily variation in refractive error and this explains the transient visual disturbances frequently reported. It may be prudent for optometrists to take into account the time of day and meal times during an eye examination. Additionally, some patients may be very anxious about the eye examination, as they often are about diabetic retinopathy (DR) screening. After an initial rise in blood glucose levels, they might actually experience a drop in blood glucose. They may also miss a meal while waiting, or change their daily routine, which might cause a hypoglycaemic episode.

Both myopic and hyperopic refractive error shifts due to changing blood glucose levels have been reported in diabetic patients. (24-30) Equivocal results are possibly due to the timescale of the reported hyperglycaemia, either being (semi-) acute or chronic. Acute hyperglycaemia occurs over the course of a day, while semi-acute hyperglycaemia persists over a few days or weeks. Chronic hyperglycaemia persists over several months, and results in both micro- and macrovascular complications. It is a leading cause of renal failure or end stage renal disease, (31) peripheral neuropathy, (32) amputations, (33) significant loss of vision or blindness due to diabetic maculopathy, (34) and death. (3)

Chronic hyperglycaemia

The long term effect of chronic hyperglycaemia has been shown to result in myopic shifts, due to the influx of water from the aqueous humour into the crystalline lens. (35,36) However, research studies investigating the impact of hyperglycaemia on the diabetic eye often include individuals who are newly diagnosed with diabetes and are undergoing (intense) treatment. This may be considered chronic hyperglycaemia since these patients have had prolonged periods of increased blood glucose prior to the onset of their treatment. Although most studies find a myopic shift in refractive error prior to diagnosis with a hyperopic shift during treatment for diabetes, the literature has not been consistent (see Table 1).

It is expected that prior to treatment, the crystalline lens will swell as a result of an influx of water during long-term hyperglycaemia and lead to an increase in myopic shift. However, Giusti found no significant changes in anterior lens curvature, anterior chamber depth, lens thickness, or axial length within four months of treatment. (26) Due to the lack of geometric change, the hyperopic shift was attributed to a decrease in refractive index of the crystalline lens. Small changes in refractive index have been shown to significantly alter refractive error. (40,41) Indeed, a reduction in equivalent refractive index of the crystalline lens with age has been used to explain the 'crystalline lens paradox'. (42-44) Here, despite the lens becoming more convex with age, (45) rather than an expected shift towards myopia, there is a tendency towards hypermetropia. (46,47) It is, therefore, more likely that refractive index is the source of any refractive change in diabetic patients. (48) One of the difficulties in interpreting the findings of investigations into the effect of hyperglycaemia during intense control of diabetes (usually following diagnosis) is that once treatment has been initiated, any subsequent changes in refractive error may be attributed to the changing blood glucose levels or as a by-product of the treatment itself.


Acute hyperglycemia

Acutely decreasing blood glucose levels may result in a myopic shift. The concentration of glucose within the crystalline lens rises with increasing blood glucose concentration. Sorbitol, converted from excess intracellular glucose, accumulates within the lens, which induces an influx of water from the aqueous humour. This will allow the lens to swell, leading to induced myopia. On the other hand, decreased glucose concentration in the aqueous humour could also cause a transient difference in osmotic pressure between the aqueous humour and crystalline lens. Due to a decrease in refractive index in the lens, a hyperopic shift may be found.

There have been few studies regarding acute hyperglycaemia in reasonably well-controlled diabetics and they are difficult to compare mostly due to variables, which include accommodation, degrees of diabetic retinopathy, measurement techniques, and inconsistent definitions of 'good' or 'poor' diabetic control.

Independent of diabetes, both objective and subjective refraction have shown that the standard deviation of repeated measures is approximately 0.30D. (51) From Table 2, it seems that despite various degrees of diabetic retinopathy, refraction and visual acuity are broadly stable in the presence of variable blood glucose levels. It is possible that only when acute blood glucose concentration rises beyond a certain (individual) threshold that measurable shifts in the anterior ocular parameters start to occur.


A differential diagnosis of 'undiagnosed diabetes' should be considered if an eye care practitioner finds an unexpected or rapid shift of >0.75D in refractive error. This type of refractive shift is usually myopic, and the patient needs referral to their general practitioner. In well-controlled diabetic patients, we do not expect to find any clinically significant fluctuation in their refractive error due to their illness. Although a refractive shift is not always apparent in patients with diabetes, it may be wise to repeat the refraction on a different day if blood glucose levels are atypically high or low at the time of refraction. This is imperative if the patient is already reporting episodes of blurry vision during fluctuating blood glucose levels.

Exam questions

Under the enhanced CET rules of the GOC, MCQs for this exam appear online at Please complete online by midnight on October 3, 2014. You will be unable to submit exams after this date. Answers will be published on and CET points will be uploaded to the GOC every two weeks. You will then need to log into your CET portfolio by clicking on 'MyGOC' on the GOC website ( to confirm your points.


Visit clinical, click on the article title and then on 'references' to download.

Byki Huntjens PhD, MSc, MCOptom, FHEA and Irene Ctori MSc, MCOptom

About the authors

Dr Byki Huntjens is an optometrist and lecturer at City University London.

Irene Ctori is an optometrist currently undertaking her PhD in macular pigment spatial profiles among ethnic groups at City University London.
Table 1 Summary of findings into refractive change during treatment
of hyperglycaemia in diabetes

Author                      N      Diabetes type

Eva et al. (1982)37         13     Newly Type 2
Saito et al. (1993)27       5      Type 1 and Type 2
Okamoto et al. (2000)38     14     Type 2
Giusti (2003)26             20     Newly Type 1
Sonmez et al. (2005)28      18     Type 2
Lin et al. (2009)30         5      Newly Type 2
Wiemer et al. (2009)24      25     Type 1 and Type 2
Agardh et al. (2011)39      53     Type 1 and Type 2

Author                      Age range

Eva et al. (1982)37         27-72 (Mean 60)
Saito et al. (1993)27       28-57 (Mean 47)
Okamoto et al. (2000)38     25-72 (Mean 50)
Giusti (2003)26             15-19 (Mean 17)
Sonmez et al. (2005)28      44-67 (Mean 56)
Lin et al. (2009)30         39-58 (Mean 48)
Wiemer et al. (2009)24      18-78 (Mean 47)
Agardh et al. (2011)39      Mean [+ o r -] SD
                            54 [+ o r -] 12

Author                      Refractive change
                             during treatment for

Eva et al. (1982)37         Hyperopic shift
Saito et al. (1993)27       Hyperopic shift
Okamoto et al. (2000)38     Hyperopic shift
Giusti (2003)26             Hyperopic shift prior to
                             treatment with a myopic
                             shift during treatment
Sonmez et al. (2005)28      9 hyperopic shift,
                             2 myopic shift,
                             7 no change
Lin et al. (2009)30         Hyperopic shift
Wiemer et al. (2009)24      No significant change
Agardh et al. (2011)39      No significant change

Table 2 Summary of findings into refractive change during acute
changes in blood glucose levels

Author                 N     Diabetes        Decrease      Refractive
                             type            in blood      change

Gwinup and             10    Not specified   8.4 mmol/l    Myopic
 Villareal (1976) 49                                        (-0.50D)
Steffes (1999)50       1     Type 1          2.8 mmol/l    Myopic
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Title Annotation:1 CET POINT
Author:Huntjens, Byki; Ctori, Irene
Publication:Optometry Today
Geographic Code:4EUUK
Date:Sep 5, 2014
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