An optometrist’s role in the diabetic care team

At the completion of this CPD activity, optometrists will have developed their knowledge of diabetic eye disease management. Including:

• Implement their own clinical approach to taking a case history of patients with diabetes or prediabetes
• Develop clinical strategies to ensure accurate grading of DR and DME
• Know the expected content of diabetes eye exam reports to be shared with fellow members of the diabetes care team
• Develop procedures to establish and reinforce the collaborative relationships among the various specialties in the diabetes care team
• Review key messages for educating patients with diabetes and/or diabetic retinal disease

NOTE: Optomery Australia members can enter their details at the bottom of this article to have it automatically added to their Learning Plan.

In Part 1 of its National Diabetes Week (10-16 July) coverage, Insight invites renowned US optometrist and diabetes educator DR A. PAUL CHOUS to share his evidence-based, practical strategies for optometric care of patients with diabetes.

A. Paul Chous, MA OD FAAO
Specialist in Diabetes Eye Care and Education
Tacoma WA USA

Every healthcare provider is seeing more patients with diabetes as the global diabetes pandemic rages on. The International Diabetes Federation (IDF) estimates 537 million people between 20 and 79 years old had diabetes in 2021 – a number that is expected to grow to 783 million by 2045.¹ 

The IDF estimates 1.5 million Australians were affected, with another three million having prediabetes, which significantly elevates risk for development of type 2 diabetes (T2D) and carries similar cardiovascular risk.² 

Global data suggest 34% of patients have some degree of diabetic retinopathy (DR), and 10% have sight-threatening diabetic retinopathy (STDR).³ Of note, up to 14.9% of patients with prediabetes also have retinal findings consistent with DR.⁴ 

All this begs the question: What is the role of optometrists in identifying, counselling and managing patients with diagnosed and undiagnosed diabetes? And how do they best collaborate with the rest of the diabetes care team? 

Defining the diabetes eye exam 

Is an eye examination of patients with diabetes distinct from that performed on patients without diabetes? Clinical practice guidelines from Optometry Australia and the American OptometricAssociation both recommend a battery of diagnostic tests as part of a comprehensive eye examination for people with diagnosed diabetes (visual acuity, refraction, ocular motility, pupil reflexes, tonometry, slit lamp examination, dilated steroscopic fundoscopy, confrontation visual field). Also, ancillary testing ‘as needed’ (fundus photography – including widefield, optical coherence tomography (OCT), gonioscopy, colour vision and contrast sensitivity assessment, automated perimetry).^5,6 

However, no group of these tests is unique to diabetes, and each arguably is or may be part of any comprehensive eye examination of any patient. 

I think the following four elements distinguish the diabetes eye examination:

1. Case history designed to ascertain metabolic control, the systemic treatment plan, medication adherence and other risk factors for vision loss

2. Consistent and meticulous examination for ocular pathologies associated with diabetes, particularly those known to cause severe vision loss

3. Focused patient education designed to attenuate risk of vision loss and stress the importance of ongoing, defined-interval surveillance. 

4. Consistent communication with other members of the diabetes care team, with particular emphasis on dilated examination, the presence/absence/severity and stability of any DR or diabetic macular oedema (DME) detected and need for any ophthalmologic referral, the recommended date for the next eye exam and any other recommendations for specific patients.

1. Case history

Case history is paramount for gauging the likelihood of finding diabetic eye disease and for reducing risk through patient education. On a percentage basis, type 1 diabetes (T1D) confers higher risk of retinopathy after five years duration than does T2D of any duration, and this risk-spread increases with time.³

Nonetheless, recent analysis shows that nearly 2% of T2D patients have proliferative disease (PDR) after five years, with 3.5 times higher risk in T2D patients who use insulin.⁷ 

It’s important to remember that insulin use doesn’t mean a patient with T2D has developed type 1 diabetes. Rather, patients with T2D become increasingly insulin-deficient over time. That said, disease duration is a definite risk factor for developing and worsening DR. (Half of the patients with T1D in the Joslin ‘Gold Medalist’ Study [50+ years living with T1D] had no or minimal DR, which suggests – somewhat paradoxically – that very long disease duration without significant DR implies protective genetics in these long-lived patients).⁸ 

Is HbA1c actually the ‘gold standard?’

After diabetes duration, blood glucose control has long been considered the second-most important risk factor for DR. Indeed, randomised trials and observational studies alike consistently show that elevated glycosylated haemoglobin (HbA1c) predicts incident and worsening DR. 

However, analysis from the vaunted Diabetes Control and Complications Trial (DCCT) has shown that HbA1c accounted for a mere 6-11% of the total risk for developing DR during the trial.⁹ Moreover, identical HbA1c values from different patients are associated with significantly different mean blood glucose levels as measured by gold standard continuous glucose monitoring (CGM) devices. This means that a patient with an HbA1c of 9% might actually have better mean glucose than a patient with an HbA1c of 7%.¹⁰  

This discrepancy and other deficiencies of HbA1c (for example: its value is weighted to the last two weeks’ glucose levels before sample collection; and it does not reflect blood glucose variability linked to microvascular complications, including DR) have led to the adoption of additional glucose metrics best accessed through use of CGM, including glucose time-in-range (TIR) that predicts DR independently of HbA1c (see Box 1 above on CGM and TIR). 

This is not to say that HbA1c is of no value, only that it isn’t the gold standard metric of good diabetes control it has long been assumed to be.

From a practical standpoint in the eye exam, a patient’s current HbA1c is of little value to clinicians except insofar as it ‘suggests’ level of control or that it has precipitously decreased within the year (the latter is associated with heightened risk of diabetic ‘re-entry retinopathy’; that is, DR develops or worsens with rapid improvement of blood glucose that re-enters a more normal range – typically a 2+ point drop in HbA1c).¹¹ 

Far more useful is to ask patients about their HbA1c history since diagnosis to assess for ‘metabolic memory’ demonstrated in every single major prospective diabetes study.¹² This refers to the long-term protective/detrimental effects of good/poor glucose control the first five-to-10 years after diabetes diagnosis that confers decreased/increased risk of DR over time, despite worsening/improving glycaemic control over time. 

If a patient has an HbA1c of 6% now but had lousy metabolic control the first 15 years after diagnosis (for example: HbA1c ranging from 8-12%), we should not be surprised to discover severe DR. In fact, recent prospective trials of anti-VEGF (vascular endothelial growth factor) therapy in severe non-proliferative diabetic retinopathy (NPDR) found that ‘good’ current glycaemic control at study entrance was not at all protective against development of sight-threatening diabetic retinopathy (STDR) – the horse is already out of the barn.¹³  

By contrast, severe hypoglycaemia itself was linked to higher risk for vision loss in the Freemantle Diabetes Study Phase II,¹⁴ possibly a reflection of glycaemic variability (that is: patients hospitalised for severe low blood glucose are more likely to have a history of severe high blood glucose levels) or the fact that hypoglycaemia is linked to apoptosis of retinal cells.¹⁵ 

In addition to glucose control, control of blood pressure and lipids, treatment of obstructive sleep apnoea, and absence of non-ocular vascular diabetes complications are linked to lower risk of DR, whereas their opposites are associated with higher risk.^16,17

Certain medications commonly used in diabetes are also linked to lower risk, including metformin, ACE inhibitors/ARBs, statins and fenofibrate^18-21 – and might be recommended to patients and other HCPs treating them.  

Patients should be asked if they consistently take prescribed medications. The case history also is a great opportunity to ask about prior adherence to annual or biannual dilated eye examinations. This also puts optometrists in a good position to recommend the frequency of future exams pending diagnostic findings. 

Patients with a history of depression, renal disease, lower extremity amputation, lower educational and socioeconomic status are at a significantly increased risk for becoming lost-to-follow up (LTFU)²² and should be assiduously pre-appointed, counselled and reminded about the importance of ongoing eyecare despite the absence of visual symptoms. 

2. Consistent and meticulous examination

Eye examination of patients with diabetes should focus on common pathologies (cataract, glaucoma, ocular surface disease, cranial neuropathy and diabetic retinopathy) with particular attention to detection and staging of any DR or DME. 

I have found a multi-modal approach combining clinical examination and retinal imaging to be most useful for diagnosing/staging of retinal disease. In addition to a steroscopic exam of the disk and macula, fundus photography is invaluable for documenting DR severity, serial comparison for progression and patient education. 

Use of red-free filters highlights microaneurysm and haemorrhage, as does fundus autofluorescence.²⁴ OCT is the most sensitive tool for detecting DME, including subclinical DME that portends increased risk of worsening macular fluid.²⁵ In my view, OCT should be routinely used in patients with any level of DR.

Evaluation of the retinal periphery increases DR severity grading in 10% of eyes and predominantly peripheral DR lesions (PPL) significantly increased risk of retinal nonperfusion, significant worsening of NPDR and PDR over four years,^26,27  making wide-field and ultrawide-field retinal imaging systems quite valuable in diabetes. 

Finally, AI systems will likely not supplant practising eyecare professionals for a number of reasons. Rather, they will likely make both optometrists and ophthalmologists better at staging DR severity, referring when treatment is most beneficial and reducing vision loss.²⁸

Figures 1A, 1B, 1C, 1D show the value of multimodal imaging in patients with DR and DME. They are multi-modal images of a 29-year-old male with T1DM x 20 years and severe NPDR with early CI-DME, OS and 20/30 visual acuity who will likely benefit from anti-VEGF therapy. Forty-five-degree imaging with AI analysis and spectral domain OCT were also used to assist with correct diagnosis/staging and persuade the patient to see a retina specialist.  

Figures 2A, 2B, show the value of multimodal imaging in patients with DR and DME. They show retinal and SD-OCT imaging of a patient with 20/20 best-corrected visual acuity and no symptoms demonstrating mild NPDR without clinically apparent DME, but subclinical DME using OCT and S-cone dysfunction with colour contrast sensitivity testing. 

It should be noted that ODs, ophthalmologists and even retina specialists frequently under-grade DR severity¹³ (several prominent retinologists have remarked to me that they are rarely certain about NPDR severity until performing ultrawide-field fluorescein angiography and OCT!), so referral of patients with moderate or worse NPDR makes absolute sense.

4. Consistent communication with other members of the diabetes care team

Ideally, eyecare providers, primary care providers and other members of the diabetes care team will openly share diagnoses and recommendations with each other, and with the patient. Communication of eye exam findings should be timely and consistent. 

In a meeting with multiple endocrinologists at the American Diabetes Association Scientific Meeting, whom I asked about their expectations from a diabetes eye exam report, they asked for the following: 

1. Confirmation the patient was dilated

2. Presence or absence of DR and stability compared to previous eye examination without abbreviations denoting disease state or laterality

3. Notice of any referral to a retina specialist 

4. A specific surveillance interval for the next dilated exam

5. Any educational recommendations pertinent to patient care. 

Ideally, communications between ECPs and other members of the diabetes care team would be reciprocal, as evidence suggests better adherence to eye examinations when PCPs send reports to ECPs than vice versa.²⁹

Patients ought to be referred to retina specialists for DR/DME if and when the diagnosis is uncertain, with unexplained vision loss, or when patients have or are anticipated to soon develop treatable disease severity (moderately severe to severe NPDR, PDR, DME or evidence of anterior segment neovascularisation). 

Communication to the retina specialist should include patient diabetes history, current medications, best-corrected visual acuity, intraocular pressure and a specific reason for referral. Imaging results are often useful, especially if serial imaging demonstrates disease progression. Ideally, retina specialists will not only send reports back to referring optometrists for ongoing care, but also copy the PCP/endocrinologist to establish and reinforce the importance of collaborative relationships between various specialties. If not, ask them to do so.

Optometrists play an important role on the diabetes care team and can improve patient outcomes significantly. By focusing on the elements described in this article, we can all help maximise patients’ ocular and systemic health and be well-respected within the diabetes care community. 

Patient Education

Key messages for educating patients with diabetes and/or diabetic retinal disease

1. Use imaging to teach patients what normal and abnormal look like

2. Use the same to motivate patients who are stable or are improving with treatment (e.g., anti-VEGF therapy)

3. Explain that DR causes no visual symptoms whatsoever at its earliest, most treatable stages; like a heart attack, everything can seem fine up until the day it isn’t

4. Pre-appoint patients for their next eye exam depending on their retinal status; reschedule patients with you after making a retinal referral to assure the appointment was kept, answer questions and bolster your relationship

5. Tell patients the worst part of an intravitreal injection, by far, is hearing that you may need one

6. Empathise with the fear of hypoglycaemia in patients using insulin or sulfonylureas – always recommend CGM for these patients, especially if they live alone

7. Not every patient should attempt tight glucose control – older age, cognitive dysfunction & multiple comorbidities are legitimate reasons for higher individualised glycaemic targets – ask the PCP so you can give complementary recommendations

8. Encourage patients to ask about ACEIs or ARBs for hypertension – these drugs protect both kidney and retinal function independently of their antihypertensive effects

9. Encourage T2DM patients with NPDR to discuss fenofibrate therapy with PCPs – statin therapy has also shown efficacy against DR progression

10. Encourage patients with pre-existing cardiovascular disease to ask the PCP about SGLT2 inhibitors and/or GLP-1 drugs to reduce risk. SGLT2 drugs are specifically beneficial for congestive heart failure and mild-moderate renal disease. Both drug classes assist with weight loss

11. Ask permission to talk about patients’ weight status by explaining it affects eye health and risk of eye disease; recommend overweight patients be assessed for obstructive sleep apnoea

12. Encourage regular aerobic and anaerobic exercise to prevent T2D and improve metabolic control in all patients with diabetes; recommend a pedometer and help patients set a daily goal based on their current level of activity – 7,000 steps daily was recently shown to reduce mortality by up to 50% in adults > 60 years [A]

14. Encourage a predominantly plant-based Mediterranean or Palaeolithic-type diet

13. Multiple studies suggest higher macular pigment is associated with lower risk of DR – recommend a lutein/zeaxanthin-rich foods or supplements [B]

14. Create and use educational handouts on minimising the risk of vision loss from diabetes; create the same for reducing the risk of developing T2D in patients at risk

15. Utilise a sight-threatening diabetic retinopathy risk calculator available at www.retinarisk.com – only accurate for patients with no or mild NPDR, but a great tool for patient education

15. Redouble all educational efforts for patients at high-risk of being LTFU, as discussed above.

SGLT2 inhibitors = sodium glucose transporter type 2
GLP-1 analogs = glucagon-like peptide-1
A. Paluch AE, Bajpai S, Bassett DR, et al. Steps for Health Collaborative. Daily steps and all-cause mortality: a meta-analysis of 15 international cohorts. Lancet Public Health. 2022;7 (3): e219-e228.
B. Chous AP, Richer SP, Gerson JD, Kowluru RA. The Diabetes Visual Function Supplement Study (DiVFuSS). Br J Ophthalmol. 2016; 100 (2): 227-34 

References 

1. International Diabetes Federation (IDF) Diabetes Atlas, 10^th ed, September 12, 2021, accessed 04/09/2022 at https://idf.org/aboutdiabetes/what-is-diabetes/facts-figures.html

2. Cai X, Zhang Y, Li M, et al. Association between prediabetes and risk of all cause mortality and cardiovascular disease: updated meta-analysis. BMJ. 2020 Jul 15;370:m2297.

3. Yau JW, Rogers SL, Kawasaki R, et al. Meta-Analysis for Eye Disease (META-EYE) Study Group. Global prevalence and major risk factors of diabetic retinopathy. Diabetes Care. 2012; 35 (3): 556-64

4. Wang, J., Zhang, RY., Chen, RP. et al. Prevalence and risk factors for diabetic retinopathy in a high-risk Chinese population. BMC Public Health 13, 633 (2013). 

5. American Optometric Association. Evidence-based Clinical Practice Guideline Eye Care of the Patient with Diabetes Mellitus, Second Edition, accessed 04/09/2022 at http://aoa.uberflip.com/i/1183026-evidence-based-clinical-practice-guideline-eye-care-of-the-patient-with-diabetes-mellitus-second-edition/0?m4=

6. Optometry Australia Clinical Guideline: Examination and management of patients with diabetes, accessed 04/09/2022 at https://www.optometry.org.au/wp content/uploads/Professional_support/Guidelines/clinical_guideline_diabetes_revised_sept_2018_final_designed.pdf

7. Gange WS, Lopez J, Xu BY, et al. Incidence of Proliferative Diabetic Retinopathy and Other Neovascular Sequelae at 5 Years Following Diagnosis of Type 2 Diabetes. Diabetes Care. 2021; 44 (11): 2518-2526.

8. Sun JK, Keenan HA, Cavallerano JD, et al. Protection from retinopathy and other complications in patients with type 1 diabetes of extreme duration: the joslin 50-year medallist study. Diabetes Care. 2011 Apr; 34 (4): 968-74.

9. Hirsch IB, Brownlee M. Beyond hemoglobin A1c—need for additional markers of risk for diabetic microvascular complications. JAMA 2010; 303: 2291–2292.

10. Beck RW, Connor CG, Mullen DM, et al. The Fallacy of Average: How Using HbA1c Alone to Assess Glycemic Control Can Be Misleading. Diabetes Care. 2017; 40 (8): 994-999.

11. Jingi, A.M., Tankeu, A.T., Ateba, N.A. et al. Mechanism of worsening diabetic retinopathy with rapid lowering of blood glucose: the synergistic hypothesis. BMC Endocr Disord 2017;17, 63. 

12. Testa R, Bonfigli AR, Prattichizzo F, et al. The “Metabolic Memory” Theory and the Early Treatment of Hyperglycemia in Prevention of Diabetic Complications. Nutrients. 2017; 9 (5): 437.

13. Brown DM, Wykoff CC, Boyer D, et al. Evaluation of intravitreal aflibercept for the treatment of severe nonproliferative diabetic retinopathy: results from the PANORAMA randomized clinical trial. JAMA Ophthalmol. 2021;1 39 (9): 946-955. doi:10.1001/jamaophthalmol.2021.2809

14. Drinkwater JJ, Davis TME, Davis WA. Incidence and predictors of vision loss complicating type 2 diabetes: The Fremantle Diabetes Study Phase II. J Diabetes Complications. 2020; 34 (6): 107560.

15. Emery M, Schorderet DF, Roduit R. Acute hypoglycemia induces retinal cell death in mouse. PLoS One. 2011; 6 (6): e21586.

16. Anwar SB, Asif N, Naqvi SAH, Malik S. Evaluation of multiple risk factors involved in the development of Diabetic Retinopathy. Pak J Med Sci. 2019; 35 (1): 156-160.

17. Smith JP, Cyr LG, Dowd LK, Duchin KS, Lenihan PA, Sprague J. The Veterans Affairs Continuous Positive Airway Pressure Use and Diabetic Retinopathy Study. Optom Vis Sci. 2019; 96 (11): 874-878.

18. Fan YP, Wu CT, Lin JL, et al. Metformin Treatment Is Associated with a Decreased Risk of Nonproliferative Diabetic Retinopathy in Patients with Type 2 Diabetes Mellitus: A Population-Based Cohort Study. J Diabetes Res. 2020 Apr 19;2020:9161039. 

19. Wang B, Wang F, Zhang Y, et al. Effects of RAS inhibitors on diabetic retinopathy: a systematic review and meta-analysis. Lancet Diabetes Endocrinol. 2015; 3 (4): 263-74. doi: 10.1016/S2213-8587(14)70256-6.

20. Kang EY, Chen TH, Garg SJ, et al. Association of Statin Therapy with Prevention of Vision-Threatening Diabetic Retinopathy. JAMA Ophthalmol. 2019; 137 (4): 363-371.

21. Meer E, Bavinger JC, Yu Y, VanderBeek BL. Association of Fenofibrate Use and the Risk of Progression to Vision-Threatening Diabetic Retinopathy. JAMA Ophthalmol. Published online April 07, 2022.

22. Chous AP. How ODs can address patients lost to folllow-up. Optometry Times 2021; 13(1). Accessed April 24, 2022 at https://www.optometrytimes.com/view/how-ods-can-address-patients-lost-to-follow-up

23. Porta M, Curletto G, Cipullo D, et al. Estimating the delay between onset and diagnosis of type 2 diabetes from the time course of retinopathy prevalence. Diabetes Care. 2014; 37 (6): 1668-74.

24. Calvo-Maroto AM, Esteve-Taboada JJ, Pérez-Cambrodí RJ, et al. Pilot Study on Visual Function and Fundus Autofluorescence Assessment in Diabetic Patients. J Ophthalmol. 2016; 2016:1287847. doi: 10.1155/2016/1287847.

25. Diabetic Retinopathy Clinical Research Network, Bressler NM, Miller KM, Beck RW, et al. Observational study of subclinical diabetic macular edema. Eye (Lond). 2012 ;26 (6): 833-40.

26. Ghasemi Falavarjani K, Tsui I, Sadda SR. Ultra-wide-field imaging in diabetic retinopathy. Vision Res. 2017; 139: 187-190.

27. Silva PS, Cavallerano JD, Haddad NM, et al. Peripheral Lesions Identified on Ultrawide Field Imaging Predict Increased Risk of Diabetic Retinopathy Progression over 4 Years. Ophthalmology. 2015 May; 122 (5): 949-56.

28. Chous, AP. Embrace, don’t fear AI in diabetic retinopathy. Optometry Times 2021; 13(5) accessed April 25, 2022 at https://www.optometrytimes.com/view/embrace-don-t-fear-ai-in-diabetic-retinopathy 

29. Storey PP, Murchison AP, Pizzi LT, et al. IMPACT OF PHYSICIAN COMMUNICATION ON DIABETIC EYE EXAMINATION ADHERENCE: Results from a Retrospective Cohort Analysis. Retina. 2016 Jan; 36 (1): 20-7.

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