This is what eye care providers need to know about type 1 diabetes

Understanding and acknowledging patient fears of hypoglycemia, good awareness of diabetes management strategies/technologies, plus consistent and reciprocal communication between optometrists and other members of the diabetes care team (including patients, caregivers, and health care providers) can have a tremendous role in patient and family quality of life while mitigating the risk of vision loss. (Adobe Stock / (JLco) Julia Amaral)

Autoimmune type 1 diabetes (T1D) affects 1.6 million Americans and about 9 million individuals worldwide.¹ More than 40% of patients receive diagnoses after age 30 years,² and incidence according to the JDRF (Juvenile Diabetes Research Foundation) is split evenly between those older than 18 years with newly diagnosed T1D and those who were 18 years or younger when they received the diagnosis (110/d in each age bracket).³ So, using juvenile diabetes to refer to T1D is incorrect.

Even though all patients with T1D require exogenous insulin for survival, approximately 30% of patients with type 2 diabetes (T2D) also require insulin therapy due to a progressive insulin secretory defect,⁴ so that using the term insulin-dependent diabetes to refer exclusively to T1D is also incorrect. Every scientific body recommends that these anachronistic terms be avoided, although their use remains common when reviewing lay and medical presentations. Semantic arguments aside, T1D is one of the most common, chronic diseases affecting pediatric populations.⁵

T1D results from lymphocytic destruction of the insulin-producing pancreatic β cells, predominantly located within the islets of Langerhans (some residual β cells have been found in the pancreatic ducts of even those with long-term T1D).⁶

T1D is divided into 3 stages: stage 1 occurs when multiple islet cell autoantibodies are present but normal insulin production remains with intact β cells; stage 2 refers to autoantibodies with reduced but sufficient β-cell mass and insulin secretion to maintain relatively normal glucose homeostasis, but with impaired glucose tolerance (eg, elevated blood glucose after a high-carbohydrate meal); and stage 3 results when β-cell loss reaches a level where glucose homeostasis is no longer possible, resulting in profound hyperglycemia and classic symptoms. The recently approved anti-CD3 monoclonal antibody teplizumab (Tzield; Provention Bio/Sanofi) delays progression from stage 2 to stage 3 T1D by a median of 2 years by mitigating, but not eliminating, autoimmune destruction of β cells.⁷

Most patients receive diagnosis with classic symptom onset, including polyuria, polydipsia, and polyphagia with weight loss. If hyperglycemia is not corrected promptly, diabetic ketoacidosis (DKA) results with marked nausea, abdominal pain, and emesis. DKA remains the leading cause of death in children with T1D⁸ due to lack of timely diagnosis and, importantly, insulin omission in adolescence and early adulthood, frequently to induce weight loss as part of what is termed “diabulimia.” Insulin omission and diabulimia are thought to affect as many as 15% of patients with T1D, with higher risk among adolescents; females; and those with anxiety, depression, and body dissatisfaction (body dysmorphic disorder).⁹ These critical and typically obvious presenting symptoms should be top of mind for every health care provider, including optometrists seeing higher-risk patients with T1D, as the probability of vascular complications and premature death is vastly higher in this population.¹⁰

In addition to the classic symptoms and signs of incident and acutely uncontrolled T1D, commonly encountered problems seen in the optometric office include large refractive shifts, crystalline lens fluid swelling, and even cataract formation (often reversible if hyperglycemia is corrected quickly).¹¹ I am often asked about prescribing refractive correction for patients with marked hyperglycemia and have found that spot glucose testing less than 180 mg/dL at time of refraction and recent glycated hemoglobin value of less than 8.0% typically result in consistent refraction and visual function, although I have encountered exceptions and, ideally, will recommend patients achieve target glucose values of HbA1c of 7.5% of less and glucose time-in-range using continuous glucose monitoring greater than 70%.

American Diabetes Associationguidelines call for patients with T1D to receive dilated retinal examination within 5 years of diagnosis and annually thereafter, with flexibility to extend the examination interval up to 2 years if there is no evidence of diabetic retinopathy (DR) during previous annual examinations.¹² If DR is present, at least annual examinations are recommended with shortened surveillance intervals as DR severity progresses, or with pregnancy, as both are known risk factors for DR progression to sight-threatening retinopathy (STR).

I recommend my patients with T1D, including pediatric patients, receive at least annual dilated eye examinations soon after diagnosis to impress upon them and their parents/caregivers the importance of routine eye care, to acclimate them to dilation (I often use just 0.5% tropicamide in children with large pupils), and to educate everyone about the asymptomatic nature of DR at its earliest stages. I use retinal images to pique the interest of adults and children and stress the profound impact of good diabetes control before the development of any DR for maintaining healthy eyes given “metabolic memory” demonstrated in every long-term diabetes study. To put a finer point on this notion, I convey the findings of the Joslin Medalist Study of patients living with T1D for 50 or more years, showing that those who get through the first 20 years of diabetes without STR were quite unlikely to develop STR in ensuing years—early, good blood glucose control pays off years down the line just like compound interest.¹³

Data demonstrate that DR and STR develop more often and sooner in patients with T1D than those with T2D, with about 20% vs 10% of patients developing proliferative diabetic retinopathy and/or diabetic macular edema after 20 years, respectively.¹⁴ Nonetheless, the majority of STR occurs in T2D given its much higher prevalence, and children who develop T2D—an increasing problem given pediatric obesity and sedentary lifestyle—are at higher lifetime risk for all vascular diabetes complications given longer anticipated life span compared with adults who develop T2D.¹⁵ It is also important to realize that about 30% of adult patients with T1D develop secondary insulin resistance¹⁶ due to aging and excess food intake, accompanied by higher insulin dosing to maintain reasonable glucose control, resulting in deposition of abdominal fat that is a hallmark of T2D—a phenomenon sometimes called “double” or “type 1.5” diabetes. To this end, appropriate food/caloric intake and physical activity are just as important for maintaining insulin sensitivity as they are for assisting with blood glucose control in patients with T1D.

Figure 1. Example of an automated insulin delivery system combining a tubeless insulin pump (a) with a continuous glucose sensor (b) and an artificial intelligence algorithmic display (c) with key metrics like current blood glucose, blood glucose change rate (arrow on display), insulin on-board (IOB; unutilized active insulin within the patient based on drug half-life), and last bolus delivered. (Images courtesy of A. Paul Chous, OD, MA, FAAO)

Newer diabetes management technologies open the possibility of maintaining near-normal blood glucose control better and sooner than before. These technologies include continuous subcutaneous insulin infusion (insulin pumps), continuous glucose monitors (CGM), semiclosed loop automated insulin delivery (AID) systems with communication between the pump and CGM (Figure 1), individualized diabetes management algorithms for carbohydrate counting and insulin dosage decisions, and super fast-acting human insulin analogs (eg, Fiasp; Novo Nordisk, and Lyumjev; Lilly) allowing more rapid correction of hyperglycemia than traditional “fast-acting insulins” (eg, aspart and lispro). These technologies also reduce the risk of disabling hypoglycemia, the fear of which prevents some patients from achieving good metabolic control of their diabetes for years, often after the development of DR and other complications.¹⁷

Optometrists should be familiar with these technologies and advocate for their consideration and prescription by PCPs and endocrinologists alike in patients with T1D, especially underserved patients of color, lower socioeconomic status, and those living in rural areas where these advancements are used significantly less often.¹⁸ And because T1D is a challenging condition to manage well and consistently—replete with hundreds of self-care decisions required every day¹⁹—it’s critical for optometrists to empathize, educate, and advocate for all our patients living with diabetes to help them navigate through an often-labyrinthine health care system.

Understanding and acknowledging patient fears of hypoglycemia, good awareness of diabetes management strategies/technologies, plus consistent and reciprocal communication between optometrists and other members of the diabetes care team (including patients, caregivers, and health care providers) can have a tremendous role in patient and family quality of life while mitigating the risk of vision loss.

References

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2. Thomas NJ, Jones SE, Weedon MN, Shields BM, Oram RA, Hattersley AT. Frequency and phenotype of type 1 diabetes in the first six decades of life: a cross-sectional, genetically stratified survival analysis from UK Biobank. Lancet Diabetes Endocrinol. 2018;6(2):122-129. doi:10.1016/S2213-8587(17)30362-5

3. JDRF your way: About JDRF. JDRF. Accessed July 19, 2023. https://www2.jdrf.org/site/SPageServer?pagename=diy_about_us

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11. Chous AP. Diabetic Eye Disease: Lessons from a Diabetic Eye Doctor. Fairwood Press; 2004.

12. American Diabetes Association. Standards of Medical Care in Diabetes-2022 Abridged for Primary Care Providers. Clin Diabetes. 2022;40(1):10-38. doi:10.2337/cd22-as01

13. 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 medalist study. Diabetes Care. 2011;34(4):968-974. doi:10.2337/dc10-1675

14. 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):556-564. doi:10.2337/dc11-1909

15. TODAY Study Group; Bjornstad P, Drews KL, Caprio S, et al. Long-term complications in youth-onset type 2 diabetes. N Engl J Med. 2021;385(5):416-426. doi:10.1056/NEJMoa2100165

16. Pathak V, Mishra I, Baliarsinha AK, Choudhury AK. Prevalence of insulin resistance in type 1 diabetes mellitus and its correlation with metabolic parameters: the double trouble. Eurasian J Med. 2022;54(2):107-112. doi:10.5152/eurasianjmed.2022.21039

17. Shepard JA, Vajda K, Nyer M, Clarke W, Gonder-Frederick L. Understanding the construct of fear of hypoglycemia in pediatric type 1 diabetes. J Pediatr Psychol. 2014;39(10):1115-1125. doi:10.1093/jpepsy/jsu068

18. Fantasia KL, Wirunsawanya K, Lee C, Rizo I. Racial disparities in diabetes technology use and outcomes in type 1 diabetes in a safety-net hospital. J Diabetes Sci Technol. 2021;15(5):1010-1017. doi:10.1177/1932296821995810

19. Montali L, Zulato E, Cornara M, Ausili D, Luciani M. Barriers and facilitators of type 1 diabetes self-care in adolescents and young adults. J Pediatr Nurs. 2022;62:136-143. doi:10.1016/j.pedn.2021.09.014