THE IMPACT OF DIABETES ON ALL LAYERS OF TEAR FILM

Diabetes fundamentally disrupts the homeostasis of the tear film – a complex tri-layered structure essential for ocular surface health.¹ Key disruptions noted in diabetic patients include:

• Mucin Layer: Diabetes-induced corneal hypoesthesia reduces the activity of goblet cells, which produce critical mucins. This decreases the wettability of the tear film and promotes ocular surface instability.¹
• Aqueous Layer: Hyperglycaemia causes microvascular damage within the lacrimal gland and diabetic peripheral neuropathy, impairing lacrimal innervation and, consequently, tear production. Patients also exhibit decreased reflex tearing and impaired corneal sensitivity.¹
• Lipid Layer: Meibomian gland dysfunction (MGD), a common comorbidity in diabetic patients, destabilises the outer lipid layer, leading to increased tear evaporation. Mechanisms include epithelial cell loss in the glands, structural abnormalities, and reduced meibum secretion.³
• Epithelial Disruption: Diabetes alters corneal epithelial cells, degrading adhesion properties and the integrity of the epithelium. The impaired neurotrophic support in diabetic patients further exacerbates adhesion disorders and basal membrane irregularity.⁴

These changes cause a destabilised tear film, setting the stage for a wide range of symptoms typical in D-DED.¹

RECOGNISING SYMPTOMS OF D-DED

Pharmacists play a critical role in identifying the hallmark symptoms of D-DED to guide patients toward proper management and medical consultation. D-DED symptoms are wide-ranging and include:

• Dryness, burning, and stinging sensations
• A gritty, sandy, or sticky feeling in the eyes
• Tired, red, and itchy eyes
• Blurred vision and light sensitivity
• Swollen eyelids and discomfort during prolonged screen time or reading.¹

It’s noteworthy that some diabetic patients may remain symptom-free despite significant ocular surface damage, highlighting the importance of proactive care and routine evaluations.¹

TREATMENT: ADDRESSING ALL TYPES OF DRY EYE DISEASE

For comprehensive management of D-DED, multidisciplinary treatment strategies are essential to address varied ocular changes.⁵ Here’s a roadmap for managing all subtypes of dry eye based on the TFOS DEWS II guidelines:

1. Educational Intervention: Patient education on the correlation between D-DED and hyperglycaemia, coupled with dietary improvements, such as increased Omega-3 fatty acid intake, supports clinical outcomes.⁵
2. Artificial Tear Formulations: These remain a cornerstone treatment for symptom relief. Advanced preservative-free options stabilise the tear film, enhance contrast sensitivity, and ensure ocular surface protection.⁵
3. Stepwise Approach per TFOS DEWS II:

• Step 1: Promote regular lid hygiene and ocular surface moisture.
• Step 2: Employ non-preserved artificial tears and anti-inflammatories. Punctal occlusions may also be beneficial.
• Step 3: For severe symptoms, introduce autologous serum tears, oral secretagogues, or therapeutic lenses.
• Step 4: Advance to procedural interventions such as amniotic membrane grafts or punctal occlusions as needed.⁵

Strategically choosing interventions that address both aqueous-deficient and evaporative DEDs is central to symptom resolution.⁵ Pharmacists must understand the mechanistic roles of these treatments to guide recommendations effectively.

RECOGNISING SYMPTOMS OF D-DED

Pharmacists play a critical role in identifying the hallmark symptoms of D-DED to guide patients toward proper management and medical consultation. D-DED symptoms are wide-ranging and include:

• Dryness, burning, and stinging sensations
• A gritty, sandy, or sticky feeling in the eyes
• Tired, red, and itchy eyes
• Blurred vision and light sensitivity
• Swollen eyelids and discomfort during prolonged screen time or reading.¹

It’s noteworthy that some diabetic patients may remain symptom-free despite significant ocular surface damage, highlighting the importance of proactive care and routine evaluations.¹