A GM conference report on Dr Simon Croxson's session from the 8th GM Conference, entitled Managing an Ageing Patient: From Midlife to Beyond.
The comprehensive diagnosis of diabetes in older patients is not always straightforward. Having diagnosed diabetes, it is important to ascertain the type.
It is important to know what we are treating to use optimum treatment and patient presentation can be misleading. For example, patients with Ketosis Prone type 2 diabetes present with diabetic ketoacidosis, but might need just a short course of insulin.1 Other people might have Latent Auto-immune Diabetes of the Adult; this is a slowly progressing form of type 1 diabetes, which may initially resemble type 2 diabetes, but will have an absolute need for insulin in due course.2 Although the type of diabetes is generally clinically apparent, it may help to clarify β-cell function by urinary C-peptide to creatinine ratio; a cut-off of 0.2nmol/mmol usually differentiates type 2 from type 1.
Hypoglycaemia in the older age group is common, poorly recognised and associated with adverse health outcomes. We need to raise professional awareness of hypoglycaemia. What makes it harder for professionals is that hypoglycaemia impairs cerebral function therefore patients are unreliable witnesses and are more likely to underestimate the frequency with which they experience hypoglycaemia. The older person developing hypoglycaemia tends to get sympathetic symptoms at a lower glucose level than younger people, and this level may be similar to the level at which neuroglycopaenia occurs; thus the elderly may be less aware of their hypos.
A survey of consecutive diabetic patients (with a partner or close relative at home) attending hospital clinics, found that patients and their partners disagreed about the frequency and nature of hypoglycaemic episodes, with 20% under-reporting by the patients. Questioning patients alone may not provide an accurate record of hypoglycaemic episode.3
The commonest symptoms of hypoglycaemia in the elderly are believed to be poor concentration, confusion, sweating, and trembling, but also include unsteadiness and light headedness suggesting hypotension. Symptoms may also change over years.
To reduce the risk of hypoglycaemia, relaxation of HbA1c targets has been proposed for frail elderly patients. The European Diabetes Working Party for Older People 2011 suggest a HbA1c target of 7.0–7.5% for non-frail older patients and 7.6–8.5% for the frail.4 The ADA / EASD 2012 guidelines emphasise a holistic approach to the risk and benefit from antihyperglycaemic medication.
In one study, patients 69 years or older with HbA1c values of 8% or greater were evaluated with continuous glucose monitoring for three days. It found that hypoglycaemic episodes were common in older adults even with high HbA1c, and generally asymptomatic. Raising HbA1c goals may not be adequate to prevent hypoglycaemia in this population.5
Another study looked at the complex interrelationship between hypoglycaemia and dementia during 12 years’ follow up of known diabetic people; 61 participants (7.8%) had a reported hypoglycaemic event first, and 148 (18.9%) developed dementia first. Those with a hypo first had a two-fold increased risk for developing dementia and those who developed dementia first, had a three-fold increased risk of future hypoglycaemia.6
Risk factors for hypoglycaemia include a recent change of agent, type of agent, hospitalisation, comorbidities, being an elderly single male, alcohol, cognitive impairment and increasing age. Because of the risk of hypoglycaemia after hospitalisation if taking insulin or sulphonylurea, patients need to be followed up after 4–6 weeks and the importance of an adequate diet must be emphasised.
There is a wide choice of newer oral and injectable therapy for diabetes in older patients including SGLT-2 inhibitors, gliptins, GLP-1 receptor agonists and insulin degludec. Appropriate use should lead to safer care.
1. Umpierrez GE, et al. Ann Intern Med 2006; 144(5): 350–57
2. Cernea S, et al. Diabetes Care 2009; 32: S246-52
3. Heller S, et al. BMJ 1999; 310(6977): 440
5. Munshi MN, et al. Arch Intern Med 2011; 171(4): 362–4
6. Yaffe K, et al. JAMA Intern Med 2013; 173(14): 1300–1306