Clinical presentation of diabetes

The clinical presentation of diabetes is heterogeneous, ranging from asymptomatic type 2 diabetes to the dramatic life-threatening conditions of diabetic ketoacidosis (DKA) and hyperosmolar non-ketotic coma (HONK). Patients with type 2 diabetes are often detected by opportunistic screening such as urinalysis or routine blood glucose tests in general practice, at health insurance checks or during attendance at hospital for an unrelated problem. This heterogeneity in presentation reflects not only the relevant diagnostic category into which the patient falls (type 1 or type 2), but also the point in the natural history of the disorder at which the diagnosis is made. Patients may present with macrovascular complications or the specific microvascular complications of diabetes.

History and initial physical examination

Having obtained a detailed history, a physical examination should be undertaken (Table 2.3). The consultation should take place in appropriate and comfortable circumstances.

Table 2.3 Components of the comprehensive diabetes evaluation

Physical examination of the patient with newly presenting type 1 diabetes is usually unremarkable, although there may be evidence of recent weight loss and occasionally signs compatible with dehydration. Features of orogenital candidiasis or cutaneous sepsis are not uncommon, but are non-specific. The presence of vitiligo is consistent with the presence of autoimmune disease.

Screening for diabetes

There has been a significant increase in our understanding of the pathogenesis of type 1 diabetes. Approximately 10% of patients have a first-degree relative with type 1 diabetes and therefore subjects at high risk could be identified using a combination of immune, genetic and metabolic markers. However, even in high risk groups, screening is imperfect and the complex methodology is not available other than for clinical trials.

In the UK Prospective Diabetes Study (UKPDS), the severity of diabetes-related tissue damage correlated with the glycated haemoglobin (HbA1c) concentration at diagnosis of type 2 diabetes. Thus, there is the prospect that earlier intervention in patients identified by screening of asymptomatic at-risk individuals may prevent or retard chronic diabetic complications. Type 2 diabetes satisfies some of the major criteria for a disorder for which screening would be appropriate. However, there is little evidence to suggest that population screening is cost effective. It is appropriate to screen ’at risk’ groups (see Section 1).

Who makes the diagnosis?

Blood glucose and urine testing are valuable pointer to diabetes. Although glucose oxidase test strips are specific for glucose, glycosuria does not invariably indicate the presence of diabetes; the converse is also true.

In the UK, the diagnosis of diabetes is most commonly made in the GP’s surgery. Routine checks, insurance medicals and consultations with opticians or urologists also highlight cases of type 2 diabetes. Diagnosis on the coronary care unit following an acute myocardial infarction is not uncommon. Less commonly, the diagnosis is made when the patient presents with an established complication such as an infected neuropathic foot lesion or symptomatic diabetic retinopathy.

Most often, the diagnosis of diabetes relies on osmotic symptoms plus an increased laboratory blood glucose level, which can be fasting (≥ 7 mmol/L) or random (≥ 11.1 mmol/L).

Initial management

Having confirmed the diagnosis of diabetes, the crucial clinical question is whether insulin treatment is required. In the young patient with acute osmotic symptoms, weight loss and ketonuria, the decision to start insulin is straightforward. Similarly, the overweight or obese middle-aged or elderly patient with minor symptoms will usually be a candidate for a trial of dietary manipulation followed by metformin. In reality very few patients (< 20%) manage with diet alone for the usually advised period of 3 months.

Other oral agents including sulphonylureas, pioglitazone, gliptins etc. can be used from diagnosis, in addition to appropriate dietary measures.

Most importantly, the patient should be treated according to clinical need. However, an attempt should be made to place the patient with diabetes within the classification system. Often this assignment to a particular category is not possible with certainty and becomes clear only later. Initial therapy, therefore, does not necessarily confirm the aetiology. The difficulty at diagnosis centres on the degree of endogenous insulin deficiency, the rate of β-cell deterioration, the degree of insulin resistance and the presence of any intercurrent illness. Thus, patients with what proves ultimately to be type 1 diabetes will sometimes be treated with a trial of oral antidiabetic drugs, usually because the clinical and biochemical features were not classical; conversely, patients with type 2 diabetes may need insulin temporarily at diagnosis, especially if there is significant intercurrent illness.

It can sometimes be difficult to decide whether a newly presenting, middle-aged, non-obese patient with moderately severe hyperglycaemia has type 2 diabetes that will respond adequately to oral antidiabetic agents or whether the patient would be better treated with insulin from the outset. In this context, it should be remembered that, although relatively uncommon in the elderly, type 1 diabetes might present at any age.

The situation is complicated by increasing awareness of subtypes of diabetes in which insulin deficiency appears to be the predominant feature but which present less dramatically than classical type 1 diabetes. Moreover, even the presence of morbid obesity does not guarantee a diagnosis of type 2 diabetes; occasionally, obese patients present with marked osmotic symptoms and/or ketonuria indicative of insulin dependence.

Identification of patients with apparently autoimmune diabetes with a relatively slow onset can be problematic; the prevalence of latent autoimmune diabetes in adults (LADA) is not known but is perhaps under diagnosed (see Section 1). The diagnosis is often made retrospectively (glutamic acid dehydrogenase (GAD) + ve, anti-islet cell + ve) following the rapid failure of treatment with oral antidiabetic agents (see Section 3, p. 97). Useful clinical pointers at diagnosis suggesting that insulin may be required include:

Dietary manipulation ± oral agents may sometimes initially produce dramatic improvements. The issue of insulin dependence is particularly difficult in African Caribbean patients who may present with ketosis, even DKA, yet who ultimately prove to have diabetes that is controllable with oral agents or even diet alone.

Personal telephone contact is best to ensure that insulin treatment is initiated with the minimum of delay.

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