Type 2 Diabetes Mellitus Clinical Presentation

Updated: May 01, 2023
  • Author: Romesh Khardori, MD, PhD, FACP; Chief Editor: George T Griffing, MD  more...
  • Print


The diagnosis of diabetes mellitus is readily entertained when a patient presents with classic symptoms (ie, polyuria, polydipsia, polyphagia, weight loss). Other symptoms that may suggest hyperglycemia include blurred vision, lower extremity paresthesias, or yeast infections, particularly balanitis in men. However, many patients with type 2 diabetes are asymptomatic, and their disease remains undiagnosed for many years.

In older studies, the typical patient with type 2 diabetes had diabetes for at least 4-7 years at the time of diagnosis. [152] Among patients with type 2 diabetes in the United Kingdom Prospective Diabetes Study, 25% had retinopathy; 9%, neuropathy; and 8%, nephropathy at the time of diagnosis. (For more information, see Diabetic Neuropathy.)

Patients with established diabetes

In patients with known type 2 diabetes, inquire about the duration of the patient's diabetes and about the care the patient is currently receiving for the disease. The duration of diabetes is significant because the chronic complications of diabetes are related to the length of time the patient has had the disease.

A focused diabetes history should also include the following questions:

  • Is the patient's diabetes generally well controlled (with near-normal blood glucose levels) - Patients with poorly controlled blood glucose levels heal more slowly and are at increased risk for infection and other complications

  • Does the patient have severe hypoglycemic reactions - If the patient has episodes of severe hypoglycemia and therefore is at risk of losing consciousness, this possibility must be addressed, especially if the patient drives or has significant underlying neuropathy or cardiovascular disease

  • Does the patient have diabetic nephropathy that might alter the use of medications or intravenous (IV) radiographic contrast material

  • Does the patient have macrovascular disease, such as coronary artery disease (CAD) that should be considered as a source of acute symptoms

  • Does the patient self-monitor his or her blood glucose levels - If so, note the frequency and range of values at each time of day

  • When was the patient's hemoglobin A1c (HbA1c; an indicator of long-term glucose control) last measured, and what was it

  • What is the patient’s immunization history - Eg, influenza, pneumococcal, hepatitis B, tetanus, herpes zoster

As circumstances dictate, additional questions may be warranted, as follows:

  • Does the patient give a history of recent polyuria, polydipsia, nocturia, or weight loss - These are symptoms of hyperglycemia

  • Has the patient had episodes of unexplained hypoglycemia - If so, when, how often, and how does the patient treat these episodes

  • Does the patient have hypoglycemia unawareness (ie, does the patient lack the adrenergic warning signs of hypoglycemia) - Hypoglycemia unawareness indicates an increased risk of subsequent episodes of hypoglycemia

  • Regarding retinopathy, when was the patient's last dilated eye examination, and what were the results

  • Regarding nephropathy, does the patient have known kidney disease; what were the dates and results of the last measurements of urine protein and serum creatinine levels

  • Does the patient have hypertension (defined as a blood pressure of 130/80 mm Hg or higher); what medications are taken

  • Does the patient have CAD

  • Regarding peripheral vascular disease, does the patient have claudication or a history of vascular bypass

  • Has the patient had a stroke or transient ischemic attack

  • What are the patient's most recent lipid levels; is the patient taking lipid-lowering medication

  • Does the patient have a history of neuropathy or are symptoms of peripheral neuropathy or autonomic neuropathy present (including impotence if the patient is male)

  • Does the patient have a history of foot ulcers or amputations; are any foot ulcers present

  • Are frequent infections a problem; at what site

Dawn phenomenon

The Dawn phenomenon, defined as a blood glucose increase of over 20 mg/dL occurring at the end of the night, appears to be common in type 2 diabetes. In a study of 248 noninsulin-treated patients with type 2 diabetes who underwent continuous glucose monitoring for 2 consecutive days, approximately half were found to have the dawn phenomenon. [153, 154] Patients with the dawn phenomenon had HbA1c levels and 24-hour mean glucose values that were significantly higher than in other patients, the mean differences being 4.3 mmol/mol for HbA1c (0.39%) and 12.4 mg/dL for average 24-hour glucose concentrations. Mean 24-hour glucose did not significantly differ between patients treated with diet alone and those treated with oral antihyperglycemic agents (ie, oral antidiabetic drugs did not eliminate the dawn phenomenon). [153, 154]


Physical Examination

Early in the course of diabetes mellitus, the physical examination findings are likely to be unrevealing. Ultimately, however, end-organ damage may be observed. Potential findings are listed in the image below.

Possible physical examination findings in patients Possible physical examination findings in patients with type 2 diabetes mellitus.

A diabetes-focused examination includes vital signs, funduscopic examination, limited vascular and neurologic examinations, and a foot assessment. Other organ systems should be examined as indicated by the patient's clinical situation.

Assessment of vital signs

Baseline and continuing measurement of vital signs is an important part of diabetes management. In addition to vital signs, measure height, weight, and waist and hip circumferences.

In many cases, blood pressure measurement will disclose hypertension, which is particularly common in patients with diabetes. Patients with established diabetes and autonomic neuropathy may have orthostatic hypotension. Orthostatic vital signs may be useful in assessing volume status and in suggesting the presence of an autonomic neuropathy.

If the respiratory rate and pattern suggest Kussmaul respiration, diabetic ketoacidosis (DKA) must be considered immediately, and appropriate tests ordered. DKA is more typical of type 1 diabetes, but it can occur in type 2.

Funduscopic examination

The funduscopic examination should include a careful view of the retina. The optic disc and the macula should be visualized. If hemorrhages or exudates are seen, the patient should be referred to an ophthalmologist as soon as possible. Examiners who are not ophthalmologists tend to underestimate the severity of retinopathy, especially if the patients' pupils are not dilated.

Whether patients develop diabetic retinopathy depends on the duration of their diabetes and on the level of glycemic control maintained. [155, 156] Because the diagnosis of type 2 diabetes often is delayed, 20% of these patients have some degree of retinopathy at diagnosis. The following are the 5 stages in the progression of diabetic retinopathy:

  • Dilation of the retinal venules and formation of retinal capillary microaneurysms

  • Increased vascular permeability

  • Vascular occlusion and retinal ischemia

  • Proliferation of new blood vessels on the surface of the retina

  • Hemorrhage and contraction of the fibrovascular proliferation and the vitreous

The first 2 stages of diabetic retinopathy are known as background or nonproliferative retinopathy. Initially, the retinal venules dilate, then microaneurysms (tiny red dots on the retina that cause no visual impairment) appear. As the microaneurysms or retinal capillaries become more permeable, hard exudates appear, reflecting the leakage of plasma.

Larger retinal arteriolar and venular calibres have been associated with lower scores on memory tests but not with lower scores on other cognitive tests. [157] This association was strong in men. Impaired arteriolar autoregulation may be an underlying mechanism of memory decrements.

Rupture of intraretinal capillaries results in hemorrhage. If a superficial capillary ruptures, a flame-shaped hemorrhage appears. Hard exudates are often found in partial or complete rings (circinate pattern), which usually include multiple microaneurysms. These rings usually mark an area of edematous retina. The patient may not notice a change in visual acuity unless the center of the macula is involved.

Macular edema can cause visual loss; therefore, all patients with suspected macular edema must be referred to an ophthalmologist for evaluation and possible laser therapy. Laser therapy is effective in decreasing macular edema and preserving vision but is less effective in restoring lost vision. (For more information, see Macular Edema in Diabetes.)

Preproliferative and proliferative diabetic retinopathy are the next stages in the progression of the disease. Cotton-wool spots can be seen in preproliferative retinopathy. These represent retinal microinfarcts caused by capillary occlusion; they appear as patches that range from off-white to gray, and they have poorly defined margins.

Proliferative retinopathy is characterized by neovascularization, or the development of networks of fragile new vessels that often are seen on the optic disc or along the main vascular arcades. The vessels undergo cycles of proliferation and regression. During proliferation, fibrous adhesions develop between the vessels and the vitreous. Subsequent contraction of the adhesions can result in traction on the retina and retinal detachment. Contraction also tears the new vessels, which hemorrhage into the vitreous.

Patients with preproliferative or proliferative retinopathy must immediately be referred for ophthalmologic evaluation because laser therapy is effective in this condition, especially before actual hemorrhage occurs.

Often, the first hemorrhage is small and is noted by the patient as a fleeting, dark area, or "floater," in the field of vision. Because subsequent hemorrhages can be larger and more serious, the patient should be referred immediately to an ophthalmologist for possible laser therapy. Patients with retinal hemorrhage should be advised to limit their activity and keep their head upright (even while sleeping), so that the blood settles to the inferior portion of the retina, thus obscuring less central vision.

Patients with active proliferative diabetic retinopathy are at increased risk of retinal hemorrhage if they receive thrombolytic therapy; therefore, this condition is a relative contraindication to the use of thrombolytic agents.

One study has shown that individuals with gingival hemorrhaging have a high prevalence of retinal hemorrhage. [158] Much of this association is driven by hyperglycemia, making it possible to use gingival tissue to study the natural course of microvascular disease in patients with diabetes.

Foot examination

The dorsalis pedis and posterior tibialis pulses should be palpated and their presence or absence noted. This is particularly important in patients who have foot infections, because poor lower-extremity blood flow can slow healing and increase the risk of amputation.

Documenting lower-extremity sensory neuropathy is useful in patients who present with foot ulcers because decreased sensation limits the patient's ability to protect the feet and ankles. This can be assessed with the Semmes Weinstein monofilament or by assessment of reflexes, position, and/or vibration sensation.

If peripheral neuropathy is found, the patient should be made aware that foot care (including daily foot examination) is very important for preventing foot ulcers and avoiding lower-extremity amputation. (For more information, see Diabetic Foot and Diabetic Foot Infections.)

Differentiation of type 2 from type 1 diabetes

Type 2 diabetes mellitus can usually be differentiated from type 1 diabetes mellitus on the basis of history and physical examination findings and simple laboratory tests (see Workup: Tests to Differentiate Type 2 and Type 1 Diabetes). Patients with type 2 diabetes are generally obese, and may have acanthosis nigricans and/or hirsutism in conjunction with thick necks and chubby cheeks.