eMedicine Specialties > Emergency Medicine > Endocrine & Metabolic

Diabetes Mellitus, Type 1 - A Review

Author: Scott R Votey, MD, Director Emergency Medicine Residency, Professor of Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA, Ronald Reagan UCLA Medical Center
Coauthor(s): Anne L Peters, MD, CDE, Director of Clinical Diabetes Programs, Professor, Department of Medicine, University of Southern California, Keck School of Medicine, Los Angeles, California, Los Angeles County/University of Southern California Medical Center
Contributor Information and Disclosures

Updated: Oct 8, 2009

Introduction

Background

Diabetes mellitus is a chronic disease that requires long-term medical attention both to limit the development of its devastating complications and to manage them when they do occur. It is a disproportionately expensive disease; in 2002, the per-capita cost of health care was $13,243 for people with diabetes, while it was $2560 for those without diabetes. The ED utilization rate by people with diabetes is twice that of the unaffected population.¹ This article focuses on the ED evaluation and treatment of the acute and chronic complications of diabetes other than those directly associated with hypoglycemia and severe metabolic disturbances, such as diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). (Please see Hypoglycemia, Diabetic Ketoacidosis, and Hyperosmolar Hyperglycemic State for more information on these disorders.)

Pathophysiology

Type 1 diabetes mellitus can occur at any age and is characterized by the marked and progressive inability of the pancreas to secrete insulin because of autoimmune destruction of the beta cells. It commonly occurs in children, with a fairly abrupt onset; however, newer antibody tests have allowed for the identification of more people with a slower onset adult form of type 1 diabetes mellitus called latent autoimmune diabetes of the adult (LADA).² The distinguishing characteristic of a patient with type 1 diabetes is that, if his or her insulin is withdrawn, ketosis and eventually ketoacidosis develop. Therefore, these patients are dependent on exogenous insulin.

Type 2 diabetes mellitus is discussed in Diabetes Mellitus, Type 2 - A Review. A variety of other types of diabetes, previously called secondary diabetes, are caused by other illnesses or medications. Depending on the primary process involved (eg, destruction of pancreatic beta cells or development of peripheral insulin resistance), these types of diabetes behave similarly to type 1 or type 2 diabetes. The most common are diseases of the pancreas that destroy the pancreatic beta cells (eg, hemochromatosis, pancreatitis, cystic fibrosis, pancreatic cancer), hormonal syndromes that interfere with insulin secretion (eg, pheochromocytoma) or cause peripheral insulin resistance (eg, acromegaly, Cushing syndrome, pheochromocytoma), and diabetes induced by drugs (eg, phenytoin, glucocorticoids, estrogens).

Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. GDM is a complication of approximately 4% of all pregnancies in the United States. Untreated GDM can lead to fetal macrosomia, hypoglycemia, hypocalcemia, and hyperbilirubinemia. In addition, mothers with GDM have increased rates of cesarean delivery and chronic hypertension. To screen for GDM, a 50-g glucose screening test should be done at 24-28 weeks of gestation.¹ This is followed by a 100-g, 3-hour oral glucose tolerance test if the patient's plasma glucose concentration at 1 hour after screening is greater than 140 mg/dL.

Although the pathophysiology of the disease differs between the types of diabetes, most of the complications, including microvascular, macrovascular, and neuropathic, are similar regardless of the type of diabetes.

Frequency

United States

In 2005, people with diabetes were estimated to account for 7% of the US population, or approximately 20.8 million people.² Of these 20.8 million people, 14.6 million have a diagnosis of diabetes, and diabetes is undiagnosed in another 6.2 million. Approximately 5-10% have type 1 diabetes, and 90-95% have type 2, and 1-5% have other types. Additionally, an estimated 54 million people have pre-diabetes.

Pre-diabetes, as defined by the American Diabetes Association, is that state in which blood glucose levels are higher than normal but not high enough to be diagnosed as diabetes. It is presumed that most persons with elevated glucose levels approaching the level needed for the diagnosis of diabetes will subsequently progress to diabetes.

International

Internationally rates of type 1 diabetes are increasing. In Europe, the Middle East, and Australia, rates of type 1 diabetes are increasing by 2-5% per year. Sardinia and Finland have the highest reported incidence of type 1 diabetes.

Mortality/Morbidity

The morbidity and mortality associated with diabetes are related to the short- and long-term complications.

• Complications include hypoglycemia and hyperglycemia, increased risk of infections, microvascular complications (eg, retinopathy, nephropathy), neuropathic complications, and macrovascular disease.
• Diabetes is the major cause of blindness in adults aged 20-74 years, as well as the leading cause of nontraumatic lower-extremity amputation and end-stage renal disease (ESRD).

Race

Whites seem to be affected more often than blacks, who have the lowest overall incidence of type 1 diabetes.

Sex

The male-to-female ratio is approximately 1:1.

Age

Long called juvenile-onset diabetes, type 1 diabetes is typically diagnosed in childhood, adolescence, or early adulthood. Although the onset of type 1 diabetes often occurs early in life, 50% of patients with new-onset type 1 diabetes are older than 20 years of age.

Clinical

History

Correctly determining whether a patient has type 1 or type 2 diabetes is important because patients with type 1 diabetes are dependent on a continuous source of exogenous insulin and carbohydrate for survival. Patients with type 2 diabetes may not need any treatment for hyperglycemia during periods of fasting or decreased oral intake. A patient whose diabetes is controlled with diet or an oral antidiabetic agent clearly has type 2 diabetes. A lean patient who has had diabetes since childhood, who has always been dependent on insulin, or who has a history of DKA almost certainly has type 1 diabetes.

Distinguishing the type of diabetes can be difficult in (1) patients who are treated with insulin and who are younger but clinically appear to have type 2 diabetes and (2) older patients with late onset of diabetes who nonetheless take insulin and seem to share characteristics of patients with type 1 diabetes. (This latter group is now said to have LADA). When in doubt, treat the patient with insulin and closely monitor his or her glucose levels. Some adolescents or young adults, mostly Hispanic or African American patients, presenting as classic DKA are subsequently found to have type 2 diabetes.

See Workup for more information on diagnosis of diabetes. See Diabetes Mellitus, Type 2 - A Review for more information on the asymptomatic patient with diabetes.

Inquire about the type and duration of the patient's diabetes and about the care the patient is receiving for diabetes.

• Type of diabetes: The diagnosis is based on history, therapy, and clinical judgment, as described above.
• Duration of diabetes: The chronic complications of diabetes are related to the length of time the patient has had the disease.
• Diabetes care: Inquire about the type of insulin being used, delivery system (pump vs injections), dose, and frequency. Also ask about oral antidiabetic agents, if any. Patients using a pump or a multiple-injection regimen have a basal insulin (taken through the pump or with the injection of a long-acting insulin analogue) and a premeal rapid-acting insulin, the dose of which is determined as a function of the carbohydrate count plus the correction (to adjust for how high the premeal glucose level is). In these patients, ask about the following:
  • Basal rates (eg, units per hour by pump, generally 0.4-1.5 units/h, may vary based on time of day). Total daily dose as basal insulin is a helpful value to know.
  • Carbohydrate ratio (ie, units of insulin per grams of carbohydrate, generally 1 unit of rapid-acting insulin per 10-15 g carbohydrate)
  • Correction dose (ie, how far the blood glucose level is expected to decrease per unit of rapid-acting insulin, often 1 unit of insulin per 50-mg/dL decrease, but individuals with insulin resistance may need 1 per 25-mg/dL decrease)
  • Some patients may be taking premeal pramlintide.

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 for losing consciousness, this possibility must be addressed, especially if the patient drives.
• Does the patient have diabetic nephropathy that might alter the use of medications or intravenous radiographic contrast material?
• Does the patient have macrovascular disease, such as coronary artery disease (CAD) that should be considered in the ED?
• Treatment monitoring
  • Does the patient self-monitor his or her blood glucose levels? Note the frequency and range of values at each time of day. An increasing number of patients monitor with continuous sensors.
  • When was the patient's hemoglobin A_1c (HbA_1c) value (an indicator of long-term glucose control) last measured? What was it?

As circumstances dictate, additional questions may be warranted.

• Hyperglycemia: Does the patient give a history of recent polyuria, polydipsia, nocturia, or weight loss?
• Hypoglycemia
  • 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.
• Microvascular complications
  • Retinopathy: When was the patient's last dilated eye examination? What were the results?
  • 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?
• Macrovascular complications
  • Hypertension: Does the patient have hypertension? What medications are taken?
  • CAD: Does the patient have CAD?
  • Peripheral vascular disease: Does the patient have symptoms of claudication or a history of vascular bypass?
  • Cerebrovascular disease: Has the patient had a stroke or transient ischemic attack?
  • Hyperlipidemia: What are the patient's most recent lipid levels? Is the patient taking lipid-lowering medication?
• Neuropathy: Does the patient have a history of neuropathy or symptoms of peripheral neuropathy or autonomic neuropathy present (including impotence if the patient is male)?
• Diabetic foot disease: Does the patient have a history of foot ulcers or amputations? Are any foot ulcers present?
• Infections: Are frequent infections a problem? At what site?

Physical

A diabetes-focused physical examination includes an assessment of 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
  • Is the patient hypertensive or hypotensive? Orthostatic vital signs may be useful in assessing the patient's volume status as well as suggesting the presence of an autonomic neuropathy.
  • If the respiratory rate and pattern suggest Kussmaul breathing, DKA must be considered immediately, and appropriate tests obtained.
• Funduscopic examination
  • Funduscopic examination should include a careful view of the retina, including both the optic disc and the macula.
  • 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.
• 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 delay 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.
  • If peripheral neuropathy is found, the patient should be made aware that foot care (including daily foot examination) is very important for the prevention of foot ulcers and lower-extremity amputation.

Causes

• Patients with type 1 diabetes are believed to have a genetic susceptibility to developing the disease.
  • Exposure to a trigger (viral, environmental, toxin) stimulates immunologically mediated destruction of the beta cells.
  • As beta-cell mass declines with ongoing immunologic destruction, insulin secretion decreases until the available insulin no longer is adequate to maintain normal blood glucose levels.
  • After 80-90% of the beta cells are destroyed, hyperglycemia develops and diabetes may be diagnosed.
• In studies of identical twin pairs in which 1 twin has type 1 diabetes, antibodies to the islet cell (IA2) and to insulin (IAA) are positive for several years in the nondiabetic twin before overt diabetes develops.

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