Nursing Management: Diabetes Mellitus



Nursing Management


Diabetes Mellitus


Janice Lazear




Learning Outcomes



1. Describe the pathophysiology and clinical manifestations of diabetes mellitus.


2. Differentiate between type 1 and type 2 diabetes mellitus.


3. Describe the collaborative care of the patient with diabetes mellitus.


4. Describe the role of nutrition and exercise in the management of diabetes mellitus.


5. Discuss the nursing management of a patient with newly diagnosed diabetes mellitus.


6. Describe the nursing management of the patient with diabetes mellitus in the ambulatory and home care settings.


7. Relate the pathophysiology of acute and chronic complications of diabetes mellitus to the clinical manifestations.


8. Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetes mellitus.



Key Terms
















Reviewed by Teressa Sanders Hunter, RN, PhD, Assistant Professor, Langston University, School of Nursing and Health Professions, Langston, Oklahoma; Jane Faith Kapustin, PhD, CRNP, BC-ADM, FAANP, Associate Professor and Assistant Dean for the Master’s and DNP Programs and Faculty Practice as Adult NP, Medical Center for Diabetes and Endocrinology, Baltimore, Maryland; Nancy Karnes, RN, MSN, CCRN, CDE, Faculty Nursing Program, Bellevue College, Bellevue, Washington; Lorraine Nowakowski-Grier, MSN, APRN, BC, CDE, Diabetes Nurse Practitioner, Christiana Care Health Services, Newark, Delaware; Susan A. Sandstrom, RN, MSN, BC, CNE, Associate Professor in Nursing (retired), College of Saint Mary, Omaha, Nebraska; and Elaine K. Strouss, RN, MSN, Associate Professor of Nursing, Community College of Beaver County, Monaca, Pennsylvania.


This chapter discusses the pathophysiology, clinical manifestations, complications, and collaborative care of diabetes mellitus. The nurse’s role in teaching to promote patient management of diet, activities, and drugs for good control of diabetes is emphasized.




Diabetes Mellitus


Diabetes mellitus (DM) is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both. Diabetes mellitus is a serious health problem throughout the world, and its prevalence is rapidly increasing. Currently in the United States an estimated 25.8 million people, or 8.3% of the population, have diabetes mellitus, and 79 million more people have prediabetes.1 Approximately 7 million people with diabetes mellitus have not been diagnosed and are unaware that they have the disease. Diabetes mellitus is the seventh leading cause of death in the United States, but it is likely to be underreported. The annual cost of diabetes exceeds $174 billion, with $116 billion in direct medical costs.2




image eNursing Care Plan 49-1   Patient With Diabetes Mellitus













































Nursing Diagnosis* Ineffective self-health management related to deficient knowledge of diabetes management and lack of adherence to diabetes management plan as evidenced by inaccurate statements regarding diabetes and its management and stated confusion regarding the pathophysiology of diabetes
Patient Goals 
Outcomes (NOC) Interventions (NIC) and Rationales

Teaching: Disease Process


• Appraise the patient’s current level of knowledge related to specific disease process to determine the scope and extent of required teaching.


• Describe the disease process.


• Discuss rationale behind management/therapy/treatment recommendations to enable patient to better understand rationale behind treatment regimen and lifestyle changes.


• Instruct patient on measures to prevent/minimize symptoms to promote management of disease.


• Discuss lifestyle changes that may be required to prevent future complications and/or control the disease process to encourage patient to actively participate in determining changes that will be acceptable.


• Describe possible chronic complications to increase awareness of the long-term effects of disease process.


• Instruct the patient on which signs and symptoms to report to health care provider to ensure prompt treatment.


• Refer the patient to local community agencies/support groups to provide continuing support and education.

Nursing Diagnosis Risk for unstable blood glucose levels related to inadequate blood glucose monitoring and lack of adherence to diabetes management plan
Patient Goal Maintains a balance of nutrition, activity, and insulin availability that results in stable, normal blood glucose levels
Outcomes (NOC) Interventions (NIC) and Rationales



Nursing Diagnosis Risk for injury related to decreased tactile sensation, episodes of hypoglycemia
Patient Goals 
Outcomes (NOC) Interventions (NIC) and Rationales

Teaching: Foot Care


• Provide information regarding the relationship between neuropathy, injury, and vascular disease and the risk for ulceration and lower extremity amputation in persons with diabetes to promote preventive measures.


• Caution about potential sources of injury to the feet (e.g., heat, cold, cutting corns or calluses, chemicals, use of strong antiseptics or astringents, use of adhesive tape, and going barefoot or wearing thongs or open-toe shoes).


• Recommend daily foot inspection over all surfaces and between the toes looking for redness, swelling, warmth, dryness, maceration, tenderness, or open areas to identify and provide early treatment of foot lesions.


• Instruct individual to inspect inside of shoes daily for foreign objects, nail points, torn linings, and rough areas to avoid injury by factors that are not felt.


• Recommend daily washing of feet using warm water and mild soap to remove irritants.


• Recommend specialist care for thick fungal or ingrown toenails, corns, or calluses to ensure safe treatment of feet.


Nursing Diagnosis Risk for peripheral neurovascular dysfunction related to vascular effects of diabetes
Patient Goals 
Outcomes (NOC) Interventions (NIC) and Rationales

Circulatory Care: Arterial Insufficiency


• Perform a comprehensive appraisal of peripheral circulation (e.g., check peripheral pulses, edema, capillary refill, color, and temperature) to establish baseline findings.


• Inspect skin for arterial ulcers or tissue breakdown to provide treatment to prevent infection and additional necrosis.


• Protect the extremity from injury (e.g., sheepskin under feet and lower legs, footboard/bed cradle at foot of bed; well-fitted shoes) to prevent conditions that favor skin breakdown.


• Maintain adequate hydration to decrease blood viscosity.


• Encourage the patient to exercise as tolerated to increase peripheral circulation.


• Instruct the patient on factors that interfere with circulation (e.g., smoking, restrictive clothing, exposure to cold temperatures, crossing of legs and feet).


• Instruct the patient on proper foot care (see Table 49-21).



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*Nursing diagnoses listed in order of priority.





The long-term complications of diabetes make it a devastating disease. Diabetes is the leading cause of adult blindness, end-stage kidney disease, and nontraumatic lower limb amputations. It is also a major contributing factor to heart disease and stroke. Adults with diabetes have heart disease death rates two to four times higher than adults without diabetes. The risk for stroke is also two to four times higher among people with diabetes. In addition, it is estimated that 67% of adults with diabetes have hypertension.1



Etiology and Pathophysiology


Current theories link the causes of diabetes, singly or in combination, to genetic, autoimmune, and environmental factors (e.g., virus, obesity). Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor utilization of the insulin that is available.


The American Diabetes Association (ADA) recognizes four different classes of diabetes. The two most common are type 1 and type 2 diabetes mellitus (Table 49-1). The two other classes are gestational diabetes and other specific types of diabetes with various causes.



TABLE 49-1


COMPARISON OF TYPE 1 AND TYPE 2 DIABETES MELLITUS




























































Factor Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus
Age at onset More common in young people but can occur at any age. Usually age 35 yr or older but can occur at any age.
Incidence is increasing in children.
Type of onset Signs and symptoms usually abrupt, but disease process may be present for several years. Insidious, may go undiagnosed for years.
Prevalence Accounts for 5%-10% of all types of diabetes. Accounts for 90%-95% of all types of diabetes.
Environmental factors Virus, toxins. Obesity, lack of exercise.
Primary defect Absent or minimal insulin production. Insulin resistance, decreased insulin production over time, and alterations in production of adipokines.
Islet cell antibodies Often present at onset. Absent.
Endogenous insulin Absent. Initially increased in response to insulin resistance. Secretion diminishes over time.
Nutritional status Thin, normal, or obese. Frequently overweight or obese. May be normal.
Symptoms Polydipsia, polyuria, polyphagia, fatigue, weight loss. Frequently none, fatigue, recurrent infections. May also experience polyuria, polydipsia, and polyphagia.
Ketosis Prone at onset or during insulin deficiency. Resistant except during infection or stress.
Nutritional therapy Essential. Essential.
Insulin Required for all. Required for some. Disease is progressive and insulin treatment may need to be added to treatment regimen.
Vascular and neurologic complications Frequent. Frequent.


Normal Insulin Metabolism.

Insulin is a hormone produced by the β cells in the islets of Langerhans of the pancreas. Under normal conditions, insulin is continuously released into the bloodstream in small pulsatile increments, with increased release when food is ingested (Fig. 49-1). Insulin lowers blood glucose and facilitates a stable, normal glucose range of approximately 70 to 120 mg/dL (3.9 to 6.66 mmol/L). The average amount of insulin secreted daily by an adult is approximately 40 to 50 U, or 0.6 U/kg of body weight.


image
FIG. 49-1 Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell. The rise in plasma insulin after a meal stimulates storage of glucose as glycogen in liver and muscle, inhibits gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis. For this reason insulin is an anabolic, or storage, hormone. The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue.


Skeletal muscle and adipose tissue have specific receptors for insulin and are considered insulin-dependent tissues. Insulin is required to “unlock” these receptor sites, allowing the transport of glucose into the cells to be used for energy. Other tissues (e.g., brain, liver, blood cells) do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function. Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate hepatic uptake of glucose and its conversion to glycogen.


Other hormones (glucagon, epinephrine, growth hormone, and cortisol) work to oppose the effects of insulin and are referred to as counterregulatory hormones. These hormones increase blood glucose levels by stimulating glucose production and output by the liver and by decreasing the movement of glucose into the cells. The counterregulatory hormones and insulin usually maintain blood glucose levels within the normal range by regulating the release of glucose for energy during food intake and periods of fasting.


Insulin is synthesized from a precursor, proinsulin. Enzymes split proinsulin to form insulin and C-peptide, and then the two substances are released in equal amounts. Therefore measuring C-peptide in serum and urine is a useful clinical indicator of pancreatic β cell function.



Type 1 Diabetes Mellitus.

Type 1 diabetes mellitus, formerly known as juvenile-onset diabetes or insulin-dependent diabetes, accounts for approximately 5% of all people with diabetes. Type 1 diabetes generally affects people under 40 years of age, and 40% develop it before 20 years of age. The incidence of type 1 diabetes has increased 3% to 5% over recent decades, and for unknown reasons it is occurring more frequently in younger children.3




image Genetic Link


Predisposition to type 1 diabetes is related to human leukocyte antigens (HLAs). (See Chapter 14 for a discussion of HLAs and disease associations.) Theoretically, when an individual with certain HLA types is exposed to a viral infection, the β cells of the pancreas are destroyed, either directly or through an autoimmune process. The HLA types associated with an increased risk for type 1 diabetes include HLA-DR3 and HLA-DR4 (see Genetics in Clinical Practice box).



image Genetics in Clinical Practice


Types 1 and 2 Diabetes Mellitus




























Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Maturity-Onset Diabetes of the Young (MODY)
Genetic Basis

Risk to Offspring

Clinical Implications



image



Idiopathic diabetes is a form of type 1 diabetes that is strongly inherited and not related to autoimmunity. It occurs only in a small number of people with type 1 diabetes, most often of Hispanic, African, or Asian ancestry.3 Latent autoimmune diabetes in adults (LADA), a slowly progressing autoimmune form of type 1 diabetes, usually occurs in people who are over the age of 35 who are not obese.4




Onset of Disease.

In type 1 diabetes the islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms. Manifestations of type 1 diabetes develop when the person’s pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose. Once this occurs, the onset of symptoms is usually rapid, and patients often are initially seen with impending or actual ketoacidosis. The patient usually has a history of recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger).


The individual with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis. Newly diagnosed patients with type 1 diabetes may experience a remission, or “honeymoon period,” for 3 to 12 months after treatment is initiated. During this time, the patient requires little injected insulin because β-cell insulin production remains sufficient for glucose control. Eventually, as more β cells are destroyed and blood glucose levels increase, the honeymoon period ends and the patient will require insulin on a permanent basis.



Type 2 Diabetes Mellitus.

Type 2 diabetes mellitus was formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (NIDDM). Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for approximately 90% to 95% of patients with diabetes.2 Risk factors for developing type 2 diabetes include being overweight or obese, being older, and having a family history of type 2 diabetes. Although the disease is seen less frequently in children, the incidence is increasing due to the increasing prevalence of childhood obesity. Type 2 diabetes is more prevalent in some ethnic populations. African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than whites.4




image Genetic Link


Although the genetics of type 2 diabetes is not yet fully understood, it is likely multiple genes are involved. Genetic mutations that lead to insulin resistance and a higher risk for obesity have been found in many people with type 2 diabetes. Individuals with a first-degree relative with the disease are 10 times more likely to develop type 2 diabetes.


Four major metabolic abnormalities have a role in the development of type 2 diabetes (see Fig. 49-2). The first factor is insulin resistance, a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, are insufficient in number, or both. Most insulin receptors are located on skeletal muscle, fat, and liver cells. When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia. In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if β-cell function is normal). This creates a temporary state of hyperinsulinemia that coexists with hyperglycemia.


A second factor in the development of type 2 diabetes is a marked decrease in the pancreas’s ability to produce insulin, as the β cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost. The underlying basis for the failure of β cells to adapt is unknown. It may be linked to the adverse effects of chronic hyperglycemia or high circulating free fatty acids.


A third factor is inappropriate glucose production by the liver. Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body’s needs at the time.


A fourth factor is altered production of hormones and cytokines by adipose tissue (adipokines). Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the pathophysiology of type 2 diabetes.5 Adipokines are thought to cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease (CVD). The two main adipokines believed to affect insulin sensitivity are adiponectin and leptin.


Individuals with metabolic syndrome are at an increased risk for the development of type 2 diabetes. Metabolic syndrome has five components: elevated glucose levels, abdominal obesity, elevated blood pressure (BP), high levels of triglycerides, and decreased levels of high-density lipoproteins (HDLs) (see Table 41-10). An individual with three of the five components is considered to have metabolic syndrome.6 Overweight individuals with metabolic syndrome can prevent or delay the onset of diabetes through a program of weight loss and regular physical activity. (See Chapter 41 for a discussion of metabolic syndrome.)




Prediabetes.

Individuals diagnosed with prediabetes are at increased risk for the development of type 2 diabetes. Prediabetes is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both. It is an intermediate stage between normal glucose homeostasis and diabetes where the blood glucose levels are elevated, but not high enough to meet the diagnostic criteria for diabetes. A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L).3 IFG is diagnosed when fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L).


Persons with prediabetes usually do not have symptoms. However, long-term damage to the body, especially the heart and blood vessels, may already be occurring. It is important for you to encourage patients to undergo screening and to provide instruction about managing risk factors for diabetes. Patients with prediabetes can take action to prevent or delay the development of type 2 diabetes. Those with prediabetes should have their blood glucose and A1C tested regularly and monitor for symptoms of diabetes, such as polyuria, polyphagia, and polydipsia. Maintaining a healthy weight, exercising regularly, and eating a healthy diet have all been found to reduce the risk of developing overt diabetes in people with prediabetes.



Gestational Diabetes.

Gestational diabetes develops during pregnancy and occurs in about 2% to 10% of pregnancies in the United States.7 Women with gestational diabetes have a higher risk for cesarean delivery, and their babies have increased risk for perinatal death, birth injury, and neonatal complications. Women who are at high risk for gestational diabetes should be screened at the first prenatal visit.8 Those at high risk include women who are obese, are of advanced maternal age, or have a family history of diabetes. Women with an average risk for gestational diabetes are screened using an OGTT at 24 to 28 weeks of gestation. Most women with gestational diabetes have normal glucose levels within 6 weeks postpartum. Be aware that women with a history of gestational diabetes have a 35% to 60% chance of developing type 2 diabetes within 10 years.7 Gestational diabetes and management of the pregnant patient with diabetes are specialized areas not covered in detail in this chapter. Consult an obstetric text for more information.



Other Specific Types of Diabetes.

Diabetes occurs in some people because of another medical condition or treatment of a medical condition that causes abnormal blood glucose levels. Conditions that may cause diabetes can result from damage to, injury to, interference with, or destruction of the β-cell function in the pancreas. These include Cushing syndrome, hyperthyroidism, recurrent pancreatitis, cystic fibrosis, hemochromatosis, and parenteral nutrition. Commonly used medications that can induce diabetes in some people include corticosteroids (prednisone), thiazides, phenytoin (Dilantin), and atypical antipsychotics (e.g., clozapine [Clozaril]). Diabetes caused by medical conditions or medications can resolve when the underlying condition is treated or the medication discontinued. (Drugs that can alter blood glucose levels are listed in eTable 49-1 available on the website for this chapter.)

Related posts:

  1. Introduction
  2. Nursing Management: Sexually Transmitted Infections
  3. Nursing Management: Integumentary Problems
  4. Fluid, Electrolyte, and Acid-Base Imbalances

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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Diabetes Mellitus

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