Chapter 19 Diabetes Type 1
Insulin-Dependent
PATHOPHYSIOLOGY
Type 1 diabetes, previously called insulin-dependent diabetes mellitus (IDDM), or juvenile-onset diabetes, is an autoimmune disease that destroys the beta cells of the pancreas, which results in insulin deficiency. Complete insulin deficiency necessitates the use of exogenous insulin to promote appropriate glucose use and to prevent complications related to elevated glucose levels, such as diabetic ketoacidosis and death.
Insulin is necessary for the following physiologic functions: (1) to promote the use and storage of glucose for energy in the liver, muscles, and adipose tissue; (2) to inhibit and stimulate glycogenolysis or gluconeogenesis, depending on the body’s requirements; and (3) to promote the use of fatty acids and ketones in cardiac and skeletal muscles. Insulin deficiency results in unrestricted glucose production without appropriate use, which leads to hyperglycemia and increased lipolysis and production of ketones and, in turn, to hyperlipidemia, ketonemia, and ketonuria. The insulin deficiency also heightens the effects of the counterregulatory hormones—epinephrine, glucagon, cortisol, and growth hormone (see Box 19-1 for these hormones’ functions).
INCIDENCE
1. Type 1 diabetes accounts for the majority of new diabetes cases in youth.
2. The onset most commonly occurs around puberty (ages 10–14 years).
3. Among preschool-aged children, the disease is more commonly diagnosed in boys.
4. Among children 5 to 10 years of age, the disease is more commonly diagnosed in girls.
5. The disease is diagnosed more often in winter than in summer.
6. Diabetic ketoacidosis is a frequent cause of morbidity and sometimes of death.
CLINICAL MANIFESTATIONS
Initial Effects
4. Recent weight loss (during a period of less than 3 weeks)
9. Dehydration (usually 10% dehydrated)
10. Diabetic ketoacidosis (Box 19-2)—hyperglycemia, ketonemia, ketonuria, metabolic acidosis, Kussmaul respirations
12. Change in level of consciousness (due to progressive dehydration, acidosis, and hyperosmolality, which results in decreased cerebral oxygenation)
Box 19-2 Signs of Diabetic Ketoacidosis
• Kussmaul respirations (deep, sighing respirations)
• Hyperglycemia (serum glucose level higher than 300 mg/dl)
• Ketonuria (moderate to large amounts; positive Ketostix result)
• Metabolic acidosis (pH <7.3; increased partial pressure of carbon dioxide [PCO2]; decreased partial pressure of oxygen [PO2]; sodium bicarbonate [NaHCO3] <15 mEq/L)
• Dehydration (as a result of polyuria and polydipsia)
• Electrolyte imbalance (falsely elevated potassium and sodium levels)
• Potential for life-threatening cardiac arrhythmias (as a result of electrolyte imbalance)
• Cerebral edema (caused by overzealous infusion of fluids)
Diagnosis is confirmed by the presence of symptoms combined with an elevated blood glucose level (higher than 200 mg/dl) and glycosuria.
COMPLICATIONS
LABORATORY AND DIAGNOSTIC TESTS
For the Individual Newly Diagnosed with Diabetes:
1. Randomly determined plasma glucose level—200 mg/dl or higher
2. Fasting plasma glucose level—higher than or equal to 126 mg/dl
3. Glycosylated hemoglobin (hemoglobin A1c) level—reflects percentage of hemoglobin to which glucose is attached
4. Blood urea nitrogen, creatinine levels—increased because of interference of ketones in measurement
5. Serum calcium, magnesium, phosphate levels—decreased as a result of diuresis
6. Serum electrolyte (potassium [K+] and sodium [Na+]) levels—may be falsely elevated as a result of hyperosmolarity
7. Complete blood count—white blood cells may be increased, with predominance of polymorphonuclear lymphocytes
8. Immunoassay—to measure level of C-peptides after glucose challenge (to verify endogenous insulin secretion)
9. Twenty-four-hour urine analysis for glucose—considered a more reliable measure of urine glucose level
MEDICAL MANAGEMENT
Children with the initial diagnosis of Type 1 diabetes are usually admitted to the hospital for stabilization and education but may be treated on an outpatient basis. Medical management includes the regulation of serum glucose, fluid, and electrolyte levels. This is accomplished through monitoring of laboratory results, administration of insulin, and intravenous (IV) administration of fluids containing the indicated additives. Secondary problems (i.e., infections) are also treated accordingly. Once glucose levels are stabilized, insulin doses are given to maintain serum glucose level. The management of these children requires a multidisciplinary approach. The child and family need ongoing education and support regarding nutrition, exercise, and daily diabetes self-management.
NURSING INTERVENTIONS
Diabetic Ketoacidosis
1. Monitor and observe child for change in status of diabetic ketoacidosis (see Box 19-2).
2. Promote child’s hydration status.
3. Monitor child’s glucose level hourly.
Recovery and Maintenance
1. Monitor and observe for signs of hypoglycemia and hyperglycemia.
3. Promote adequate nutritional intake (see Box 19-3 for nutritional recommendations).
4. Monitor and establish appropriate relationship between insulin dose, dietary requirements, and exercise.
5. Provide emotional support to individual and family to promote psychosocial adaptation to diabetes.
Box 19-3 Nutritional Requirements in Diabetes
Dietary Plans
Two exchange systems are used by diabetic individuals: the American Diabetic Association (ADA) exchange group and the British Diabetic Association exchange system.
• The ADA exchange group has six exchange lists, which are for milk, fruit, vegetables, bread, meat, and fat. The exchange lists give the equivalent amounts of calories and nutrients.
• The British Diabetic Association exchange focuses on carbohydrate intake only. A liberal intake of protein is allowed and fats are less restricted. Many children and adolescents prefer carbohydrate counting because it allows for more flexibility in dietary management than the exchange system.
General Information
• Foods high in fiber retard carbohydrate absorption.
• Foods have different glycemic responses (glycemic index).
• Long periods between eating must be avoided.
• Extra food must be consumed for increased activity (10 to 15 g of carbohydrate for every 30 to 45 minutes of activity).
• Quantity of food needed between meals will vary according to increase or decrease in physical activity.
Discharge Planning and Home Care
American Diabetes Association. Clinical practice recommendations (2004) diagnosis and classification of diabetes mellitus. Diabetes Care. 2004;26(2):S5. (Supp I):
Betschart J. Diabetes in the life cycle and research. In: Franz M, ed. A core curriculum for diabetes education. Chicago: American Association of Diabetes Educators, 2001.
Diabetes Research in Children Network Study Group. The effects of aerobic exercise on glucose and counterregulatory hormone concentrations in children with type I diabetes. Diabetes Care. 2006;29(1):20.
Dowshen S, Ben-Joseph EA. Type I diabetes: What is it? Kidshealth. 2005;14(1):32.
