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Hesi Diabetes Type 1 Case Study


This is a 9 year old boy who has enjoyed his usual state of good health until his polyuria started 2 months ago. He began to lose weight and reported worsening nocturia over this same period. His appetite increased although lately he has more episodes of stomachaches. Today, he had a noticeably sweet smell to his breath and he was breathing faster than usual so his mother brought him to his pediatrician.

Exam: VS T 37.0, RR 44, P 92, BP110/60, oxygen saturation 100% on room air. His weight was 25 kg (25%tile). He is alert and cooperative. His skin is warm to his wrists and ankles. His oral mucous membranes are tacky. His capillary refill is 3 seconds over his chest. His skin was otherwise normal. His thyroid gland is approximately 1.5 times the normal size. His heart rate is regular. He is slightly tachypneic with clear breath sounds. His reflexes are normal. His abdomen has normal bowel sounds has no tenderness. His genitalia and pubic hair are in Tanner stage I. The rest of the physical examination is unremarkable.

His pediatrician suspects new onset diabetes mellitus. A urine dipstick in the office shows 4+ glucose and 2+ ketones. No other dipstick abnormalities are noted. He is clinically stable. He is hospitalized for further management and treatment. His initial lab studies show Na 132, K3.3, Cl 99, bicarb 11, glucose 380, BUN 21, creatinine 0.4. He is started on an IV fluid infusion and subcutaneous insulin.


Prior to the purification of insulin, type 1 diabetes mellitus was uniformly lethal. Although we have made significant strides in the evaluation and management of diabetes, it remains a significant health problem in the general population. In the pediatric subset of the population, type 1 diabetes mellitus is especially challenging since so many factors need to be balanced. The basics on balancing all of these factors will be covered in this chapter.

In United States, the overall risk of developing type 1 diabetes mellitus is 0.2-0.4 percent in Caucasians. In siblings of patients with type 1 diabetes, the risk is approximately 6%. Children of fathers who have type 1 diabetes mellitus have a 6% risk of developing the problem. Children of mothers with type 1 diabetes mellitus have only a 3% chance of developing the problem. The overall incidence of the disease is 18.2 in 100,000/year among people less than 20 years old. The incidence is much higher in Scandinavian countries than in Asian countries.

The National Diabetes Data Group in 1979 divided the heterogeneous condition of diabetes mellitus into two main groups. Type 1 diabetes mellitus has also been called insulin-dependent (IDDM), juvenile onset, ketosis prone, or brittle diabetes. In this type of diabetes mellitus, islet cells are destroyed by an autoimmune process and insulin that these islet cells produce must be replaced. With our current understanding, type 2 diabetes mellitus is primarily an insulin resistant state with a gradual decrease in beta cell function. It was formally known as non insulin-dependent diabetes (NIDDM), adult-onset diabetes, or stable diabetes. Clinical diabetes mellitus can also result from a large number of pathologic processes. Beta cell destruction due to pancreatitis, cystic fibrosis, or surgery can lead to an insulinopenic state that requires insulin injections. Medications including streptozocin, cyclosporin, and corticosteroids can also lead to clinically high blood sugars.

Approximately 2 percent of the American population have some form of diabetes mellitus. Approximately 85 percent of all patients (adults and children) with diabetes mellitus are categorized as type 2. Since type 2 diabetes mellitus is often very subtle, the number of undiagnosed cases of diabetes mellitus is significant. The other 15 percent of patients with diabetes mellitus nationwide are categorized as type 1. In the pediatric population, type 1 diabetes makes up a larger proportion of the cases. Although our estimates are quite crude, some centers report that approximately 98 percent of their children with diabetes have the Type 1 variety. This estimate will certainly be revised in the future as we recognize more type 2 diabetes in children.

Insulin is the primary hormone that suppresses hepatic glucose production, proteolysis, and lipolysis. It is secreted in a biphasic manner in response to glucose. The first phase of insulin release is followed by a nadir and then by a relatively prolonged second phase of insulin release. Catecholamines, cortisol, growth hormone, glucagon, and gastrointestinal hormones among other hormones modulate the insulin response to glucose.

Due to the portal circulation in the gut, blood draining the islet cells of the pancreas goes to the liver before returning to the heart. This portal circulation exposes the liver to an immediately high concentration of insulin soon after a meal. When treating diabetes with exogenously administered insulin into the systemic circulation, we need to remember that this does not duplicate the physiologic state.

Insulin is an anabolic hormone that increases the transport of glucose into cells. With this transport, insulin will decrease the serum glucose. At the cellular level, glucose does not act alone. In reality, the insulin/glucagon ratio is important for determining the body's response to insulin. A high insulin state will induce glucose uptake and inhibit amino acid release in muscle cells. In the liver, insulin will decrease glucose release and decrease ketone body formation. In fat cells, insulin will increase glucose uptake and decrease lipolysis.

In our most current models, type 1 diabetes mellitus is an autoimmune disease. In our current understanding of the problem, people with type 1 diabetes mellitus have an underlying genetic predisposition to developing diabetes. On top of this predisposition, they are exposed to an environmental insult that triggers the immune response. In this way, not everyone who is genetically susceptible to type 1 diabetes mellitus will develop the problem. The identical twin of the patient with type 1 diabetes mellitus has a 25 to 50 percent risk of developing the problem in their lifetime.

Important genes for transmitting this susceptibility to diabetes include the human leukocyte antigens (HLA) that allow for some of the communication between white blood cells. The HLA-DR and HLA-DQ molecules are especially important. These are antigen-presenting structures that T-cells recognize. The antigens in these presenting molecules are the targets for the immune response. Mutations that lead to defects in the structure of this antigen presenting molecule predisposes to type 1 diabetes mellitus. One of the important residues in the structure of the HLA molecules is at position 57. Homozygosity for aspartic acid at this site confers nearly 100% protection against type 1 diabetes. Conversely, a non-aspartic residue at this spot can lead to a nearly 100 fold increase in the incidence of disease.

On top of this genetic predisposition, an environmental insult is likely to be required for the development of diabetes. The environmental factors are quite varied and we are only now beginning to isolate some of them. Congenital rubella cases provide compelling evidence that some of these environmental triggers are viral proteins. Approximately 20 percent of babies with congenital rubella will develop type 1 diabetes mellitus. Most of these cases do not appear until adolescence. Other viruses such as Coxsackie virus, cytomegalovirus, and hepatitis viruses have been implicated.

Polyuria, polydipsia, weight loss, fatigue, polyphagia, anorexia, deteriorating school performance, failure to thrive, and nocturnal enuresis can occur. Clinical symptoms become apparent when the blood sugar rises above the renal threshold and glycosuria induces an osmotic diuresis. Insulinopenia allows hormone sensitive lipase to cut long fatty-acid chains into two carbon acetate fragments which are converted to ketoacids. Patients will present in varying degrees of decompensation as the serum pH decreases and as the dehydration progresses. New onset type 1 diabetes will frequently present with diabetic ketoacidosis of varying severity.

Secondary enuresis, unexplained weight loss, and polyuria should raise suspicions about diabetes. Testing should include random glucose levels, electrolytes, and ketones. The measurement of hemoglobin A1C and insulin can also be helpful. 90% of children will have elevated anti-insulin, anti-islet cell, or anti-GAD (Glutamic acid dehydrogenase) antibodies. Rarely, an IV or oral glucose tolerance test to evaluate for the degree of insulin-producing capacity may be considered in borderline cases, mostly to confirm type 2 diabetes.

Normal glucose levels should be

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