Question

Discuss differences in types of insulins and consideration to peaks and self-monitoring of blood glucose (SMBG).

Discuss ketoacidosis and the best ways to avoid it.

Consider and discuss growth/development and other stresses affecting children in regard to blood sugar/DKA?

Discuss hospital management of DKA and the educational/support needs of children/families.

Answer 1

1)Discuss differences in types of insulins and consideration to peaks and self-monitoring of blood glucose (SMBG).

Ans)Types of Insulins

There are three main groups of insulins: Fast-acting, Intermediate-acting and Long-acting insulin.

Fast-acting insulin:

Is absorbed quickly from your fat tissue (subcutaneous) into the bloodstream.

Is used to control the blood sugar during meals and snacks and to correct high blood sugars

Includes:

Rapid Acting Insulin Analogs (Insulin Aspart, insulin Lyspro, Insulin Glulisine) which have an onset of action of 5 to 15 minutes, peak effect in 1 to 2 hours and duration of action that lasts 4-6 hours. With all doses, large and small, the onset of action and the time to peak effect is similar, The duration of insulin action is, however, affected by the dose – so a few units may last 4 hours or less, while 25 or 30 units may last 5 to 6 hours. As a general rule, assume that these insulins have duration of action of 4 hours.

Regular Human Insulin which has an onset of action of 1/2 hour to 1 hour, peak effect in 2 to 4 hours, and duration of action of 6 to 8 hours. The larger the dose of regular the faster the onset of action, but the longer the time to peak effect and the longer the duration of the effect.

Intermediate-acting insulin:

Is absorbed more slowly, and lasts longer

Is used to control the blood sugar overnight, while fasting and between meals

Includes:

NPH Human Insulin which has an onset of insulin effect of 1 to 2 hours, a peak effect of 4 to 6 hours, and duration of action of more than 12 hours. Very small doses will have an earlier peak effect and shorter duration of action, while higher doses will have a longer time to peak effect and prolonged duration.

Pre-Mixed Insulin which is NPH pre-mixed with either regular human insulin or a rapid- acting insulin analog. The insulin action profile is a combination of the short and intermediate acting insulins.

Long-acting insulin:

Is absorbed slowly, has a minimal peak effect, and a stable plateau effect that lasts most of the day.

Is used to control the blood sugar overnight, while fasting and between meals

Includes

Long acting insulin analogs (Insulin Glargine, Insulin Detemir) which have an onset of insulin effect in 1 1/2-2 hours. The insulin effect plateaus over the next few hours and is followed by a relatively flat duration of action that lasts 12-24 hours for insulin detemir and 24 hours for insulin glargine.Self-monitoring of blood glucose (SMBG) should be part of a regular management plan for patients with diabetes. Self-monitoring of blood glucose provides information regarding an individual's dynamic blood glucose profile. This information can help with the appropriate scheduling of food, activity, and medication. It is also required for understanding of the timing of blood glucose variations. Lack of regular SMBG predicts hospitalization for diabetes-related complications. Self-monitoring of blood glucose is an essential tool for people with diabetes who are taking insulin or for those who experience fluctuations in their blood glucose levels, especially hypoglycemia. Application of practical aspects that aid in easy management of SMBG makes the task of checking blood glucose more achievable. For patients taking insulin and adjusting their dose, SMBG is needed for self-management. For others receiving oral medication, profiling glucose trends and the confirmation of high or low blood glucose can be a useful addendum to successful management.

2)Discuss ketoacidosis and the best ways to avoid it.

Ans) What is diabetic ketoacidosis?

Diabetic ketoacidosis (say: key-toe-acid-OH-sis), or DKA for short, happens when your body has high blood sugar (also called glucose) and a build-up of acid. If it isn’t treated, it can lead to coma and even death. It mainly affects persons with type 1 diabetes. But, it can happen with other types of diabetes, including type 2 diabetes and diabetes during pregnancy.

What causes DKA?

The main cause of DKA is not having enough insulin. This raises the blood glucose levels, but stops the body from using the glucose for energy. To get calories, the body starts to burn fat. This causes a build-up of acid in the body. A high level of blood glucose can cause excessive urination, which leads to a lack of fluids in the body (dehydration).

What are triggering factors?

The most common triggering factors are “skipping” insulin doses and illnesses, especially infections that raise your body’s need for insulin.

How can I prevent DKA?

You should work with your doctor to have a plan if your blood glucose level gets too high. Make sure that you know how to reach your doctor in an emergency. Careful monitoring is needed, especially if you are sick.

What should I do?

Check your blood glucose level at least every three to four hours if you are sick. Check your glucose level every one to two hours if you have critical blood glucose values. Ask your doctor what your critical level should be. Most patients should watch their glucose levels closely when they are higher than 250 mg per dL. Keep testing at least every four hours during the night.

Test your urine for ketones or your blood for beta-hydroxybutyrate every four hours or if your blood glucose is over 250 mg per dL.

If you are not eating, do NOT stop your insulin completely. Your body needs insulin even if you are not eating. Call your doctor if you do not know how to change your insulin dose.

If your blood glucose is high, take extra insulin to control it. Call your doctor if you do not have an extra insulin dose or if the extra dose is not working.

Drink lots of sugar-free, caffeine-free liquids. Sip small amounts every few minutes if you are feeling sick to your stomach.

If your blood glucose is more than 250 mg per dL, do not eat or drink foods that are high in carbohydrates.

Contact your doctor if you have:

• Vomiting more than once

• Stomach pain

• Diarrhea five or more times in six hours

• Two blood glucose level tests higher than 300 mg per dL

• A blood glucose level less than 70 mg per dL more than once or symptoms of low blood sugar

• Trouble breathing

• Moderate or large ketones if you are using urine test strips

• High beta-hydroxybutyrate levels if you are using blood test strips

If you have signs of infection, including fever, cough, sore throat, or pain when you go to the bathroom, see your doctor to make sure you are getting the right treatment.

If you are on an insulin pump, make sure that you have short-acting insulin, long-acting insulin, and needles in case your pump is not working right. You also should have an emergency phone number to call for help with your pump.

3)Consider and discuss growth/development and other stresses affecting children in regard to blood sugar/DKA?

Ans) The adage “A child is not a miniature adult” is most appropriate when considering diabetic ketoacidosis (DKA). The fundamental pathophysiology of this potentially life-threatening complication is the same as in adults. However, the child differs from the adult in a number of characteristics.

1) The younger the child, the more difficult it is to obtain the classical history of polyuria, polydipsia, and weight loss. Infants and toddlers in DKA may be misdiagnosed as having pneumonia, reactive airways disease (asthma), or bronchiolitis and therefore treated with glucocorticoids and/or sympathomimetic agents that only compound and exacerbate the metabolic derangements. Because the diagnosis of diabetes is not suspected as it evolves, the duration of symptoms may be longer, leading to more severe dehydration and acidosis and ultimately to obtundation and coma. Even in developed countries, some 15–70% of all newly diagnosed infants and children with diabetes present with DKA (1–8). Generally, the rates of DKA are inversely proportional to rates of diabetes in that community, but throughout the U.S., the overall rates of DKA at diagnosis have remained fairly constant at ∼25% (6). DKA, defined by blood bicarbonate <15 mmol/l and/or pH <7.25 (<7.3 if arterial or capillary), was present in 23.3% of a carefully analyzed cohort. However, the prevalence of DKA decreased significantly with age from 36% in children <5 years of age to 16% in those >14 years but did not differ significantly by sex or ethnicity (6).

2) The higher basal metabolic rate and large surface area relative to total body mass in children requires greater precision in delivering fluids and electrolytes. The degree of dehydration is expressed as a function of body weight, i.e., 10% dehydration implies 10% loss of total body weight as water. However, the calculation of basal requirements, although a constant per unit of surface area, must be carefully adjusted when calculating per unit mass because the amount of fluid per kilogram declines as the infant or child grows.

3) Cerebral and other autoregulatory mechanisms may not be as well developed in younger children. Hence, greater severity at presentation in younger children together with less maturity of autoregulatory systems combine to predispose children to cerebral edema, which occurs in ∼0.5–1% of all episodes of DKA in children and is the most common cause of mortality in children with DKA (9–12). Only a minority of deaths in DKA are attributable to other causes, such as sepsis, other infections (including mucormycosis), aspiration pneumonia, pulmonary edema, acute respiratory distress syndrome, pneumomediastinum, hypo- or hyperkalemia, cardiac arrhythmias, central nervous system (CNS) hematoma or thrombosis, and rhabdomyolysis. Currently, the etiology, pathophysiology, and ideal treatment are poorly understood, but these are areas of intense investigation. Because cerebral edema occurs in the context of DKA, reduction of the incidence of DKA should be a major goal of treating children with diabetes. The reported mortality rates in children with DKA are constant in national population-based studies varying from ∼0.15 to 0.3%. Once cerebral edema develops, death occurs in some 20–25%, and significant morbidity, including pituitary insufficiency, occurs in 10–25% of survivors. Where medical services are less well developed, the risk of dying from DKA is greater, and children may die before receiving treatment. Overall, cerebral edema accounts for ∼60–90% of all DKA-related deaths in children.

4) Whereas delay in diagnosis is the major cause of DKA in previously unrecognized disease in younger children, omission of insulin is the leading cause of recurrent DKA, most prevalent among adolescents. In this group, some 5% of patients account for >25% of all admission for DKA.

These important differences between children and adults require careful attention to issues of management. Here, we briefly review the pathophysiology of DKA in childhood and discuss recommended treatment protocols. Current concepts of cerebral edema are presented. We conclude with recommendations and strategies for the prediction and prevention of DKA and, hence, its complications in infants, children, and adolescents.

These considerations and recommendations are in agreement with those recently endorsed by the Lawson Wilkins Pediatric Endocrine Society (LWPES), European Society for Pediatric Endocrinology (ESPE), and the International Society for Pediatric and Adolescent Diabetes (ISPAD).

4) Discuss hospital management of DKA and the educational/support needs of children/families.

Ans)Diabetic ketoacidosis (DKA) is biochemically defined as a venous pH <7.3 or serum bicarbonate concentration <15 mmol/L, serum glucose concentration >200 mg/dL (11 mmol/L) together with ketonemia, glucosuria, and ketonuria.1,2 Rarely, DKA may occur with normal circulating glucose concentrations if there has been partial treatment or with pregnancy.3,4 The severity of DKA is determined by the degree of acidosis:

Mild: venous pH >7.2 and <7.3, bicarbonate <15 mmol/L

Moderate: venous pH >7.1 and <7.2, bicarbonate <10 mmol/L

Severe: venous pH <7.1, bicarbonate <5 mmol/L.

Pathophysiology

DKA is the result of a critical relative or absolute deficit of insulin, resulting in intracellular starvation of insulin-dependent tissues (muscle, liver, adipose), stimulating the release of the counter-regulatory hormones glucagon, catecholamines, cortisol, and growth hormone. The counter-regulatory hormonal responses may also be the result of stress-induced proinflammatory cytokines.5 They stimulate lipolysis and proteolysis, hepatic and renal glucose production, and hepatic oxidation of fatty acid to ketone bodies.6 Unlike during physiologic fasting, absence of citric acid cycle processing of glucose impedes the processing of these ketones for energy The frequency of new-onset diabetes presenting as DKA varies widely by geographic region, and correlates inversely with the regional incidence, and therefore the level of awareness in the community of pediatric diabetes. In Europe this frequency varies from 11% to 67%.7 In Australia the frequency between 1985 and 2000 was 26%,8 and in New Zealand 63% in 1988/89 and 42% in 1995/96.9 Children <5 years of age are more likely to have DKA at diagnosis as are those who are in social or economic situations that do not permit ready access to medical care.2,7–14 In patients from Colorado, DKA was seen at onset in 28.4%; the odds ratio for uninsured patients compared with insured patients was 6.2, with significantly greater severity in the uninsured group.12 Long-term reductions in frequency of DKA at onset have been reported following intensive education of the medical and lay community.8–10 DKA at the time of diagnosis has been estimated to occur in as many as 25% of children with type 2 diabetes (T2D).2

It is not uncommon for previously undiagnosed patients in DKA to have been seen in physicians’ offices or emergency rooms without adequate history and laboratory study that could have made the diagnosis before they became critically ill. A high index of suspicion is particularly warranted for infants and young children whose symptoms may be nonspecific.

Recurrent DKA Among 1243 patients in Colorado, the risk of recurrent DKA was eight episodes per 100 patient years; 20% of the patients accounted for 80% of the episodes. The risk factors for recurrent DKA were poor metabolic control or previous episodes of DKA, female gender (peripubertal or adolescent), psychiatric disorders including eating disorders, difficult or unstable family circumstances, limited access to medical services, and insulin pump therapy.12 Only rapid- or short-acting insulin is used in pumps, so that interruption of insulin delivery for any reason rapidly leads to insulin deficiency. In the 1970s and 1980s, the establishment of treatment teams with intensive education of families on sick day management and 24-hour availability demonstrated a profound reduction in recurrent DKA, which is almost invariably due to intentional omission of insulin administration.15,16

Diagnosis and Initial Evaluation

Hyperglycemic hyperosmolar state (HHS) defined as serum glucose >600 mg/mL (33 mmol/L), serum osmolality >320 mOsm/L, and minimal ketonemia/ketonuria, is being seen with increasing frequency as the presenting indication of T2D and may be associated with mild-tomoderate acidosis from severe dehydration, leading to confusion with DKA.17 Conversely, patients with type 1 diabetes (T1D) may have features of HHS, especially if they have been satisfying their polydipsia with fluids containing a high concentration of glucose.18 HHS has a substantial mortality rate and requires aggressive reconstitution of the circulatory volume.17–20

Body weight should be determined for calculation purposes. Dehydration can be estimated as 5% if there is reduced skin elasticity, dry mucous membranes, tachycardia, and deep breathing, and up to 10% with capillary refill time greater than 3 seconds and sunken eyes . Calculations of fluid deficit are commonly based on 10% dehydration, which in most cases is a modest overestimate that does not appear to have clinical significance.21–22 The level of consciousness should be recorded using the Glasgow Coma Scale. An initial venous blood sample should be tested for glucose; electrolytes; pH; urea nitrogen; creatinine; osmolality; ketones or beta-hydroxybutyrate; hemoglobin and hematocrit or complete blood count, while keeping in mind that DKA is associated with leukocytosis

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