insulin (14 units of insulin glargine plus 12 units of insulin aspart for meal

coverage = 26 units):

Table 53-17

Factors that Can Alter Blood Glucose Control

Diet

Insufficient calories (e.g., alcoholism, eating disorders, anorexia, nausea, and vomiting)

Overeating (e.g., during the holidays)

Irregularly spaced, skipped, or delayed meals

Dietary content (e.g., fiber, carbohydrate content)

Physical Activity

See Table 53-19

Stress

Infection

Surgery/trauma

Psychological

Drugs

Certain medications can increase or decrease blood glucose levels. It is important to assess for potential effects

on the blood glucose when starting new medications

Hormonal Changes

Menstruation: Glucose concentrations may increase premenstrually and return to normal after menses

Pregnancy

Puberty: hyperglycemia probably related to high growth hormone levels

Gastroparesis

Delays gastric emptying time. Peak insulin action and meal-related glucose excursions may become mismatched

Altered Insulin Pharmacokinetics

See Table 53-8

Insulin Injection Technique

Measuring

Timing

Technique

Inactive Insulin

Outdated insulin

Improperly stored insulin (heat or cold)

Crystallized insulin

Because most single servings of carbohydrate contain 15 g, A.H. decides to start

with a ratio of 1 unit for every 15 g or single serving of carbohydrates she consumes

at each meal. If A.H. were using regular insulin for meal coverage, she could use the

“450 rule”: 450 divided by the total daily insulin dose yields grams of carbohydrate

covered by 1 unit of insulin.

To evaluate the accuracy of her insulin-to-carbohydrate ratio, A.H. will need to

check her BG values 2 hours after each meal (postprandial) to assess the

appropriateness of her ratio. She agrees to test her BG level 8 times/day and return in

2 weeks.

CASE 53-2, QUESTION 12: A.H. is getting more comfortable with carbohydrate counting and adjusting her

insulin doses accordingly. A review of her food diary reveals that for the most part, she is able to determine the

appropriate serving sizes for 15 g of carbohydrate. She admits to difficulty determining carbohydrate amounts

when eating out. As a result, A.H. notices that her preprandial BG concentrations exceed her goal of 80 to 130

mg/dL on occasion.

7 Sometimes they are as high as 200 mg/dL. Evaluate A.H.’s BG trends. How should

occasional preprandial glucose concentrations that exceed the desired goal of 80 to 130 mg/dL be managed?

Once the basal insulin dose and insulin-to-carbohydrate insulin dose have been

established, one can begin to teach A.H. how to use a correction factor to adjust her

dose of insulin when preprandial BG concentrations fall above or below the range of

BG concentrations that have been established as her goal of therapy (80–130 mg/dL

per the ADA; Table 53-15).

A correction insulin dose is used to compensate for unusually high BG

concentrations (high-sugar correction). To re-emphasize, this assumes there are no

unusual changes in the patient’s overall diet or exercise patterns (Table 53-18

explains the effects of exercise on BG). Many clinicians favor rapid-acting insulin

versus regular insulin because its action is brief and patients do not have to worry

about residual effects 3 to 4 hours after its injection. This is particularly valuable

when correctional doses of insulin are needed at bedtime.

1.

2.

The patient’s sensitivity to insulin, as reflected by his/her TDD on a unit per

kilogram basis, is a major determinant of any algorithm developed. A general

approach is to give an additional 1 to 2 units of supplemental rapid-acting insulin for

each 30- to 50-mg/dL elevation above the target level.

93 An alternative method of

estimating the drop in a person’s BG per unit of regular insulin is the “1,500 rule.”

99

The derived value is referred to as the “sensitivity factor”: The rule was modified to

the “1,800 rule” for use with rapid-acting insulin (insulin lispro, aspart, or glulisine).

Because these insulins tend to drop the BG level faster and farther, 1,500 turns out to

be too aggressive. Others have recommended other numerators such as 1,600, 1,700,

2,000, and 2,200.

107 For this case, the “1,700 rule” will be used. The calculation for

A.H. would be as follows:

Thus, 1 unit of insulin aspart for A.H. will drop her BG level by about 70 mg/dL.

People with a lower-sensitivity factor (higher-insulin requirements) typically

achieve a smaller reduction in BG per unit of insulin compared with those with a

higher-sensitivity factor (lower-insulin requirement). Thus, an algorithm of 1 unit of

insulin aspart for every 70-mg/dL excursion above her goal of 120 mg/dL is a

reasonable place to begin. If this dose of insulin is insufficient, one can decrease the

BG excursion required per unit of insulin dose (e.g., 50 mg/dL). Correctional insulin

doses also are used for sick day management (see Case 53-5). The following is an

example of a high-sugar correction algorithm for A.H:

Glucose Concentrations (mg/dL) Insulin Aspart

<80 1 unit less

80–120 Usual dose

120–190 1 unit extra

191–260 2 units extra

261–330

a 3 units extra

331–400

a 4 units extra

aCheck urine or blood ketone levels. If ketones are positive and BG concentrations remain >300 mg/dL for ≥12

hours, call the physician for directions.

Table 53-18

Exercise in Patients with Diabetes

Test blood glucose before, during, and after exercise

For moderate exercise (e.g., bicycling or jogging for 30–45 minutes), ↓ the preceding dose of regular or rapidacting insulin by approximately 30%–50%. If glucose concentration is normal or low before exercise,

supplement the diet with a snack containing 10–15 g of carbohydrate

3.

4.

5.

6.

7.

8.

To avoid ↑ absorption of regular insulin by exercise, inject into the abdomen or exercise 30–60 minutes after

injection. Avoid exercise when rapid-acting insulin is peaking

Individuals with low glycogen stores may be predisposed to the hypoglycemic effects of exercise. Examples

include alcoholics, fasted individuals, or patients on extremely hypocaloric (<800 calories), low-carbohydrate

(<10 g/day) diets

Patients taking insulin are more susceptible to hypoglycemia than those taking oral insulin secretagogues

(sulfonylureas, glinides). Patients with type 2 diabetes treated with diet are unlikely to develop hypoglycemia

Watch for postexercise hypoglycemia. Individuals who have been exercising during the day will likely need to

↑ their carbohydrate intake and should test their blood glucose during the night to detect nocturnal

hypoglycemia. Hypoglycemia can occur 8–15 hours after exercise

If the glucose concentration is >240–300 mg/dL, the patient should not exercise. This indicates severe insulin

deficiency. These patients are predisposed to hyperglycemia secondary to exercise

Patients with severe proliferative retinopathy or retinal hemorrhage should avoid jarring exercise or exercise

that involves moving the head below the waist

EVALUATING FASTING HYPERGLYCEMIA

CASE 53-2, QUESTION 13: A.H. returns after 1 month. She is currently using 14 units of insulin glargine

each evening, 1 unit of insulin aspart for each 15 g of carbohydrate ingested at mealtime, and a high-sugar

correction factor of 1 unit of insulin aspart for every 70 mg/dL above 130 mg/dL. Presuming that her diet is

consistent, her SMBG results are as follows:

Time Glucose Concentration mg/dL

7 AM 140–180

Noon 120–150

5 PM 90–130

11 PM 90–120

3 AM 60–90

p. 1099

p. 1100

Overall, A.H. feels her diabetes is in good control. Her energy level has returned to normal, and her nocturia

has diminished, but she occasionally gets up 1 or 2 times nightly to urinate. A.H. has also noticed that

nightmares or “sweats” sometimes awaken her. When this occurs, she generally has something to eat because

she is “famished.” She is able to get back to sleep, but wakes up the next morning with a “splitting headache”

and a “hungover” feeling. A.H.’s weight remains the same, and she has begun to develop some consistency in

her dietary patterns with the help of a dietitian. She has been consistently correcting her prelunch and predinner

insulin doses by adding or subtracting 2 units from her premeal insulin doses based on her premeal BG values.

The A1C from her last visit is 7.3%. Evaluate A.H.’s BG values. What are possible causes of A.H.’s fasting

hyperglycemia?

When evaluating morning hyperglycemia, several causes must be considered:

An insufficient basal dose of insulin. If the basal dose is insufficient, hepatic

glucose output during the fasting state will be excessive, thereby producing

hyperglycemia.

Insufficient dinner coverage with insulin aspart, resulting in hyperglycemia that

persists into the morning. This can be distinguished from an insufficient basal

insulin by assessing glucose control at bedtime.

Reactive hyperglycemia in response to a nocturnal hypoglycemic episode (Somogyi

effect or rebound hyperglycemia).

An excessive bedtime snack.

The dawn phenomenon (see Case 53-3).

The presence of normoglycemia at bedtime, low BG concentrations at 3 AM, and

symptoms of nocturnal hypoglycemia (nightmares, sweating, hunger, morning

headache) in A.H. are consistent with a rebound hyperglycemic reaction in the

morning (i.e., posthypoglycemic hyperglycemia, also referred to as the Somogyi

effect).

108

Theoretically, this effect occurs after any episode of severe hypoglycemia and is

secondary to an excessive increase in glucose production by the liver that is

activated by insulin counter-regulatory hormones such as cortisol, glucagon,

epinephrine, and growth hormone. The waning effects of the basal insulin dose can

also be a cause of fasting hyperglycemia because insulin is needed to suppress

hepatic glucose output during the fasting state; however, this is not likely in A.H.’s

case. Asymptomatic nocturnal hypoglycemia can occur in patients taking more than

necessary doses of insulin in the evening and may potentially cause rebound

hyperglycemia in the morning. By correcting the nocturnal hypoglycemia,

normalization of A.H.’s fasting hyperglycemia also may be achieved. Thus, a

decrease in the daily dose of insulin glargine is warranted. A.H. should continue to

monitor her BG concentrations at 3 AM to determine whether her BG levels return to

normal.

Caveat: If A.H. were using NPH BID to supply her basal insulin, one option would

be to shift the evening injection of NPH from before dinner to bedtime. This

preferred method effectively shifts the peak action of NPH to the early morning, when

she is awake, and decreases the risk of nocturnal hypoglycemia.

93,109,110 This peak

action also corresponds to the dawn phenomenon (see Case 53-3) and the breakfast

meal.

Another option if a patient is using NPH and experiencing nocturnal hypoglycemia

is to change from NPH to either insulin glargine or insulin detemir because these

insulins are associated with less nocturnal hypoglycemia.

111,112 When switching from

NPH insulin to insulin detemir, a one-to-one dose conversion may be used although

higher doses of detemir may be required. In one crossover study of Type 1 diabetes

patients, the average detemir basal dose was approximately double that of the NPH

basal dose.

113 However, when switching from NPH insulin to insulin glargine, a oneto-one dose conversion is utilized only when a patient is using NPH insulin once

daily. If a patient is taking NPH insulin twice daily, then the total daily insulin dose

should be decreased by 20% when switching to insulin glargine. In this case of AH,

the daily dose of NPH should be decreased by 20% to determine the insulin glargine

dose to err on the conservative side.

76

Although A.H.’s prelunch BG values are above her goal, this may be attributable

to the fasting BG being elevated and then continuing to be elevated mid-morning, like

a domino effect. It is important to first correct fasting hyperglycemia and generally

correct one BG concentration at a time.

MIXING INSULINS

CASE 53-2, QUESTION 14: If A.H. were to use NPH as basal insulin, how should she be instructed to

measure and withdraw this insulin mixture?

Although mixing two insulins in the same syringe has become less common with

use of basal-bolus therapy (because insulin glargine and detemir cannot be mixed)

and the use of rapid-acting insulin pen devices, the procedure used to mix and

withdraw NPH and mealtime insulin (regular or rapid-acting insulin) is basically the

same as that described in Case 53-2, Question 8. The major difference is that an

adequate volume of air must be injected into the NPH vial before the regular or

insulin aspart is measured and withdrawn. Also, the mealtime clear insulin is

measured and withdrawn into the insulin syringe first to avoid contamination of the

vial of regular, aspart, lispro, or glulisine insulin with NPH. For example,

contamination with NPH ultimately alters the NPH to regular insulin ratio that is

administered. When patients withdraw NPH insulin first, the vial of regular insulin

eventually becomes cloudy. In contrast, contamination of the NPH insulin with

regular insulin is insignificant because the protamine contained in NPH can bind the

regular insulin (see Case 53-2, Question 15). The procedure A.H. should use to mix

her insulins is described in the following section, using her morning dose as an

example.

After dispersing the NPH insulin suspension, inject 14 units of air into the NPH vial

and withdraw the needle.

Inject 7 units of air into the insulin aspart vial, and withdraw the 7 units of insulin as

described in Case 53-2, Question 8.

Insert the needle into the NPH vial, and pull the plunger down to the 21-unit mark

(14 units of NPH plus 7 units of insulin aspart).

STABILITY OF MIXED INSULINS

CASE 53-2, QUESTION 15: Will mixing NPH with a rapid-acting or regular insulin blunt the rapid action of

the mealtime insulins? How stable are other insulin mixtures?

Regular insulin and all of the rapid-acting insulin analogs (aspart, lispro, and

glulisine) may be mixed with NPH. In general, it is recommended to mix the insulins

just before administration. See Table 53-19 for details on compatibility and stability

of insulin mixtures. However, with the increased use of insulin pen devices, mixing

of insulins in the same syringe has become a less common practice.

PREMEAL HYPERGLYCEMIA

CASE 53-2, QUESTION 16: After reducing the dose of insulin glargine to 14 units each evening, A.H.’s

FPG is now 110 to 125 mg/dL. However, her noon BG concentrations remain in the 120- to 150-mg/dL range.

Are there any other changes that you would recommend to make at this time?

p. 1100

p. 1101

Table 53-19

Compatibility of Insulin Mixtures

105

Mixture Proportion Comments

Regular + NPH Any proportion The pharmacodynamic profiles of regular and

NPH insulin are unchanged when premixed and

stored in vials or syringes for up to 3 months

Regular + normalsaline Any proportion Use within 2–3 hours of preparation

Regular + insulin diluting solution Any proportion Stable indefinitely

Rapid-acting + NPH

70–72 Any proportion The absorption rate and peak action of the rapidacting insulins are blunted; total bioavailability is

unaltered. Rapid-acting insulin and NPH should

be mixed just before use (within 15 minutes)

Insulin glargine and detemir

76,82 Do not mix with other

insulins

Pharmacodynamics could be modified

NPH, neutral protamine Hagedorn.

When evaluating mid-morning hyperglycemia, it is important to remember that the

FPG concentration can contribute up to 50% of this plasma glucose excursion.

Therefore, a key to the control of mid-morning hyperglycemia may be to normalize

the fasting glucose concentration. However, for A.H., the reduction in the insulin

glargine has now corrected the reactive fasting hyperglycemia.

Hyperglycemia before a meal can be a result of several factors. The following are

possible explanations for A.H.’s mid-morning hyperglycemia:

An insufficient dose of insulin aspart before breakfast. For A.H., this means that her

insulin-to-carbohydrate ratio needs to be adjusted.

Excessive carbohydrate ingestion at breakfast or inaccurate (under) counting of the

carbohydrates ingested. Patients having difficulty accurately counting their

carbohydrates should meet with a dietitian or diabetes educator for education;

this is often necessary periodically throughout their lives as a refresher, just like

many other skills require.

Poor synchrony between meal intake and insulin action. This could be caused by

administration of rapid-acting insulin too long before or after the meal (e.g., ≥30

minutes). If regular insulin is used, this could be caused by administering regular

insulin just before or after meals.

An insufficient dose of evening insulin glargine to suppress hepatic glucose

production (glycogenolysis and gluconeogenesis) during the fasting state or the

dawn phenomenon (see Case 53-3). However, in A.H.’s case, her FBG values

are in target, so this is not likely.

The following interventions may be considered:

Adjust her insulin-to-carbohydrate ratio to increase her insulin aspart dose at

breakfast. The ratio should be changed to 1 unit of aspart for every 10 or 12 g

(which are typical ratios used) of carbohydrate for the breakfast meal. This

assumes a patient is technically able to use a different “ratio” at different

mealtimes.

Alter the carbohydrate content of the meals. This may include decreasing the amount

of carbohydrate in the breakfast meal, changing the type of carbohydrate ingested,

or adding fiber to that meal to minimize glucose excursions.

Adjust the high-sugar correction factor if the glucose excursions appear to be caused

by reduced insulin sensitivity in the morning. For example, the high-sugar

correction can be adjusted to give 1 unit of aspart for every 50 mg/dL above 130

mg/dL.

PREPRANDIAL HYPOGLYCEMIA

CASE 53-2, QUESTION 17: A.H. is now taking insulin glargine 12 units each night and using an insulin-tocarbohydrate ratio of 1:15 (1 unit of insulin aspart for every 15 g of carbohydrate) at lunch and dinner and 1:12

at breakfast. She is continuing with the same high-sugar premeal correction of 1 unit of insulin aspart for every

70 mg/dL more than her premeal BG target of 120 mg/dL. Two weeks later, she brings in her BG records.

Time Glucose Concentration (mg/dL)

7 AM 110–120

Noon 90–115

5 PM 60–110

11 PM 80–110

3 AM 110–120

A.H. feels that she is now “back to normal.” She has no signs or symptoms of hyperglycemia, and her weight

has remained stable. Occasionally, she becomes hypoglycemic before dinner, but this most often occurs when

her dinner is delayed because of a hectic work schedule. Evaluate A.H.’s BG trends. What could be the cause

of her predinner hypoglycemia, and how could she be managed?

A.H.’s BG concentrations indicate that her basic insulin regimen is generally

adequate to achieve the overall goal of preprandial BG concentrations of less than 80

to 130 mg/dL.

The hypoglycemia A.H. is experiencing before dinner could be caused by

insufficient carbohydrate intake at lunch (inaccurate carbohydrate counting),

increased activity during the day, or an excessive dose of insulin aspart (insulin-tocarbohydrate ratio too high). Thus, the problem could be resolved by augmenting

A.H.’s lunch meal, adjusting the lunch insulin-to-carbohydrate ratio to 1 unit of

insulin aspart for every 18 (or 20) g of carbohydrate, or adding a mid-afternoon

snack.

DAWN PHENOMENON

CASE 53-3

QUESTION 1: R.D., a 37-year-old man, has had Type 1 diabetes since age 14. During the past 2 years, he

has been very well controlled on the following insulin regimen: insulin glargine 20 units each morning with insulin

lispro 3 to 4 units depending on carbohydrate

p. 1101

p. 1102

intake before meals. On this regimen, his BG concentrations for the past 2 weeks have been as follows:

Time Glucose Concentration (mg/dL)

7 AM 140–170

Noon 100–120

5 PM 100–130

11 PM 115–140

3 AM 100–120

What are the likely causes of R.D.’s fasting hyperglycemia?

As discussed in Case 53-2, Question 13, fasting hyperglycemia may be the result

of insufficient doses of insulin in the evening and, possibly, reactive hyperglycemia.

In R.D.’s case, the dawn phenomenon also must be considered.

98 The dawn

phenomenon is a rise in the BG concentration that occurs between 4 and 8 AM after a

physiologic nadir in the BG concentration that occurs between midnight and 3 AM.

This 30- to 40-mg/dL increase in the morning BG concentration cannot be attributed

to increases in counter-regulatory hormones secondary to an antecedent

hypoglycemic event, but it may be secondary to rising growth hormone levels. This

phenomenon is inconsistently observed in individuals with Type 1 and Type 2

diabetes as well as nondiabetic individuals; furthermore, it is inconsistently present

from one day to the next.

114

R.D.’s normal 3 AM BG concentration indicates that posthypoglycemic

hyperglycemia is an unlikely cause of his fasting hyperglycemia. Thus, the modest

increase in his BG concentration between 3 and 8 AM may be attributed to the waning

effects of insulin or the dawn phenomenon. In both cases, an increase in R.D.’s daily

dose of insulin glargine would be indicated. Another option would be to switch R.D.

to an insulin pump. He has demonstrated a desire and the ability for intensive

management with multiple daily injections, frequent SMBG, record-keeping skills,

the ability to make appropriate insulin dose adjustments, and accurate carbohydrate

counting. The advantage to using a pump is the ability to program an increase in the

basal infusion rate in the early-morning hours (e.g., beginning around 2 to 3 AM and

continuing until 7 to 9 AM).

Type 1 Diabetes in Children

DIAGNOSIS AND CLINICAL PRESENTATION

CASE 53-4

QUESTION 1: J.C., a 7-year-old, 30-kg (95th percentile), 50 inches tall (90th percentile) girl, was brought to

the emergency department by her parents because of nausea, vomiting, and a persistent stomach pain

secondary to the flu. For the past week, J.C. had flulike symptoms, resulting in a 6-lb weight loss. Initial

laboratory values revealed a BG of 600 mg/dL, serum pH of 6.8 with bicarbonate level of 13 mEq/L, plasma

ketone level of 5.2 mmol/L, and positive ketonuria. J.C. was diagnosed with diabetic ketoacidosis (DKA)

secondary to new-onset Type 1 diabetes. In retrospect and on further questioning, J.C.’s parents realized that

she probably had symptoms as early as 4 weeks before her hospitalization. While on a driving vacation, she

drank large quantities of juice and had to stop hourly to urinate. She began experiencing enuresis, which her

parents attributed to her increased fluid intake. What signs and symptoms are consistent with the diagnosis of

Type 1 diabetes in a child?

The diagnosis of Type 1 diabetes in children is generally straightforward.

Presenting symptoms include a several-week history of polyuria, polydipsia,

polyphagia, and weight loss, with hyperglycemia, glucosuria, ketonemia, and

ketonuria. J.C.’s presentation is typical for a child newly diagnosed with diabetes

who is brought in for medical attention because of severe symptoms related to the flu.

An acute viral illness can trigger autoimmune destruction of the pancreas and

abdominal pain, which may masquerade as gastroenteritis. Abdominal pain is a

common presenting symptom of DKA.

115 J.C.’s weight loss probably represents fluid

and caloric loss secondary to uncontrolled diabetes as well as decreased caloric

intake from the flu. The symptoms of polyuria are less obvious in an infant and are

frequently missed until metabolic derangement has occurred. Unlike J.C., infants

frequently present with severe dehydration and metabolic acidosis despite a negative

history of diarrhea or significant vomiting.

GOALS OF THERAPY

CASE 53-4, QUESTION 2: What are the goals of therapy for J.C.? Do the results of the DCCT apply to

children such as J.C.? Are there age-specific goals?

Current ADA guidelines recommend an A1C goal of <7.5% for all pediatric

groups and adolescents (<19 years old) such as J.C. with diabetes mellitus.

Individualization of goals however is still encouraged.

7

Additional targets should also be kept in mind, including (a) to achieve normal

growth and development, (b) to facilitate positive psychosocial adjustment to

diabetes, and (c) to prevent acute and chronic complications. Attainment of these

goals requires a tremendous amount of support and education for the parents and can

best be provided by a multidisciplinary team of professionals, including a pediatric

endocrinologist, nurse educator, pharmacist, dietitian, and mental health

professional.

116

Growth serves as an important clinical indication of overall general health and

well-being in children with diabetes. Height and weight should be measured at each

visit and plotted on standard growth grids. If, at the time of diagnosis, a child has

fallen behind in height or weight, prompt and appropriate treatment should quickly

return the child to the appropriate percentile and pattern of growth. An overweight

child should be encouraged to achieve a more appropriate percentile of weight

gradually, over the course of several months.

117

Although recommendations for glycemic control are based on data from studies

mostly in adult patients with diabetes, achieving the same near-normalization of BG

levels in children and adolescents is recommended. However, special consideration

must be given to the unique risks and consequences of hypoglycemia in young

children. A cohort of adolescents included in the DCCT was analyzed separately.

118

Similar to the adults in the DCCT, adolescents had sustained benefits from intensive

management with little further progression to proliferative retinopathy 4 years after

the DCCT was terminated.

119 Thus, J.C.’s pediatrician must strive for the best

glucose control that she, her family circumstances, and currently available treatment

regimens will permit.

The risk of hypoglycemia is of great concern in children younger than 6 years of

age as they can have a form of hypoglycemic unawareness that results partly from

their reduced capacity to communicate symptoms of hypoglycemia, but may be

contributed to by less-developed counter-regulatory mechanisms.

38

In addition, food

intake and physical activity are unpredictable in this age group. These factors must be

taken into consideration when determining an A1C goal in this patient population

where the long-term benefits of achieving a lower A1C need to be weighed against

the risk of hypoglycemia.

116 Per the ADA recommendations, the ultimate goal

p. 1102

p. 1103

is to achieve the best A1C possible without experiencing symptoms of

hypoglycemia. The management of diabetes in children 6 to 12 years of age, such as

J.C., is particularly challenging because many children require insulin with lunch or

at other times when they are away from home. Administration of insulin at school

demands flexibility and close communications between the parents, the healthcare

team, and school personnel. (Table 53-4).

38,116,120 The greatest amount of evidencebased data exists for adolescents with diabetes (13–19 years). As mentioned,

teenagers included in the DCCT achieved a mean A1C level of 8.06% in an era

before the availability of rapid-acting or basal insulins. As stated previously, an A1C

goal of less than 7.5% is recommended in this age group.

38,116,120

INSULIN THERAPY

CASE 53-4, QUESTION 3: How should J.C. be started on insulin? Is the use of an insulin pump appropriate

in children such as J.C.?

Generally, rapid-acting and basal insulin analogs are used in children to reduce the

risk of hypoglycemia. Insulin requirements are generally based on body weight, age,

and pubertal status. Newly diagnosed children with Type 1 diabetes usually require

an initial TDD of approximately 0.5 to 1.0 unit/kg.

116 The small insulin requirements

of infants and toddlers may be delivered by using diluted insulin (e.g., 10 units/mL,

U-10; or 50 units/mL, U-50)

70,71

to measure doses in less than 1-unit increments.

Diluents are available for insulin aspart and lispro. Insulin syringes and pens that

deliver insulin in 0.5-unit increments are also very useful in pediatric patients. Most

children are treated with basal-bolus regimens. These regimens have demonstrated

lower FBG levels with less nocturnal hypoglycemia versus regimens using NPH in

children and adolescents.

121