type i dm in pediatric prepared by: dr moslah jabari pediatric endocrinologist assistant professor...

Type I DM in Type I DM in PediatricPediatric

Prepared by:

Dr Moslah JabariPediatric Endocrinologist

Assistant Professor in Pediatrics

• Introduction• Insulin regimen• Insulin dose• Diet• Monitoring• Hypoglycemia• Management during infection• Management during surgery• Screening for chronic complication

DIAGNOSTIC CRITERIA FOR IMPAIRED GLUCOSE TOLERANCE AND DIABETES

MELLITUS

Diagnostic Criteria of Impaired Glucose Tolerance and Diabetes Mellitus Table

Symptoms include polyuria, polydipsia, and unexplained weight loss with glucosuria and ketonuria. A fasting glucose concentration of 99 mg/dL is the upper limit of “normal”.

Etiologic Classification of Diabetes Mellitus Table

Epidemiology:

The incidence among school-age children is about 1.9/ 1,000 in USA with annual incidence about 14.9 new cases/ 100,000 children.

• Sex: M:F ratio is 1:1.• Age at presentation: Peaks occur in 2 age

groups. At 5-7 yr of age and puberty

• Seasonal variations: More frequent in the autumn and winter months.

Etiology:

The Mechanisms that lead to failure of

pancreatic ß-cell function increasingly point

to an auto immune destruction ofpancreatic islet ß cells in

predisposed individuals.

Evidences supporting the auto immune basis of type 1 DM (T1DM)

1. Type 1 DM is commonly associated with auto immune diseases as celiac disease, Addison disease, and thyroiditis.

2. Auto antibodies as (GAD)and islet cell cytoplasm antibodies (ICA) and insulin auto antibodies (IAA) are detected in the sera of newly diagnosed patients.


3. Genetic predisposition (the increased protection and susceptibility to T1DM)

The Genetics of type 1 DM cannot be classified according to a specific model of inheritances. The most important genes are located within the MHC HLA class II region on chromosome 6p21, accounting for about 60% of genetic susceptibility for the disease.


a. The inheritance of HLA-DR3 or DR4 antigens (susceptibility haplotypes) increases the risk for developing type 1 DM two to 3 folds. The inheritance of both antigens increases the risk 7-10 fold.

b. Role of HLA Class : Certain alleles of class II HLA genes appear to have the strongest associations with diabetes, the most significant association is with HLA-B39, which confers high risk for type 1A diabetes.


c. The inheritance of certain genotype HLA-DRB1-0401 DQB1-302 DQA1-0301 confer high risk susceptibility.

d. The inheritance of certain genotype provide significant protection as

HLA-DRB1-0403 DQB1-0301 DQA1-0102


The homozygous absence of aspartic acid at position 57 of the HLA-DQ ß-chain confers about 100 fold relative risk for the development of T1DM.

e. Insulin gene locus: It is found to be associated with risk of T1DM and it is estimated that this locus accounts for about 10% of the familiar risk of T1DM.


4. EnvironmentFactors such as viral infections, chemicals, seasonal factors, and dietary factors have been suspected of contributing to differences in the incidence and prevalence of type 1 DM in various ethnic populations.


a. Viral Infections: A variety of viruses and mechanisms may contribute to the development of T1DM in genetically susceptible hosts. Enteroviral, congenital rubella, and mumps infection leads to the development of ß-cell auto immunity with high frequency and to T1DM in some cases. Congenital rubella infection is associated with diabetes (up to 40%).


b. Diet

• Breast-feedingMay lower the risk of T1DM, either directly or by delaying exposure to cow’s milk protein.


• Early introduction of cow’s milk protein and early exposure to gluten in cereals have both been implicated in the development of auto immunity and it has been suggested that this is due to the “leakiness” of the immature gut to protein antigen

• s. Antigens that have been implicated include ß-lactoglobulin, which is homologous to the human protein glycodelin (PP14), a T-cell modulator. Other studies have focused on bovine serum abumin as the inciting antigen,.


• Other dietary factors that have been suggested at various times as playing a role in diabetes risk include Omega-3 fatty acids, Vitamin D, ascorbic acid, zinc, and Vitamin E

• Vitamin D has a role in immune regulation, decreased Vitamin D levels in pregnancy or early childhood may be associated with diabetes risk; but the evidence is not yet conclusive.


c. Psychologic stress: Several studies show an increased prevalence of stressful psychologic situations among children who subsequently developed T1DM. Whether these stresses only aggravate pre-existing auto immunity or whether they can actually trigger auto immunity remains unknown.

Pathogenesis and natural history of type 1 diabetes mellitus

A genetically susceptible host develops auto immunity against his or her own ß cells. What triggers this auto immune response remains unclear at this time. In some ( But not all) patients, this auto immune process results in progressive destruction of ß cells until a critical mass of ß cells are destroyed and the patient becomes totally dependent on exogenous insulin for survival.

Pathogenesis and natural history of type 1 diabetes mellitus

1.Initiation of auto immunity.2. Preclinical auto immunity with progressive loss of ß-cell function.3. Onset of clinical disease.4. Transient remission (honeymoon period).5. Established disease.6. Development of complications.

Pathophysiology

In normal individuals, there are normal swings between the postprandial, high-insulin anabolic state and fasted, low-insulin catabolic state that affect 3 major tissues: liver, muscle, and adipose tissue.

Influence of feeding (High Insulin) or of fasting (Low Insulin) on some Metabolic processes in liver, muscles and adipose tissue.

Tissue Postprandial State(High Plasma

Insulin)

Fasted State(Low Plasma

Insulin)

Liver • Glucose uptake, glycogen synthesis, absence of gluconeogenesis• Lipogenesis• Absence of ketogenesis

• Glucose production (glycogenolysis + gluconeogenesis)• Absence of lipogenesis• Ketogenesis

Muscle • Glucose uptake and oxidation, and glycogen synthesis• Protein synthesis

• Absence of glucose uptake• Glycogenolysis•Proteolysis and amino acid release

Adipose Tissue

• Glucose uptake• Triglyceride uptake• Lipid synthesis

• Absence of glucose uptake•Absence of triglyceride uptake• Lipolysis and fatty acids release

1. Hyperglycemia- (fasting and increases after eating): due to glucose production (glycogenolysis and gluconeogenesis) and absence of glucose uptake by muscle and adipose tissues.

2. Glucosuria - When blood glucose level exceeds the renal tubular maximum (Tm) of glucose (180 mg/dL). Calories are lost in urine a compensatory hyperphagia. If the Hyperphagia does not keep pace with the glucosuria, loss of body fat ensues with clinicalweight loss.

Influence of feeding (High Insulin) or of fasting (Low Insulin) on some Metabolic processes in liver, muscles and adipose tissue.

3. Metabolic Acidosis- Insulinopenia, diminished energy production from glucose lipolysis. Peripheral utilization of fatty acids is incomplete and they are converted to ketone bodies in the liver. Accumulation of ketoacids (acetoacetic, ß-hydroxybutyric acids) will lead to metabolic acedosis. Ketoacidosis leads Kussmaul respiration (deep rapid breathing), fruity breath odor (acetone), diminished neurocognitive function, and possible coma.

4. Dehydration and loss of electrolytes Ketones in association with cations are excreted in urine- loss of fluid and electrolytes, also hyperglycemia will lead to osmotic diuresis.

5. Hyperosmolality - It is due to dehydration and hyperglycemia.Serum osmolality in mOsm/kg=2 (serum Na) glucose mg/ dL /18 + BUN mg/ dL /3.

• 6. Impaired level of consciousness- it is due to dehydration, hyperosmolality, metabolic acidosis, and diminished cerebral oxygen utilization.

Clinical Manifestations

Different clinical presentations

1. The classic presentation of diabetes in children is a history of polyuria, polydipsia, hyperphagia, and loss of weight (loss of body fat). The duration of these symptoms is often less than 1 mo. Hyperphagia occurs as a compensatory mechanism when calories are lost in the urine (glucosuria).


2. Enuresis (due to polyuria) in a previously

toilet-trained child.

3. Insidious onset with lethargy, weakness,

and weight loss (in spite of an increased Apetite).

4. Pyogenic skin infections or monolial vaginitis ( in teenage girls due to chronic glucosuria).


5. Diabetic ketoacido sis- it is the clinical presentation of 20%-40% of new-onset diabetic children and in children with known diabetes who omit insulin doses or who do not successfully manage the precipitating factors (trauma, infection, vomiting, and psychologic disturbances).


• The early manifestations may be mild (nausea, vomiting, polyuria and dehydration).

• Kussmaul respiration (deep rapid respiration due to metabolic acidosis in an attempt to excrete excess CO2) with an odor of acetone on the breath (acetone is formed by non enzymatic conversion of acetoacetate).


• Abdominal pain or rigidity (DD: appendicitis, pancreatitis), nausea, and emesis.

• Severe dehydration • Cerebral obtundation and ultimately

coma.

Diagnosis of T1DM

1. Hyperglycemia- Non fasting blood glucose value exceeding 200 mg/ dL with typical symptoms.

2. Glucosuria

DD

The differential diagnosis of diabetes mellitus is not difficult, since this is virtually the only condition that gives rise to hyperglycemia, glucosuria and ketosis.

. Renal glucosuria

Isolated Congenital disorder.

Renal tubular disorder (Fanconi syndrome, Renal disorders due to intoxication by heavy metals {lead} or outdated tetracycline or inborn errors of metabolism {cystinosis}).

DD

. Causes of metabolic acidosis

Uremia, gastroenteritis with metabolic acidosis, hypoglycemia, lactic acidosis, salicylate intoxication, sepsis and encephalitis.

. Physical stress

Transient hyperglycemia with glucosuria, this is induced by counter regulatory hormones.

New-Onset Diabetes without Ketoacidosis

• Excellent diabetes control involves many goals• to maintain a balance between tight glucose control

and avoiding hypoglycemia• to eliminate polyuria and nocturia, to prevent

ketoacidosis• permit normal growth and development with minimal

effect on lifestyle.

initiation and adjustment of insulin,• extensive teaching of the child and caretakers• reestablishment of the life routines.

• Each aspect should be addressed early in the overall care.

• therapy can begin in the outpatient setting, with complete team staffing by a pediatric endocrinologist, experienced nursing staff, dietitians with training as diabetes educators, and a social worker.

• Close contact between the diabetes team and family

must be assured. Otherwise, initial therapy should be

done in the hospital setting.

Types of InsulinTypes of Insulin• Rapid Acting:

– Insulin lispro (Humalog) ®

– Insulin aspart (Novolog) ®

– Insulin glulisine (Apidra) ®

• Short-acting:

– Regular

• Intermediate-acting:

– NPH

• Long-acting:

– Insulin glargine (Lantus) ®

– Insulin detemir (Levemir) ®

Rapid (lispro, aspart, glulisine)

Hours

Long (glargine)

Short (regular)

Intermediate (NPH)

Long (detemir)

InsulinLevel

0 2 4 6 8 10 12 14 16 18 20 22 24

Pharmacokinetics of Insulin ProductsPharmacokinetics of Insulin Products

Adapted from Hirsch I. N Engl J Med. 2005;352:174-183.

Normal Insulin SecretionNormal Insulin Secretion

Basal (background) insulin needs0

10

20

30

40

50

0 2 4 6 8 10 12 14 16 18 20 22 24

Seru

m in

sulin

(µU

/mL)

Time

Meal Meal Meal Bolus (meal) insulin needs

60

Common Insulin Regimens• The goal of treatment in type 1 DM is to provide

insulin in as physiologic a manner as possible.• Insulin replacement is accomplished by giving a basal

insulin and a preprandial (premeal) insulin• The basal insulin is either long-acting (glargine or

detem • The preprandial insulin is either rapid-acting (lispro,

aspart, or glulisine) or short-acting (regular)

• For patients on intensive insulin regimens (multiple daily

injections or insulin pumps), the preprandial dose is based on

the carbohydrate content of the meal (the carbohydrate ratio)

• plus a correction dose if their blood glucose level is elevated

• This method allows patients more flexibility in caloric intake

and activity, but it requires more blood glucose monitoring and

closer attention to the control of their diabetes.

http://emedicine.medscape.com/article/1982274-overview

4:00 16:00 20:00 24:00 4:00

Breakfast Lunch Dinner

8:0012:008:00

Glargine or detemir

Plas

ma

insu

linBasal/Bolus Treatment Program With Rapid-

Acting and Long-Acting Analogs

Bed




Subcutaneous Insulin Dosing

Age (years)

0-5

5-12

12-18

Target Glucose (mg/dL)

100-200

80-150

80-130

Target Daily Insulin (units/kg/d)

0.6-0.7

0.7-1.0

1.0-1.2

Basal Insulin (% of total daily dose)

25-30

40-50

40-50

Bolus Units added per 100 mg/dL above target

Insulin Units Added per 15 g at Meal

0.5 0.5

0.75 0.75

1.0-2.0 1.0-2.0

A four-step dosing A four-step dosing scheduleschedule

The basal insuline glargine should be 25-

30% of the total dose in toddlers and 40-

50% in older children. The remaining

portion of the total daily dose is divided

evenly as bolus injections for the three

meals.

Newly diagnosed children in the “honeymoon” may only

need 60-70% of a full replacement dose. Total daily dose

per kg increases with puberty.

Newly diagnosed children who do not use carbohydrate

dosing should divide the nonbasal portion of the daily

insulin dose into equal doses for each meal

• For example: a 6 yr old child who weighs 20 kg needs about

(0.7 U/kg/24 hr ? 20 kg) = 14 U/24 hr with 7 U (50%) as basal and

7 U as total daily bolus

• . Give basal as glargine at bedtime. Give 2 U lispro or aspart

before each meal if the blood glucose is within target

• subtract 1 U if below target; add 0.75 U for each 100 mg/dL

above target (round the dose to the nearest 0.5 U). For finer

control, extra insulin may be added in 50-mg/dL increments.

Indeed, bolus-basal treatment with multiple

injections is better adapted to the

physiologic profiles of insulin and glucose

and can therefore provide better glycemic

control than the conventional two-to-three

dose regimen. This approach allows insulin

doses to be changed as needed to correct

hyperglycemia, supplement for additional

anticipated carbohydrate intake, or subtract

for exercise.

Some families may be unable to administer four daily injections.

In these cases, a compromise may be needed:

A three-injection regimen: Combining NPH with a rapid analog

bolus at breakfast, a rapid acting analog bolus at supper, and

NPH at bed time. This regimen may provide fair glucose control.

A two-injection regimen: This would require NPH combined with

a rapid analog bolus at breakfast and supper. However, such a

schedule would provide poor coverage for lunch and early

morning, and would increase the risk of hypo glycemia at

midmorning and early night.

a. The total daily insulin requirement is calculated.

b. 2/3 of the daily dose is given before breakfast and 1/3

before supper (if the total dose is 30 U, 20 U will be given

before breakfast and 10 U before supper).

c. Each injection consists of intermediate and regular

insulins in proportions of 2: 1 or 3:1 (20 U before breakfast

=14U of NPH + 6 U of regular insulin, and 10 U before

supper= 6 U of NPH + 4 U of regular insulin).

Fine adjustment of insulin dose

• NPH in the morning dose has primary influence on

before supper blood glucose (after about 12 hr).

• Morning regular insulin has primary influence on before

lunch blood glucose (after about 6 hr).

• NPH in the evening dose has primary influence on

breakfast blood glucose (after about 12 hr).

• Evening regular insulin has primary influence on before

bed blood glucose (after about 6 hr).

Fine Adjustment of the Two Injection Fine Adjustment of the Two Injection RegimenRegimen

Examples

Before lunch blood glucose level

• If the level is less than 80 mg/dL, decrease the dose of A.M

regular insulin by 1-2 units.

• If the level is more than 150 mg/dL, increase the dose of

A.M regular insulin by 1-2 units.

Before supper blood glucose level

• If the level is less than 80 mg/dL, decrease the dose of A.M-

NPH by 1-3 units.

• If the level is more than 150 mg/dl, increase the dose of

A.M- NPH by 1-3 units and so on.

INSULIN DOSAGEINSULIN DOSAGEInsulin requirement is based upon the body weight, age, and pubertal stage of the child

In general, the newly diagnosed child requires an initial total daily insulin dose of 0.5 to 1.0 units/kg.

Prepubertal children usually require lower doses, and the dose requirement may be as low as 0.25 units/kg for a variable period following diagnosis.

Higher doses are needed in pubertal children, patients in ketoacidosis, or in patients receiving glucocorticoid therapy.

INSULIN DOSAGEINSULIN DOSAGEIn infants and toddlers who receive their insulin by syringe, the insulin dose may be so small that dilution is required to allow for easier and more precise administration.

The smallest dose of insulin that can be accurately administered without dilution using a syringe is 0.5 units.

Many insulins can be diluted either at a specialized pharmacy or at home with proper training.

Specific diluent for many insulin preparations is available from the insulin manufacturer.

Some insulin pumps can deliver much smaller doses of insulin, of the order of 0.025 units at a time, often obviating this problem.

INSULIN DOSAGEINSULIN DOSAGE

On average, 1 unit of insulin is required to cover:

•20 grams of carbohydrates in most young children (1 to 6 years of age)

•10 to 12 grams of carbohydrates in older prepubertal children

•8 to 10 grams in pubertal adolescents

Monitoring • Success in the daily management of the diabetic child can be measured by the

competence acquired by the family, and subsequently by the child, in

assuming responsibility for daily “diabetic care.” Their initial and ongoing

instruction in conjunction with their supervised experience can lead to a sense

of confidence in making intermittent adjustments in insulin dosage for dietary

deviations, for unusual physical activity

• and even for some minor intercurrent illnesses, as well as for otherwise

unexplained repeated hypoglycemic reactions and excessive glycosuria. Such

acceptance of responsibility should make them relatively independent of the

physician for their ordinary care. The physician must maintain ongoing

interested supervision and shared responsibility with the family and the child.

• Self-monitoring of blood glucose (SMBG) is an essential component

of managing diabetes. Monitoring often also needs to include

insulin dose, unusual physical activity, dietary changes,

hypoglycemia, intercurrent illness, and other items that may

influence the blood glucose.

• These items may be valuable in interpreting the SMBG record,

prescribing appropriate adjustments in insulin doses, and teaching

the family. If there are discrepancies in the SMBG and other

measures of glycemic control (such as the HbA1c), the clinician

should attempt to clarify the situation in a manner that does not

undermine their mutual confidence

• Parents and patients should be taught to use these devices and measure

blood glucose at least 4 times daily—before breakfast, lunch, and supper

and at bedtime. When insulin therapy is initiated and when adjustments

are made that may affect the overnight glucose levels,

• SMBG should also be performed at 12 a.m. and 3 a.m. to detect nocturnal

hypoglycemia. Ideally, the blood glucose concentration should range from

approximately 80 mg/dL in the fasting state to 140 mg/dL after meals. In

practice, however, a range of 60-220 mg/dL is acceptable

• based on age of the patient (Blood glucose measurements that are

consistently at or outside these limits, in the absence of an identifiable

cause such as exercise or dietary indiscretion, are an indication for a

change in the insulin dose.

• If the fasting blood glucose is high, the evening dose of long-acting

insulin is increased by 10-15% and/or additional fast-acting insulin (lispro

or aspart) coverage for bedtime snack may be considered.

• If the noon glucose level exceeds set limits, the morning fast-acting

insulin (lispro or aspart) is increased by 10-15%

• If the pre-supper glucose is high, the noon dose of fast-acting insulin is

increased by 10-15%.

• If the pre-bedtime glucose is high, the pre-supper dose of fast-acting

insulin is increased by 10-15%.

• Similarly, reductions in the insulin type and dose should be made if the

corresponding blood glucose measurements are consistently below

desirable limits.

Hypoglycemic Reactions Hypoglycemic Reactions • Hypoglycemia is the major limitation to tight control of glucose levels.

Once injected, insulin absorption and action are independent of the

glucose level, thus creating a unique risk of hypoglycemia from an

unbalanced insulin effect. Insulin analogs may help reduce but cannot

eliminate this risk.

• Most children with T1DM can expect mild hypoglycemia each week,

moderate hypoglycemia a few times each year, and severe hypoglycemia

every few years. These episodes are usually not predictable,

• although exercise, delayed meals or snacks, and wide swings in glucose

levels increase the risk.

Infants and toddlers are at higher risk because they have more variable

meals and activity levels, are unable to recognize early signs of

hypoglycemia, and are limited in their ability to seek a source of oral

glucose to reverse the hypoglycemia.

The very young have an increased risk of permanently reduced cognitive

function as a long-term sequela of severe hypoglycemia. For this reason, a

more relaxed degree of glucose control is necessary until the child

matures

Hypoglycemia can occur at any time of day or night.

Early symptoms and signs (mild hypoglycemia) may occur with a suddendecrease in blood glucose to levels that do not meet standard criteriaFor hypoglycemia in nondiabetic children.

The child may show pallor, sweating, apprehension or fussiness, hunger, tremor, and tachycardia, all due to the surge in catecholamines as thebody attempts to counter the excessive insulin effect. Behavioralchanges such as tearfulness, irritability, aggression, and naughtiness aremore prevalent in children.

As glucose levels decline further, cerebral glucopenia occurs with drowsiness,

personality changes, mental confusion, and impaired judgment (moderate

hypoglycemia) progressing to inability to seek help and seizures or coma

(severe hypoglycemia). Prolonged severe hypoglycemia can result in a

depressed sensorium or Stroke like focal motor deficits that persist after the

hypoglycemia has resolved.

Although permanent sequelae are rare, severe hypoglycemia is frightening

for

the child and family and can result in significant reluctance to attempt even

Moderate glycemic control afterward.

• Recurrent hypoglycemic episodes associated with tight metabolic

control may aggravate partial counter-regulatory deficiencies,

producing a syndrome of hypoglycemia unawareness and reduced

ability to restore euglycemia (hypoglycemia-associated autonomic

failure). Avoidance of hypoglycemia allows some recovery from this

unawareness syndrome

• The most important factors in the management of hypoglycemia are an understanding by

the patient and family of the symptoms and signs of the reaction and an anticipation of

known precipitating factors such as gym or sports activities. Tighter glucose control

increases the risk.

• Families should be taught to look for typical hypoglycemic scenarios or patterns in the

home blood glucose log, so that they may adjust the insulin dose and avert predictable

episodes.

• A source of emergency glucose should be available at all times and places, including at

school and during visits to friends. If possible, it is initially important to document the

hypoglycemia before treating, because some symptoms may not always be due to

hypoglycemia.

• Most families and children develop a good sense for true hypoglycemic episodes and can

institute treatment before testing. Any child suspected of having a moderate to severe

hypoglycemic episode should also be treated before testing.

• It is important not to give too much glucose; 5-10 g should be given

as juice or a sugar-containing carbonated beverage or candy, and

the blood glucose checked 15-20 minutes later. Patients, parents,

and teachers should also be instructed in the administration of

glucagon when the child cannot take glucose orally.

• An injection kit should be kept at home and school. The

intramuscular dose is 0.5 mg if the child weighs less than 20 kg and

1.0 mg if more than 20 kg. This produces a brief release of glucose

from the liver. Glucagon often causes emesis, which precludes

giving oral supplementation if the blood glucose declines after the

glucagon effects have waned. Caretakers must then be prepared to

take the child to the hospital for IV glucose administration,

Dawn PhenomenonDawn Phenomenon• There are several reasons that blood glucose levels increase in the early morning

hours before breakfast. The most common is a simple decline in insulin levels

and is seen in many children using NPH or Lente as the basal insulin at supper or

bedtime. This usually results in routinely elevated morning glucose.

• The thought to be due mainly to overnight growth hormone secretion and

increased insulin clearance. It is a normal physiologic process seen in most

nondiabetic adolescents, who compensate with more insulin output. A child with

T1DM cannot compensate and may actually have declining insulin levels if using

evening NPH or Lente. The dawn phenomenon is usually recurrent and modestly

elevates most morning glucose levels.

Somogyi phenomenonSomogyi phenomenon• Rarely, high morning glucose is due to the Somogyi

phenomenon, a theoretical rebound from late night or

early morning hypoglycemia, thought to be due to an

exaggerated counter-regulatory response.

• It is unlikely to be a common cause, in that most children

remain hypoglycemic (do not rebound) once nighttime

glucose levels decline. Continuous glucose monitoring

systems may help clarify ambiguously elevated morning

glucose levels.

Brittle DiabetesBrittle Diabetes• The term has been used to describe the child, usually an adolescent female, with

unexplained wide fluctuations in blood glucose, often with recurrent DKA, who is

taking large doses of insulin.

• An inherent physiologic abnormality is rarely present because these children usually

show normal insulin responsiveness when in the hospital environment.

• Psychosocial or psychiatric problems, including eating disorders, and dysfunctional

family dynamics are usually present, which preclude effective diabetes therapy

• . Hospitalization is usually needed to confirm the environmental effect, and

aggressive psychosocial or psychiatric evaluation is essential. Therefore, clinicians

should refrain from using “brittle diabetes” as a diagnostic term.

Management During Infections Management During Infections • Although infections are no more common in diabetic children than in nondiabetic

ones, they can often disrupt glucose control and may precipitate DKA.

• In addition, the diabetic child is at increased risk of dehydration if hyperglycemia

causes an osmotic diuresis or if ketosis causes emesis.

• Counter-regulatory hormones associated with stress blunt insulin action and

elevate glucose levels. If anorexia occurs, however, lack of caloric intake increases

the risk of hypoglycemia.

• Although children younger than 3 yr tend to become hypoglycemic and older

children tend toward hyperglycemia, the overall effect is unpredictable. Therefore,

frequent blood glucose monitoring and adjustment of insulin doses are essential

elements of sick day guidelines

• The overall goals are to maintain hydration, control glucose levels, and avoid

ketoacidosis.

• This can usually be done at home if proper sick day guidelines are followed and

with telephone contact with health care providers. The family should seek advice if

home treatment does not control ketonuria, hyperglycemia, or hypoglycemia, or if

the child shows signs of dehydration.

• A child with large ketonuria and emesis should be seen in the emergency

department for a general examination, to evaluate hydration, and to determine

whether ketoacidosis is present by checking serum electrolytes, glucose, pH, and

total CO2.

• A child whose blood glucose declines to less than 50-60 mg/dL (2.8-3.3 mmol/L)

and who cannot maintain oral intake may need IV glucose, especially if further

insulin is needed to control ketonemia.

Management During SurgeryManagement During Surgery• Surgery can disrupt glucose control in the same way as can intercurrent

infections. Stress hormones associated with the underlying condition as well

as with surgery itself decrease insulin sensitivity.

• This increases glucose levels, exacerbates fluid losses, and may initiate DKA.

On the other hand, caloric intake is usually restricted, which decreases

glucose levels. The net effect is as difficult to predict as during an infection.

• Vigilant monitoring and frequent insulin adjustments are required to

maintain euglycemia and avoid ketosis.

• Maintaining glucose control and avoiding DKA are best

accomplished with IV insulin and fluids. A simple insulin adjustment

scale based on the patient's weight and blood glucose level can be

used in most situations

• The IV insulin is continued after surgery as the child begins to take

oral fluids; the IV fluids can be steadily decreased as oral intake

increases. When full oral intake is achieved, the IV may be capped

and subcutaneous insulin begun. When surgery is elective, it is best

performed early in the day, allowing the patient maximal recovery

time to restart oral intake and subcutaneous insulin therapy.

• When elective surgery is brief (less than 1 hr) and full oral intake is

expected shortly afterward, one may simply monitor the blood

glucose hourly and give a dose of insulin analog according to the

child's home glucose correction scale.

• If glargine or detemir is used as the basal insulin, a full dose is given

the evening before planned surgery. If NPH or Lente is used, one

half of the morning dose is given before surgery. The child should

not be discharged until blood glucose levels are stable and oral

intake is tolerated.

type i dm in pediatric prepared by: dr moslah jabari pediatric endocrinologist assistant professor...

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