1. Jon Galea, D.D.S. Children’s National Medical Center November 9, 2001
DIABETES
Jon Galea, D.D.S.
Children’s National Medical Center
November 9, 2001
Unless otherwise noted in the footer, all information was gathered from Dr. Oski’s book on Pediatric medicine

2. Type I (Insulin-Dependent) Diabetes Mellitus
A common and serious disease of childhood and adolescence
A new case is diagnosed every hour
Can shorten life by 15 years
Long-term management is challenging to child, family and health care team
Rarely does any disease require as much self-care management as does IDDM
jdrf, 2001

3. DEFINITION
Type I diabetes is the most common form found in children. Other names used in the past include; juvenile-onset, brittle or ketosis-prone diabetes.
Type I diabetics are unable to produce insulin and therefore require and external source of insulin to prevent ketosis and maintain life

4. EPIDEMIOLOGY Prevalence Incidence Seasonal distribution
Among children and adolescents most studies report a rate of 1.2 to 1.9 cases per 1,000 Gender
Males and females equally affected
Incidence
Increases with age, peaking at early to middle puberty
Seasonal distribution
Most newly diagnosed cases occur in the cooler months

5. Diagnosis
Diagnosis is usually quite easy with the child showing the classic signs including:
Polyuria
Polydipsia
Polyphagia
Weight loss
Lethargy

6. Diagnostic Glucose Levels
In addition to the classic symptoms, glucose levels must be elevated
Random plasma glucose  200mg/dL (1.11mmol/L)
If asymptomatic:
Fasting plasma glucose  126mg/dL (7.0 mmol/L) or
2- hour plasma glucose level with a glucose tolerance test  200mg/dL
Requires repeat testing on another day to confirm
Normal blood glucose levels are within a range of 60mg/dL- 150mg/dL

7. ETIOLOGY
Development of Type 1 Diabetes appears to have genetic as well as external causative factors
Since < 50% of identical twins are both affected with Type 1 DM it is believed that only a susceptibility is inherited and not actually DM itself
Overall, only 5% of type 1 DM patient’s siblings develop the disease
Significant geographic variation in the incidence of Type 1 DM exists

8. Genetics
There is no one diabetic gene but rather evidence of genetic variations that raise or lower the susceptibility to beta-cell destruction
Inheritance of HLA antigens DR3 and DR4 increase the risk of developing Type 1 DM
DR3 or DR4 = 3x-5x > risk
DR3 and DR4 together = 10x > risk
95% of Type 1 DM patients have one or both of these antigens
DQ antigen variation is also implicated with greater risk

9. External Factors External environmental factors may include:
Viral infections
Dietary factors
Environmental toxins
Stress

10. Pathogenesis
80% of beta-cell mass must be destroyed before glucose intolerance is noticeable
Beta-cell destruction is usually immune-mediated and takes place over the course of months or years
Immunologic markers present in Type 1 DM patients:
Islet cell antibodies (ICAs)
Insulin autoantibodies (IAAs)
Process may be a slow ,constant progressive destruction or may have an intermittent course with periods of destruction followed by remission

11. Pathophysiology Normal Insulin Levels Absent or low Insulin levels
With food ingestion insulin acts as an anabolic hormone and converts glucose into energy storage forms of glycogen, protein and adipose tissue
Absent or low Insulin levels
Stored energy is broken down in a lysis reaction and the uptake of ingested glucose is inhibited
Mild insulin deficiency  hyperglycemia
Severe insulin deficiency  ketonuria, ketonemia and acidosis

12. Clinical Presentation
Most children present with the classic symptoms: 3 P’s, weight loss and lethargy
In young children and infants, it is easier to miss the diagnosis due to difficulty in recognizing the symptoms.
At this age, many of them present with severe ketoacidosis
Most children with new-onset IDDM have symptoms of < one month, however, milder cases can take months to diagnosis
Important to inquire about urination patterns and question why a patient with dehydration continues to urinate regularly
Honeymoon Phase
Begins 1-3 months after diagnosis and can last for months
Period of relative well-being
Honeymoon phase: requires less exogenous insulin because the body’s remaining beta-cells are still producing insulin. Eventually these cells die off and honeymoon is over. Patient and family can become complacent and go into denial. Important that a close relationship is maintained with physician as this phase comes to an end

13. Goals of Treatment Normal Development Management of Type 1 Diabetes
Poorly controlled IDDM patients can have delayed skeletal and sexual maturation
Excessively controlled (too much insulin) can lead to rapid weight gain
Management of Type 1 Diabetes
Education  Independence
Frequent monitoring of blood glucose levels
Altering caloric intake or insulin doses to account for athletes
Ready supply of glucose for those teens that drive
Wearing of Medic-Alert bracelets

14. Goals of Treatment Avoid Metabolic Abnormalities
Monitor blood glucose and urinary ketones several times per day
Glycosylated hemoglobin levels (HbA1c) monitored every 3 months
Measures average blood glucose levels over a 2 month period
Blood lipid levels monitored routinely and dietary changes made if necessary
Be vigilant during times of illness or infection as insulin doses often require adjustment

15. Management Insulin Preparations available Types
Standard beef and pork mix
Disadvantage of containing beef component is that it is antigenic
Purified pork and human forms
Most commonly used
Human form may have shorter duration of action in children
Types
Regular
Rapid acting
Peaks at 2-4h
Duration for 3-6h
Standard form used to treat hyperglycemia, ketosis and DKA

16. Management Insulin lispro Neutral protamine Hagedron (NPH) or lente
New to the market
Biosynthetic analogue of regular insulin
Peaks at ½-1h
Duration of3h
Faster acting than regular and more closely resembles pancreatic insulin secretion
Neutral protamine Hagedron (NPH) or lente
Intermediate acting
Peaks at 4-14h
Duration of 10-20h
Ultralente
Long-acting insulin
Minimal peak
Duration 18-36h

17. Management
Schedule
Most children and adolescents require at least two injections per day of short and long acting insulin to achieve metabolic control
Injections usually before breakfast and dinner
Absorption rate is variable depending on injection site
Warmer more exercised sites have more rapid absorption
Total daily dosage breakdown
2/3 in the AM
1/3 in the PM
Type of insulin breakdown
1/3 regular and 2/3 NPH or
½ regular and ½ NPH
Other regimens are often required to achieve metabolic stability and must be tailored to the individual patient

18. Management
Nutrition
Timing of meals and snacks should minimize blood glucose variability
3 meals, mid afternoon snack
Bedtime snack for those getting evening NPH
Diet breakdown
50-55% carbohydrate
Most should be complex carbs
20% protein
30% fat
Low cholesterol & saturated fats

19. Management
Exercise
Leads to better metabolic control, decreased insulin requirements, improved self-esteem and body image
Extra calories may be required to prevent hypoglycemia
When metabolic control is poor,the stress of exercise can cause further degradation of metabolic control

20. Management Monitoring
Blood glucose levels usually measured before meals and snacks and at approximately 3am (lowest nighttime reading if evening NPH taken)
Targeted blood glucose levels
Fasting & preprandial = mg/dL
Postprandial = < mg/dL
3am = >65-80mg/dL
Urinary ketones
Especially when blood glucose levels > 250mg/dL, febrile or nauseous/vomiting
Essential in avoiding DKA episodes

21. Management Education Fundamental to diabetes management and control
Parents and children need to understand the acute and chronic complications associated with IDDM
Important to tailor education according to patient’s age and parents educational background
Some families are never quite able to manage diabetes control independently and require close attention by the diabetes management team

22. Complications Acute Effects Hypoglycemia Hyperglycemia and ketosis
Blood glucose < 50-60mg/dL
Usually occurs if glucose levels kept to close to normal
Mild symptoms
Adrenergic (tremors, sweating, hunger, palpations)
Moderate symptoms
Adrenergic plus neuroglycopenic (headache, irritability, confusion, sleepiness weakness, impaired judgment)
Severe symptoms
Unresponsiveness, coma convulsions
Mild and moderated symptoms treated by ingestion of simple sugars (10-15g glucose)
Severe reactions require IV glucose or parenteral injection of glucagon
Hyperglycemia and ketosis
Left untreated can lead to Diabetic ketoacidosis

23. Complications Chronic Effects Autoimmune Disease Joint Dysfunction
Especially thyroid dysfunction (monitor periodically)
Joint Dysfunction
Limited mobility ( marker of long-term poor control)
Growth Disturbances
Short stature and delayed maturation (poor control)
Retinopathy
Most develop background retinopathy over year period
20-50% develop proliferative retinopathy
5-10% become blind
Annual ophthalmologic exams recommended

24. Complications Nephropathy Neuropathy Macrovascular Complications
30-40% develop end-stage renal disease
Marked by proteinuria, hypertension and elevated serum creatinine or urea nitrogen
Must monitor several times yearly and consult with nephrologist
Low protein diets, but this raises concerns in growing children
Neuropathy
Relatively uncommon in children and adolescents
Linked to duration of disease and degree of hyperglycemia
Macrovascular Complications
IDDM’s prone to CAD, CVD and PVD at earlier age than non-diabetics
Must discourage smoking and high fat diet
CAD= coronary artery disease
CVD= cerebrovascular disease
PVD= peripheral vascular disease

25. Diabetic Ketoacidosis (DKA)
DKA occurs with severe insulin deficiency in addition to elevated counter-regulatory (stress) hormones such as glucagon, cortisol, growth hormones and catecholamines all of which antagonize the effects of insulin
DKA pathway
 glucose levels (hyperglycemia)  osmotic diuresis  polyuria & polydipsia  dehydration & lipolysis   fatty acid oxidation  ketone production  metabolic acidosis  electrolyte imbalance (hypercalcemia)

26. Features of DKA Classic Neurological Respiratory Polyuria Polydipsia
Weight loss
Neurological
Altered level of consciousness
Headache
Respiratory
Fruity breath
Hyperventilation
Gastrointestinal
Anorexia
Abdominal pain
Diarrhea
Nausea/vomiting
Genitourinary
dehydration

27. Complications of DKA Complications Cerebral edema
Unpredictable and often fatal complication of DKA
Usually occurs when the biochemical imbalances are improving
Children <5 years and newly diagnosed IDDM patients are at greatest risk

28. Complications of DKA Possible causes for Cerebral edema Treatment
Too rapid a drop in blood glucose
Failure of serum sodium to increase
Excessive fluid administration
Tonicity of intravenous fluids
Use of bicarbonate
Treatment
Intubate and hyperventilate to  intracranial pressure
80% fluid maintenance
head of bed elevated 30°
Mannitol 1g/kg IV bolus if needed

29. Laboratory analysis of DKA
Serum
Metabolic acidosis with wide anion gap
Hyperglycemia with high serum osmolality
Dehydration (with elevated urea and creatinine)
Hyperkalemia, hyponatremia
Urine
Ketonuria
Glucosuria

30. Management of DKA Supportive
Monitor electrolytes, gas, serum osmolality and glucose q1h
Monitor BUN, creatinine, calcium and phosphate q4h
Monitor urinary ketones with each void
Neurovitals q1h if altered level of consciousness

31. Management of DKA Fluid replacement Initial Maintenance
NS or LR bolus 10-20cc/kg over 1 hour and repeat if unstable
Rehydrate in order to perfuse kidneys and increase urinary glucose output  decreased blood glucose
Maintenance
Switch to 0.45% NaCl and correct 50% of deficit over 8h and remaining over 16h
Add glucose once serum glucose levels approach normal
Add 20 mEqu KCl/500cc fluid if potassium levels are normal or low and patient is urinating

32. Management of DKA Insulin Potassium 0.1U/kg/h IV of Regular insulin
If acidosis not improved in 2h increase insulin dosage to U/kg/h
Continue IV insulin until glucose and acidosis have corrected then switch to subcutaneous insulin
Potassium
Both hyper/hypokalemia can cause death and therefore must be monitored q1-2h
40mEq/L may be added to IV fluids if K levels are normal or low
Don’t administer in the presence of renal failure

33. Management of DKA Phosphate Bicarbonate
If serum phosphate< 2mEq/L  add phosphate at a rate of 1.5 mEq/kg/L over 8-12h
Monitor calcium levels concurrently
Bicarbonate
Only in severe metabolic acidosis
1-2mEq/kg/L HCO3 over 2h

34. Management of DKA Converting to Subcutaneous Insulin
Indicated when patient is clinically stable, normal vitals, normal glucose levels, absence of acidosis and patient can take fluids PO without vomiting
If known IDDM start on regular insulin regimen
If new IDDM, add up total dosage of Regular Insulin given at time of DKA and then give 2/3rds in am and 1/3rd in pm with 2/3rds of NPH and 1/3rd Regular given at each time. Continue IV insulin for minutes after first subcutaneous dose then d/c.
Best to make transition during the daytime
Adjust insulin dosage based on regular serum glucose and urine ketone checks

35. Dental Management Medical History
Inquire about blood glucose levels and frequency of hypoglycemic episodes
Inquire about type of medication used to control blood glucose levels
Hypoglycemic potentiating drugs
Salicylates, dicumerol, beta-adrenergic blockers, MAO inhibitors, sulfonamides & angiotensin converting enzyme inhibitors
Hyperglycemic potentiating drugs
Epinephrine, corticosteroids, thiazides, oral contraceptives, phenytoin, thyroid products and calicum channel blockers
IDDM patients undergoing surgical procedures may need their insulin dosage adjusted
Lalla & D'Ambrosio, 2001

36. Dental Management Scheduling of appointments
Morning appointments best in order to coincide with peak cortisol levels
Be sure appointment doesn’t coincide with peak insulin activity
Don’t want to precipitate a hypoglycemic attack
Diet
Make sure patient adheres to normal diet and medication routine
If sedation required and NPO necessary make sure patient adjusts insulin dose according to physicians orders
Lalla & D'Ambrosio, 2001

37. Dental Management Blood glucose monitoring
If <70mg/dL, an oral carbohydrate should be given before treatment
If hypoglycemic attack occurs during treatment, stop and give 15g of fast acting carbohydrate (glucose tablets or gel)
If patient becomes unconscious, administer 25-30mL of 50% dextrose solution or 1mg of glucagon IV. Glucagon can also be given IM or subQ at a rate of 0.1mg/kg up to a max of 1mg
Lalla & D'Ambrosio

38. Dental Management Post treatment precautions
Infection and delayed wound healing is common in poorly controlled diabetics
Antibiotic coverage necessary for surgical procedures or obvious oral infection
If patient’s diet altered post treatment, insulin dose should be adjusted per physicians order
Avoid aspirin type medications
Lalla & D'Ambrosio, 2001

39. Oral manifestations Periodontal disease
Especially in poorly controlled patients
Possibly due to reduced polymorphonuclear leukocyte function or collagen instability
Periodontal disease can have an adverse effect on glycemic control
With delayed wound healing and increased chance for infection, best to treat periodontal condition conservatively
Prevention and more frequent recall best approach
Smoking increases the risk for periodontal disease in the IDDM patient
Lalla and D'Ambrosio,2001

40. Oral manifestations Salivary gland dysfunction Fungal infections
Xerostomia
Parotid gland enlargement
Fungal infections
Oral candidiasis, including median rhomboid glossitis and angular cheilitis
Possibly due to xerostomia, increased salivary glucose or impaired immune system
Oral burning/taste alteration
Burning sensation
Possibly due to peripheral neuropathy, xerostomia or candidasis
Lalla and D'Ambrosio,2001

41. Oral manifestations Lichen planus Dental caries
Taste alteration
Maybe related to xerostomia or impaired glucose receptors
Lichen planus
Some studies show elevation in IDDM patients
Dental caries
If patient is xerostomic or has elevated salivary glucose levels, caries rate may be higher
Traumatic ulcers and irritation fibromas
Higher prevalence thought to be associated with impaired wound healing
Lalla and D'Ambrosio,2001