Diabetes Mellitus patients in dental management

1. Diabetes Mellitus patients in dental management shabeel pn

2. Introduction • Diabetes mellitus is a metabolic disorder characterized by relative or absolute insufficiency of insulin, and resultant disturbances of carbohydrate metabolism. • The major function of insulin is to counter the concerted action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels.

3. Epidemiology • 6% (16 million persons) of the general population in the US have diabetes mellitus. • Almost 20% of adult older than 65 y/o have DM. • A dental practice serving an adult population of 2,000 can expect to encounter 40-80 persons with diabetes, about half of whom will be unaware of their condition. National Institutes of Health, Aug 2001

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5. Etiologic classification of DM • There are two types of Diabetes Mellitus: • Type 1, insulin-dependent or, juvenile-onset diabetes (IDDM) • Type 2, non-insulin-dependent, adult-onset diabetes (NIDDM) • Other specific types JADA, Oct 2001

6. Type 1 (IDDM) • Autoimmune destruction of the insulin-producing beta cells of pancreas. • 5-10% of DM cases. • Common occurs in childhood and adolescence, or any age. • Absolute insulin deficiency. • High incidence of severe complications. • Prone to autoimmune diseases. (Grave’s, Addison, Hashimoto’s thyroiditis)

7. Type 2 (NIDDM) • Result from impaired insulin function. (insulin resistance) • Constitutes 90-95% of DM • Specific causes of this form are unknown. • Risk factors : age, obesity, alcohol, diet, family Hx and lack of physical activity..etc.

9. Other specific types • Genetic defects of beta-cell functions • Decrease of exocrine pancreas • Endocrinepathothies • Drug or chemical usage • Infections ………….

10. Gestational diabetes mellitus (GDM) • Defined as any degree of glucose intolerance with onset or first recognition during pregnancy. • 4% of pregnancy in US.

11. Pathophysiology • Healthy people blood glucose level maintained within 60 to 150 mg/dL. • Insulin synthesized in beta cells of pancreas and secreted rapidly into blood in response to elevations in blood sugar. • Promoting uptake of glucose from blood into cells and its storage as glycogen • Fatty acid and amino acids converted to triglyceride and protein stores.

12. Pathophysiology • Lack of insulin or insulin resistance, result in inability of insulin-dependent cells to use glucose. • Triglycerides broken down to fatty acids blood ketones↑  diabelic ketoacidosis.

13. Pathophysiology • As blood sugar levels became elevated (hyperglycemia), glucose is excreted in the urine and excessive of urination occurs due to osmotic diuresis (polyuria). • Increased fluid loss leads to dehydration and excess thirst (polydipsia). • Since cells are starved of glucose, the patient experiences increased hunger (polyphagia). • Paradoxically, the diabetic patient often loss weight, since the cells are unable to take up glucose.

14. Complications • People with DM have an increased incidence of both microvascular and macrovascular complications.

15. Diagnosis • A casual plasma glucose level of 200 mg/dL or greater with symptoms presented. • Fasting plasma glucose level of 126 or greater.(Normal <110 mg/dL,IGT,IFG) • Oral glucose tolerance test (OGTT) value in blood of 200 mg or greater. ADA recommend >45 y/o screened every 3 years. Diabetes Care, 2000 National Institutes of Health, Aug 2001

16. Medical management • Objective : maintain blood glucose levels as close to normal as possible. • Good glycemic control inhibits the onset and delay of type 1 DM, similar in type 2 DM.

17. Medical management • Glycated hemoglobin assay (HbA1c ) reflects mean glycemia levels over the proceding 2~3 months. (normal < 7%) • HbA1c also a predictor for development of chronic complications.

18. Medical management • Exercise and diet control • Insulin : rapid, short, intermediate, long acting. • Oral antidiabetic agents

19. Oral manifestations and complications No specific oral lesions associated with diabetes. However, there are a number of problems by present of hyperglycemia. • Periodontal disease • Microangiopathy altering antigenic challenge. • Altered cell-mediated immune response and impaired of neutrophil chemotaxis. • Increased Ca+ and glucose lead to plaque formation. • Increased collagen breakdown.

20. Oral manifestations and complications • Salivary glands • Xerostomia is common, but reason is unclear. • Tenderness, pain and burning sensation of tongue. • May secondary enlargement of parotid glands with sialosis. • Dental caries • Increase caries prevalence in adult with diabetes. (xerostomia, increase saliva glucose) • Hyperglycemia state shown a positive association with dental caries.

21. Oral manifestations and complications • Increased risk of infection • Reasons unknown, but macrophage metabolism altered with inhibition of phagocytosis. • Peripheral neuropathy and poor peripheral circulation • Immunological deficiency • High sugar medium • Decrease production of Ab • Candical infection are more common and adding effects with xerostomia

22. Oral manifestations and complications • Delayed healing of wounds • Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. • Increase prevalence of dry socket. • Miscellaneous conditions • Pulpitis : degeneration of vascular. • Neuropathies : may affect cranial nerves. (facial) • Drug side-effects : lichenoid reaction may be associated with sulphonylurea. (chlopropamide) • Ulcers New Zealand Journal, Jan 1985

23. Dental management considerations To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental tx. • Medical history : take hx and assess glycemic control at initial appt. • Glucose levels • Frequency of hypoglycemic episodes • Medication, dosage and times. • Consultation

24. Dental management considerations • Scheduling of visits • Morning appt. (endogeneous cortisol) • Do not coincide with peak activity. • Diet • Ensure that the patient has eaten normally and taken medications as usual. • Blood glucose monitoring • Measured before beginning. (<70 mg/dL) • Prophylactic antibiotics • Established infection • Pre-operation contamination wound • Major surgery

25. Dental management considerations • During treatment • The most complication of DM occur is hypoglycemia episode. • Hyperglycemia • After treatment • Infection control • Dietary intake • Medications : salicylates increase insulin secretion and sensitivity avoid aspirin.

26. Emergency management • Hypoglycemia • Initial signs : mood changes, decreased spontaneity, hunger and weakness. • Followed by sweating, incoherence, tachycardia. • Consequenced in unconsiousness, hypotention, hypothermia, seidures, coma, even death.

27. Emergency management • 15 grams of fast-acting oral carbonhydrate. • Measured blood suguar. • Loss of conscious, 25-30ml 50% dextrose solution iv. over 3 min period. • Glucagon 1mg. • 911, 119

28. Emergency management • Severe hyperglycemia • A prolonged onset • Ketoacidosis may develop with nausea, vomiting, abdominal pain and acetone odor. • Difficult to different hypo- or hyper-.

29. Emergency management • Hyperglycemia need medication intervention and insulin administration. • While emergency, give glucose first ! • Small amount is unlikely to cause significant harm. JADA, Oct 2001

30. Conclusion

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33. 1.Liver glucose glucose TG glycerol-po4 glycerol +FA glycerol FA+ALB 2.Adipose ketone body ATP+co2 acetyl coA TG FA Glycerol-po4 glucose • glucose 3.Muscle glucose glucose