dental management of diabetic patients
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Dental management of
diabetic patients
Presented by :Chitrang kolawale
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Introduction Diabetes mellitus is a metabolic disordercharacterized by relative or absolute insufficiency of insulin, and resultant disturbances of carbonhydratemetabolism.
The major function of insulin is to counter theconcerted action of a number of hyperglycemia-generating hormones and to maintain low bloodglucose levels.
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Epidemiology 6% (16million persons) of the general population in
the US have diabetes mellitus.
Almost 20% of adult older than 65 y/o haveDM.
A dental practice serving an adult population of 2,000can 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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Etiologic classification
of DM There are two types of DiabetesMellitus:
Type 1, insulin-dependent or, juvenile-onset diabetes(IDDM)
Type 2, non-insulin-dependent, adult-onset diabetes
(NIDDM)
Other specific types
J ADA, Oct 2001
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Type 1 (IDDM)
Autoimmune destruction of the insulin-producingbeta 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. (Graves, Addison,
Hashimotos thyroiditis)
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Type 2 (NIDDM)
Result from impaired insulin function. (insulinresistance)
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.
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ComparisonComparison Type 1 Type 2
Clinical onset <20 years onset >30 years
normal weight obesity
decreased blood insulin normal or increased blood
insulin
anti-islet cell antibodies no anti-islet cell
antibodies
Genetics ketoacidosis common ketoacidosis rare
human leukocyte antigen
(HLA)-D linked
No HLA association
Pathogenesis autoimmunity,
immunopathologic
mechanisms
insulin resistance
severe insulin deficiency relative insulin deficiency
Islet Cells insulitis early no insulitis
marked atrophy and
fibrosis
focal atrophy and amyloid
deposits
severe beta-cell depletion mild beta-cell depletion
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Other specific types
Genetic defects of beta-cell functions
Decrease of exocrine pancreas
Endocrinepathothies
Drug or chemical usage
Infections.
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Gestational diabetes mellitus
(GDM)
Defined as any degree of glucose intolerance
with onset or first recognition during
pregnancy.
4% of pregnancy in US.
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P
athophysiology Healthy people blood glucose level maintained
within 60 to 150 mg/dL.
Insulin synthesized in beta cells of pancreas andsecreted rapidly into blood in response to elevationsin 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.
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P
athophysiology 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.
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P
athophysiology As blood sugar levels became elevated (hyperglycemia),
glucose is excreted in the urine and excessive of urinationoccurs 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 thecells are unable to take up glucose.
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C
omplications People with DM have an increased incidence of both
microvascular and macrovascular complications.
Major organs/systems showing changes Long term complications
Cardiovascular system: heart,
brain, blood vessels
myocardial infarct; atherosclerosis;
hypertension; microangiopathy;
cerebral vascular infarcts; cerebral
hemorrhage
Pancreas islet cell loss; insulitis (Type 1); amyloid
(Type 2)
Kidneys nephrosclerosis; glomerulosclerosis;arteriosclerosis; pyelonephritis
Eyes retinopathy; cataracts; glaucoma
Nervous system autonomic neuropathy; peripheral
neuropathy
Peripherals peripheral vascular atherosclerosis;
infections; gangrene
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Diagnosis A casual plasma glucose level of 200 mg/dL or
greater with symptoms presented.
Fasting plasma glucose level of 126 orgreater.(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
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Medical management Objective : maintain blood glucose levels as
close to normal as possible.
Good glycemic control inhibits the onset anddelay of type 1 DM, similar in type 2 DM.
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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.
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Medical management Exercise and diet control
Insulin : rapid, short, intermediate, long acting.
Oral antidiabetic agents
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Oral manifestations and
complications No specific oral l esion s a ssociated with diabetes. H owever,
ther e ar e a number o f probl em s by pr esent o f hypergl ycemia.
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.
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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.
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Oral manifestations and
complications Increased risk of infection
Reasons unknown, but macrophage metabolism altered with inhibitionof phagocytosis.
Peripheral neuropathy and poor peripheral circulation
Immunological deficiency
High sugar medium
Decrease production of Ab
Candical infection are more common and adding effects withxerostomia
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Oral manifestations and
complications Delayed healing of wounds
Due to microangiopathy and ultilisation of protein for energy, mayretard 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
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Dental management
considerationsT o minimize the r isk o f an int rao perative emerg ency ,
cl inician s need t o con sider some issues bef or e initiating
dent al tx. Medical history :Assess glycemic control at initial appt.
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times.
Consultation
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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
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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 sensitivityavoid aspirin.
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Emergency management
Hypoglycemia
Initial signs : mood changes, decreased
spontaneity, hunger and weakness.
Followed by sweating, incoherence, tachycardia.
Consequenced in unconsiousness, hypotention,
hypothermia, seizures, coma, even death.
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Emergency management
15 grams of fast-acting oral carbonhydrate.
Measured blood sugar.
Loss of conscious, 25-30ml 50% dextrose solution iv.over 3 min period.
Glucagon 1mg.
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Emergency management
Severe hyperglycemia
A prolonged onset
Ketoacidosis may develop with nausea, vomiting,abdominal pain and acetone odor.
Difficult to differentiate between hypo- or hyper-.
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Emergency management
Hyperglycemia need medication intervention andinsulin administration.
While emergency, give glucose first ! Small amount is unlikely to cause significant harm.
J ADA, Oct 2001
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Conclusion