Diabetes Mellitus 2024: A Presentation PDF

Diabetes Mellitus Dr Janice Chuang Specialist in Special Needs Dentistry BDS (Singapore), DClinDent (SND) (Queensland), MRACDS (SND) Acknowledgements to Dr Lydia See and Dr Claudia Lo...

Diabetes Mellitus Dr Janice Chuang Specialist in Special Needs Dentistry BDS (Singapore), DClinDent (SND) (Queensland), MRACDS (SND) Acknowledgements to Dr Lydia See and Dr Claudia Lopez Silva DENT4060 May 2024 Learning objectives Understand the pathophysiology of diabetes mellitus and complications Understand the medical management of diabetes mellitus Understand the potential consequences of diabetes mellitus on oral health Understand the dental management considerations in the patient with diabetes Outline 1. Definition 2. Pathophysiology 3. Laboratory markers 4. Medical management 5. The relationship between oral health and diabetes mellitus 6. Dental management considerations  1. Definition of diabetes “ Diabetes mellitus (DM) is a group of metabolic disorders sharing the common feature of hyperglycaemia caused by defects in insulin secretion, insulin action, or, most commonly, both” (Robins and Cotran 2021) Classification of diabetes Type 1: autoimmune disease; onset usually in childhood/early adulthood Type 2: lifestyle-associated with genetic risk factors Gestational diabetes: abnormal blood homeostasis during pregnancy Others e.g. pancreatic disease, medication-induced (e.g. long- term corticosteroids), genetics (Down syndrome)  Epidemiology Diabetes worldwide Diabetes 10% 90% Diabetes No diabetes 90% 10% Type I Type 2 Diabetes in Australia 1 in 20 Australians (5.1% of the total population) living with diabetes in 2021 Older Australians aged 80-84: 1 in 5 persons Diabetes contributed to about 19,300 deaths in 2021 Australian Institute of Health and Welfare 2023. Diabetes. Diabetes: Australian facts, Summary - Australian Institute of Health and Welfare (aihw.gov.au) Insulin Glucose stimulates insulin production and release Insulin increases the rate of glucose transport from bloodstream into cells in the body Type I 2. Pathophysiology Type II Beta cell Insulin destruction resistance Insulin Relative deficiency insulin Often deficiency immune mediated Clinical presentation Hyperglycemia Polyuria Polydipsia Polyphagia Hyperglycaemia Results in Fluid lost through Lack of glucose leads to glucose increased urinary urine may lead to utilization by many excretion in the volume dehydration and cells of the body urine = glycosuria The 3 Ps loss of electrolytes = thirsty leads to cellular starvation The patient often increases intake of food but in many cases still loses weight A sequence of events Acute complications in DM (crisis states) Diabetic ketoacidosis Acute hyperosmolar hyperglycaemic state Acute hypoglycemia  Diabetic ketoacidosis (acute) Infection Intoxication Signs of Hyperglycemia Deficient insulin Infarction availability dehydration Metabolic 5Is Inappropriate GI symptoms acidosis withdrawal of Hyperventilation Hyperketonemia Lipid oxidation insulin and metabolism. Coma* Ketonuria Intercurrent illness A complication of (mainly) type I diabetes Laboratory marker: Random blood glucose + Blood ketone levels Hyperosmolar hyperglycaemic state (acute) Prolonged hyperglycemia and dehydration Hyperglycemia Insulin deficiency without No acidosis ketoacidosis No Ketonuria Urinary output drops A complication of type 2 diabetes Hypoglycaemia (acute) Due to insulin overdose or inadequate calorific intake Symptoms Signs Patients at risk Shakiness, anxiety, Tremors, tachycardia, altered The elderly palpitations, increased consciousness (lethargy and T1D sweating, hunger obtundation or personality T2D with CVD change), blood glucose level CKD of immune deficiencies More prone to infections Decreased PMN and macrophage function (chemotaxis, phagocytosis, killing) Decreased cytokine response following stimulation Increased susceptibility to Skin infections Mucosal candidosis Periodontal disease Poor wound healing Chronic complications of DM Chronic hyperglycaemia → microvascular & macrovascular complications Macrovascular Non enzymatic glycosylation of vascular basement membranes NEG of large and medium sized vessels – Atherosclerosis and its resultant complications: IHD, MI, stroke – Risk of MI is tripled! – Peripheral vascular disease – leading cause of non traumatic amputations Chronic complications of DM Chronic hyperglycaemia → microvascular & macrovascular complications Microvascular NEG of small vessels (arterioles) – hyaline arteriolosclerosis – Renal arterioles – glomerulosclerosis (scarring of small vessels in the kidney) – Reduces renal blood flow and hence GFR > nephropathy Osmotic damage – Schwann cells > peripheral neuropathy – Pericytes of retinal blood vessels > retinopathy > blindness – Lens > Cataracts Chronic complications of DM Atherosclerosis, IHD, MI, stroke Nephropathy Retinopathy Peripheral and autonomous neuropathy Impaired wound healing Periodontal disease Robbins basic pathology. 2012  3. Laboratory markers Tests Diabetes Fasting Plasma Glucose ≥126 mg/dL (≥7.0 mmol/L) on two Type 1 DM diagnosed after occasions. Fasting is defined as no caloric Acute onset of symptoms intake for at least 8 hours. Metabolically unstable Require immediate Non-Fasting Random Glucose ≥200 mg/dL (11.1 mmol/L). Obtained at evaluation and treatment any time of day without regard to time since last meal Oral Glucose Tolerance 2 hours: ≥ 200. Measurement of plasma Type 2 DM usually is glucose at two hours after consuming 75 diagnosed by means of grams Routine laboratory of glucose dissolved in water assessments After clinical evaluation Hb A1c ≥6.5% Outline 1. Definition 2. Pathophysiology 3. Laboratory markers 4. Medical management 5. The relationship between oral health and diabetes mellitus 6. Dental management considerations Management Type 1 Diabetes Mellitus Insulin regimens for both Basal (overnight fasting and between-meal) Prandial insulin (glucose excursions above basal at mealtime) Medical nutrition therapy Regular exercise but ensure education about the effects of exercise on blood glucose levels to avoid significant hypo- or hyperglycaemia (Handelsman, Bloomgarden et al. 2015) The Royal Australian College of General Practitioners. General practice management of type 2 diabetes: 2016–18. East Melbourne, Vic: RACGP, 2016. Management T2D (Diabetes Management Algorithm, Endocr Pract. 2020) Glucose- lowering agents CRICOS PROVIDER NO. 00025B CRICOS PROVIDER NO. 00025B  Oral manifestations in poorly controlled diabetes mellitus (Adapted from Kudiyirickal and Pappachan 2008) Acknowledgments Dr Daniel Sundaresan  5. Oral manifestations in poorly controlled diabetes mellitus Periodontal Periimplantitis Caries disease Diabetes a recognised systemic risk factor  Periodontal disease Risk is 2x higher in persons with diabetes 3x higher in persons with poorly-controlled diabetes Granulomatous tissue at the gingival margin and spontaneous suppuration (Lamster, Lalla et al. 2008,Mealey 2006, Taylor 2002)  Bidirectional relationship Untreated periodontitis = Poorer diabetes control Poor – 6 times higher risk of Periodon- worsening diabetes Diabetes titis control Control More diabetes-related complications – Heart attack, stroke, diabetic foot, kidney damage, eye damage (Mealey and Rose 2008) (Lamster, 2012) Predisposition to infection Oral fungal infections 6. Dental management considerations Assess severity of DM and DM control Current medication Random blood glucose levels and HbA1c Extent of diabetic end-organ disease If insulin dependent: frequency of hypoglycaemic episodes Advise the patient about poor wound healing and risk of infection Ensure regular recall Periodontal disease Caries risk Opportunistic infections 6. Dental management considerations Avoid medical emergencies Timing of dental treatment – minimise disruption to routine Ensure patient does not skip meals Invasive treatment: maintain usual caloric intake and medication regimen Consider checking RBG at start of appointment Especially for insulin dependent diabetics with Labile blood glucose levels Regularly experience hypoglycemias Identification and treatment of hypoglycaemia in the dental office Symptoms of hypoglycaemia Shakiness, anxiety, palpitations, increased sweating, hunger Signs of hypoglycaemia Tremors, tachycardia, altered consciousness (lethargy and obtundation or personality change), Blood glucose level below 4.0 mmol/L https://www.diabetesaustrali a.com.au/blood-glucose- monitoring (Kidambi and Patel 2008) Hypoglycemic emergency Signs and symptoms Emergency management Mild Terminate dental treatment immediately Hunger Fatigue Awake/alert patient Sweating Administer 15 g oral carbohydrate (i.e., glucose tablet, 180 mL orange juice, Nausea 15–25 mL sugar) Abdominal pain Monitor blood glucose and repeat carbohydrate dosing as necessary Headache If not improvement, repeat the dose of glucose Tachycardia If improvement, the patient should eat a longer acting carbohydrate Irritability Moderate Uncooperative patient Incoherence Seek emergency medical assistance Uncooperative Belligerence Unconscious patient Resistive behaviour Seek emergency medical assistance Severe Unconscious Seizure (Kidambi and Patel 2008) Sodium glucose co-transporter 2 (SGLT2) inhibitors Dapagliflozin (Forxiga, Qtern or Xigduo XR) Empagliflozin (Jardiance, Jardiamet or Glyxambi) Risk of diabetic ketoacidosis with surgical procedures Consider ceasing SGLT2 inhibitor for a day prior to extraction Medication may be restarted once the patient's condition has stabilised following surgery and oral intake is normal Extractions in poorly controlled diabetics 1. Should we proceed with extractions? Risk of non-treatment > risk of treatment Acute pain/infection can progress Asymptomatic hyperglycemia – rarely an rapidly (immunocompromised host) emergency. Infection put patient at risk of DKA Look out for signs of DKA. Stop if patient feels unwell, call EMS if necessary 2. Post-op antibiotics? Weigh against risks: antibiotic resistance, ADR, gut dysbiosis Counsel patient on risk of post-op infection & delayed healing Arrange post-op review  Prophylactic antibiotics are not usually considered “well controlled Type 2 diabetics on diet control or oral hypoglycaemics can be treated the same as non diabetic patients” (Sambrook and Goss 2018) “Specialist referral for insulin dependent diabetics requiring extraction should be considered” (Power, Sambrook et al. 2019) (Sambrook and Goss 2018) Thank you