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DIABETES Paediatrics and Adolesence Dr Aisling Myers Clinical Lecturer Classification Type 1 (Autoimmune, Idiopathic) Type 2 Others Genetic defects of β-cell function (e.g. MODY) Pancreatic diseases (e.g. cystic fibrosis) Endocrinopathies (e.g. Cushing Syndrome) Iatrogenic (e.g. Glucocorticoids) Infections (e.g. Congenital Rubella) Other syndromes (e.g Prader Willi Syndrome) Gestational Diabetes – Type 1 Most common metabolic disease in the young Third most common chronic disorder in childhood after asthma and cerebral palsy Life threatening, life long Incidence rising, presenting at younger age Chronic hyperglycaemia Defect in insulin secretion / action Normoglycaemia Uncontrolled Diabetes Mellitus Insulin deficiency Pathogenesis Deficiency of insulin secretion Prone to ketoacidosis T-cell mediated pancreatic islet β-cell destruction β-cell destruction – occurs at variable rate Process begins months/years before presentation with clinical symptoms. ? Viral trigger Clinically symptomatic when ~ 90% of β-cells destroyed HLA genes – 8-10 fold risk if HLA-DR3 or HLA-DR4 Serological Markers Serological markers present in 85-90% at presentation Autoimmune pathologic process Islet cell Autoantibodies (ICA) Insulin Autoantibodies (IAA) Glutamic Acid Decarboxylase (GAD) Epidemiology Over 50% diagnosed before 15 yrs T1DM – accounts for >90% of childhood and adolescent diabetes Type 2 – becoming more common Incidence variable - Highest in Finland. 12 – 15% will have affected first degree relative 3 times more likely to develop diabetes if father also affected vs mother Screening unethical unless part of trial – no effective methods of prevention Diagnosis 1 Symptoms……plus Hyperglycaemia (random blood sugar >11mmol/litre) Or Fasting blood sugar >7.0 mmol/litre Or 2hr post prandial sugar >11 mmol/litre Or OGTT Diagnosis 2 Presentation Polyuria, polydipsia, weight loss Glycosuria, Ketonuria Diabetic Ketoacidosis (DKA) – urgent Non-ketotic hyperosmolar state Recent onset enuresis in previously trained child Vaginal candidiasis (prepubertal) Vomiting Chronic weight loss, failure to thrive Recurrent skin infections Management Urgent (same day) referral to multidisciplinary paediatric diabetes care team Admission or home based care Admit: DKA <2 yrs old Social / Emotional issues Family living long distance from hospital Peripheral hospital DKA Clinical history Clinical signs Polyuria, polydipsia, wgt loss, abdo pain, weakness, vomiting, confusion, stupor, coma. Dehydration, smell of ketones, lethargy, drowsiness, Kussmaul breathing Biochemical signs Ketones (blood/urine), hyperglycaemia (>11), acidosis (pH < 7.3), other electrolyte abnormalities DKA Airway Breathing Circulation (ABC) Admit ICU IV access x 2 Oxygen Fluid resuscitation / IV Insulin / Potassium Electrolyte monitoring (hrly, 2hrly, 4hrly) – K+ Close monitoring Sepsis/Infection Neurological deterioration Cerebral oedema Insulin Subcutaneous insulin when clinically well and tolerating food / fluids Injection sites Abdomen Thighs Buttocks Insulin Preparations Preparation Onset Duration Rapid acting* 15 mins 2 – 5 hours Short acting 30 – 60 mins Up to 8 hours Intermediate acting Long acting 1 – 2 hours 16 – 35 hours 1 – 2 hours > 24 hours Insulin Regimens 1, 2 or 3 injections per day: rapid or short acting insulin premixed or self mixed with intermediate acting insulin MDI regimen: rapid or short acting insulin before meals with intermediate or long acting insulin Insulin pump therapy (CSII) – most physiological. Requires commitment , competence and good family support Phases of Diabetes Preclinical diabetes Presentation Partial remission (“Honeymoon” Phase) Months or years prior to presentation Antibodies (Islet cell, Insulin, Glutamic Acid Decarboxylase) - positive 80% of cases transient decrease in insulin requirements Duration – weeks to months Important to inform parents that this phase is transient Chronic Lifelong insulin therapy Education Insulin Monitoring glycaemic control (HbA1C) Diet Exercise Smoking / Alcohol / Substance misuse Intercurrent illness (sick days) Hypoglycaemic episodes Avoidance, detection, management Multidisciplinary Team Consultant and diabetic team Diabetic Nurse Specialists Dietician Psychology Social Worker Ophthalmology Chiropody GP Follow-Up Aim for frequent blood sugar monitoring (usually 4 BM’s daily – fingerprick) Aim for pre-prandial sugar: 4 – 8 mmol/L Aim for post-prandial sugar: < 10mmol/L Adjust insulin doses accordingly Liaise with diabetic team (phone / clinic) Monitor sugars more often during intercurrent illness Clinic Visits Monitor growth (height, weight, BMI) Pubertal development HbA1C (< 7.5%) Check injection sites Review foot care Annual screen Retinopathy Nephropathy (Microalbuminuria, Blood Pressure) Associated conditions Thyroid disease Coeliac Disease Ongoing Care Constant re-education Encourage family involvement Psychology (NB in teenage years) Tailor insulin therapy and delivery methods to each patient / family Screen for complications Transition to adult care – smooth Surgical Procedures In centres with facilities for care of children/young people with diabetes Agree protocol for safe management. Ensure first on list. Inform anaesthetic team Check regular blood sugars Check electrolytes (K) Check for glycosuria, ketonuria Complications Short Term / Ongoing Hypoglycaemia DKA Sick days Lipohypertrophy (48%) Psychological Long Term Retinopathy Nephropathy Neuropathy Macrovascular Disease Hypoglycaemia Carry T1DM identification (bracelet) Rapid access to CHO and blood sugar monitor Educate carers re glucagon administration and advice to seek medical assistance if failing to respond (seizures can occur if untreated) Patients – increase awareness and respond appropriately Avoid over corrections at meals especially at night – overnight or fasting hypo Avoid very low HbA1C DKA Untreated – stupor, coma, death Follow proposed guidelines for institution Initial management in HDU Transfer to paeds ICU if not responding Outrule co-existing sepsis Monitor closely for signs of deterioration Impaired consciousness Suspected cerebral oedema Sick Days Sick Day Rules Extra blood sugars Check for ketones Hrly / 2 hrly snacks If persistent vomiting or if not tolerating – bring to hospital Regular phone contact with nurse specialist/team NEVER OMIT INSULIN Psychological / Social Issues Emotional / Behavioural Family Conflict Anxiety / Depression Eating Disorders Cognitive Disorders Behavioural / Conduct Disorders Non – compliance Complications Long Term - Retinopathy Visual impairment Blindness Poor glycaemic control Laser treatment if sight threatening Ophthalmology check annually from 12 years or if diagnosed >5yrs Long Term - Nephropathy Renal failure Hypertension Early morning urine for microalbuminuria Albumin:Creatinine ratio Monitor BP at clinic visits Screen annually from 12 yrs or if diagnosed > 5yrs Long Term - Macrovascular Stroke Ischaemic Heart Disease Peripheral Vascular Disease Associated Conditions/Complications Impaired growth and development Late pubertal development Obesity (excessive exogenous insulin assoc with high energy intake) Autoimmune conditions Hypothyroidism Hyperthyroidism Coeliac Disease Addison’s Disease Other types of Diabetes Type 2 Diabetes Rising prevalence – associated with increasing obesity Type 2 Diabetes Insulin resistance Acanthosis nigricans High insulin or c-peptide levels Dyslipidemia Polycystic ovarian syndrome More common in ethnic minority groups Japan – more common than T1DM Type 2 Diabetes Commonly presents in mid-puberty Confused with MODY (monogenic maturity onset diabetes of the young) Screen if obese, positive family history or signs of insulin resistance Lifestyle changes – diet, exercise Pharmacotherapy – not licensed in children Early intervention – best prevention Neonatal Diabetes Very rare (1 in 400,000 births) Insulin requiring hyperglycaemia in first 3-6 mths of life May be associated with IUGR (intra uterine growth retardation) 50% cases transient Permanent – associated with pancreatic aplasia, genetic mutations Predisposition to impaired glucose tolerance and Type 2 diabetes in later life Cystic Fibrosis (CFRD) Insulin deficiency Insulin resistance Infections Medications (steroids, bronchodilators) Occurs late in disease (adolescence, early adulthood) Cirrhosis contributes to insulin resistance Onset of CFRD – poor prognostic indicator Poor control – promotes catabolism Screening – OGTT as part of annual screen >10yrs Insulin doses usually smaller than in classic T1DM MODY Maturity Onset Diabetes of the Young Single gene disorder causing β cell dysfunction Autosomal dominant family history Endogenous insulin secretion Not prone to ketoacidosis No signs of insulin resistance Usually require less insulin than classic T1DM Mutations found in >80% of patients (5) Other causes Drug-induced diabetes Neurosurgery (Dexamethasone) Oncology (chemotherapy) Stress Hyperglycaemia Reported in up to 5% attendances to A&E Acute illness, trauma, post seizure, fever Recheck blood sugar series when well Islet Cell Transplantation Islet cells replaced with harvested donor cells Typically receive cells from up to 3 donors Experimental therapy Shortage of donor material Still require insulin therapy Anti-rejection drugs – severe side effects The Future Key Points Lifelong disease Never omit insulin Healthy lifestyle for all the family Good glycaemic control Screen for complications Prevention better than cure! 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