Transcript DIABETES-AISLING

DIABETES
Paediatrics and
Adolesence
Dr Aisling Myers
Clinical Lecturer
Classification
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Type 1 (Autoimmune, Idiopathic)
Type 2
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Others
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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
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Normoglycaemia
Uncontrolled Diabetes Mellitus
Insulin deficiency
Pathogenesis
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Deficiency of insulin secretion
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Prone to ketoacidosis
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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
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HLA genes – 8-10 fold risk if HLA-DR3 or HLA-DR4
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Serological Markers
Serological markers present in 85-90% at
presentation
 Autoimmune pathologic process
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Islet cell Autoantibodies (ICA)
 Insulin Autoantibodies (IAA)
 Glutamic Acid Decarboxylase (GAD)
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Epidemiology
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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
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Symptoms……plus
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Hyperglycaemia (random blood sugar
>11mmol/litre)
Or
Fasting blood sugar >7.0 mmol/litre
Or
2hr post prandial sugar >11 mmol/litre
Or
OGTT
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Diagnosis 2
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Presentation
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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
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Urgent (same day) referral to multidisciplinary
paediatric diabetes care team
Admission or home based care
Admit:
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DKA
<2 yrs old
Social / Emotional issues
Family living long distance from hospital
Peripheral hospital
DKA
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Clinical history
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Clinical signs
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Polyuria, polydipsia, wgt loss, abdo pain, weakness,
vomiting, confusion, stupor, coma.
Dehydration, smell of ketones, lethargy, drowsiness,
Kussmaul breathing
Biochemical signs
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Ketones (blood/urine), hyperglycaemia (>11), acidosis
(pH < 7.3), other electrolyte abnormalities
DKA
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Airway Breathing Circulation (ABC)
Admit ICU
IV access x 2
Oxygen
Fluid resuscitation / IV Insulin / Potassium
Electrolyte monitoring (hrly, 2hrly, 4hrly) – K+
Close monitoring
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Sepsis/Infection
Neurological deterioration
Cerebral oedema
Insulin
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Subcutaneous insulin
when clinically well
and tolerating food /
fluids
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Injection sites
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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
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Phases of Diabetes
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Preclinical diabetes
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Presentation
Partial remission (“Honeymoon” Phase)
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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
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Lifelong insulin therapy
Education
Insulin
 Monitoring glycaemic control (HbA1C)
 Diet
 Exercise
 Smoking / Alcohol / Substance misuse
 Intercurrent illness (sick days)
 Hypoglycaemic episodes
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Avoidance, detection, management
Multidisciplinary Team
Consultant and diabetic team
 Diabetic Nurse Specialists
 Dietician
 Psychology
 Social Worker
 Ophthalmology
 Chiropody
 GP
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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
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Clinic Visits
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Monitor growth (height, weight, BMI)
Pubertal development
HbA1C (< 7.5%)
Check injection sites
Review foot care
Annual screen
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Retinopathy
Nephropathy (Microalbuminuria, Blood Pressure)
Associated conditions
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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
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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
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Complications
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Short Term / Ongoing
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Hypoglycaemia
DKA
Sick days
Lipohypertrophy (48%)
Psychological
Long Term
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Retinopathy
Nephropathy
Neuropathy
Macrovascular Disease
Hypoglycaemia
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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
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Impaired consciousness
 Suspected cerebral oedema
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Sick Days
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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
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Psychological / Social Issues
Emotional / Behavioural
 Family Conflict
 Anxiety / Depression
 Eating Disorders
 Cognitive Disorders
 Behavioural / Conduct Disorders
 Non – compliance
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Complications
Long Term - Retinopathy
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Visual impairment
Blindness
Poor glycaemic
control
Laser treatment if
sight threatening
Ophthalmology check
annually from 12
years or if diagnosed
>5yrs
Long Term - Nephropathy
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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
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Stroke
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Ischaemic Heart
Disease
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Peripheral Vascular
Disease
Associated
Conditions/Complications
Impaired growth and development
 Late pubertal development
 Obesity (excessive exogenous insulin
assoc with high energy intake)
 Autoimmune conditions
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Hypothyroidism
 Hyperthyroidism
 Coeliac Disease
 Addison’s Disease
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Other types of Diabetes
Type 2 Diabetes
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Rising prevalence – associated with
increasing obesity
Type 2 Diabetes
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Insulin resistance
Acanthosis nigricans
 High insulin or c-peptide levels
 Dyslipidemia
 Polycystic ovarian syndrome
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More common in ethnic minority groups
 Japan – more common than T1DM
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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
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Neonatal Diabetes
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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)
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Insulin deficiency
Insulin resistance
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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
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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)
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Other causes
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Drug-induced diabetes
Neurosurgery (Dexamethasone)
 Oncology (chemotherapy)
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Stress Hyperglycaemia
Reported in up to 5% attendances to A&E
 Acute illness, trauma, post seizure, fever
 Recheck blood sugar series when well
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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
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The Future
Key Points
Lifelong disease
 Never omit insulin
 Healthy lifestyle for all the family
 Good glycaemic control
 Screen for complications
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Prevention better than cure!
Thank You