What’s New in Paediatric T1DM
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Transcript of What’s New in Paediatric T1DM
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What’s New in Paediatric T1DM
TCH Paediatric Multidisciplinary Diabetes Team10 July 2013
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Learning objectives• Recognise clinical signs and symptoms to allow for
the earliest possible diagnosis and referral of children with new-onset T1DM.
• Describe current insulins and regimen options available in 2013.
• Develop an understanding of the various technologies available for the management of T1DM at home.
• Understand strategies for and review sick-day management plans for children with T1DM in your practice.
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Case study1• 4 yr old boy• GP presentation: 3 week history of
weight loss, polyuria and polydipsia. • 2 day history of sore throat• Woke up in the morning with ‘heavy
breathing’• Past medical and family history were
unremarkable.
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Case study2Physical examination• Alert• GCS score 15/15• Kussmaul breathing present• PR 136 bpm, RR 44, BP 92/58• >5% dehydration• Dry cracked lips• Weight 16kg (~3kg weight loss in 4 weeks)• Pharyngitis
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Case study3• At GP surgery: BGL 25mmol/L – referred to
ED In ED:• Capillary blood gas: pH 7.18, bicarbonate
(HCO3) 12 mmol/L, BGL 25 mmol/L, Na 136 mmol/L (corrected = 142) , K 4.9 mmol/L
Corrected Na = measured Na + 0.3 (glucose – 5.5)
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Case study4Management:• 10ml/kg bolus Normal saline• Re-assessed: PR 118, RR 36, BP 96/58• IV insulin infusion: 0.1U/kg/hr• Fluids: N/S + 40mmol/L KCL at maintenance
+ 5% replacement over 48 hrs• Transferred to HDU – further management
as per DKA protocol
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Case study5At resolution of ketoacidosis:• Initiated on MDI: Levemir at bedtime;
Novorapid with meals using an insulin dosing card.
• DNE / Dietician / Social work involvement
• Discharged home on day 5 with nightly contact with on-call Paediatric Endocrinologist for dose adjustments
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• Type 1 diabetes
– β-cell destruction• Type 2 diabetes
– Progressive insulin secretory defect• Other specific types of diabetes
– Genetic defects in β-cell function, insulin action
– Diseases of the exocrine pancreas– Drug- or chemical-induced
• Gestational diabetes mellitus (GDM)
Diabetes Care 2013;36(suppl 1):S11.
Classification of Diabetes
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A1C ≥6.5%OR
Fasting plasma glucose≥7.0 mmol/L
OR2-h plasma glucose ≥11.1 mmol/L during
an OGTTOR
A random plasma glucose ≥11.1 mmol/L
Diabetes Care 2013;36(suppl 1):S13; Table 2.
Criteria for diagnosis of Diabetes
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Categories of increased risk for diabetes (prediabetes)
IFG: 5.6–6.9 mmol/LOR
IGT: 2-h plasma glucose in the 75-g OGTT7.8–11.0 mmol/L
ORA1C 5.7–6.4%
*For all three tests, risk is continuous, extending below the lower limit of a range and becoming disproportionately greater at higher ends of the range.
Diabetes Care 2013;36(suppl 1):S13; Table 3.
Criteria for Prediabetes
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• Autoimmune destruction of the pancreatic islet cell
• Hallmark = lymphocytic infiltration of islets
• Progresses over years• Leads to insulin deficiency• Glucagon production is
preserved but impaired action
Pathogenesis of T1DM
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Diabetic Medicine 2009; 26(6): 596-601
Australian incidence (NDR) in children 0-14 years between 2000-2006
Incidence of T1DM in Australia
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Genetics of T1DM 1
• Susceptibility to T1DM is an inheritable trait BUT >85% cases occur in the absence of first-degree relative
• Lifetime risk: first-degree relative (5%) vs general population (0.3%)
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Genetics of T1DM 2
• Twin concordance: monozygotic (30-50%) vs dizygotic (6-10%)
• Risk increases with early age at diagnosis: 3-5 fold increase risk if first degree relative diagnosed <5 years age
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Genetics of T1DM 3Susceptibility loci: HLA-DR3 and HLA-DR4• At least one locus: 95% T1DM vs 3%
general population
Protective loci: HLA-DR2, HLA-DR5, and HLA-DQB1*0602• 1 in 15,000 people with HLA-DQB1*0602
develop T1DM
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Environmental factors in T1DM
• Cow’s milk protein exposure (bovine serum albumin and β-lactoglobulin)
• Vitamin D deficiency• Viruses: coxsackie A or B, enterovirus, rubella,
cytomegalovirus, ECHO virus, EBV, mumps, retrovirus• Drugs & toxins: eg alloxan-like or streptozotocin- like
agents that induce oxidant beta-cell damage• Stress
The Environmental Determinants of Diabetes in the Young (TEDDY) study
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Islet-specific autoantibodies1• Islet cell autoantibodies (ICA)• Glutamic acid decarboxylase autoantibodies
(GADA)• Insulinoma-associated 2 autoantibodies (IA-2A)• Insulin autoantibodies (IAA)• Zinc transporter autoantibodies (ZnT8A).
Multiple and specific combinations of autoantibodies more predictive
Diabetes Care 2009;32:2269-74
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Islet-specific autoantibodies2• Not causative • Present months to years before onset of
symptoms• Persist for varying duration after onset• 90-95% T1DM have at least one at
diagnosis
Cell Mol Life Sci 2007;64:865-72Ann Intern Med 2004;140:882-6J Clin Endocrinol Metab 2004;89:3896-902.Diabetes 1999;48:460-8
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Atkinson MA & Eisenbarth GS. Lancet 2001; 358; 221-229
The Pathogenesis of T1DM
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Meal
Normal glucose homeostasis
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Insulin secretion
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Fasting blood glucose is not an appropriate screen test for T1DM
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Clinical Presentation• Polyuria – 95%• Weight loss – 61%• Fatigue – 52%
Polyuria is often missed on history
The EURODIAB studyDiabetologia 2001;44(Suppl 3):B75-80.
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• Utilize intensive therapy aimed at near-normal BG and A1C levels
• Prevent diabetic ketoacidosis and severe hypoglycemia
• Achieve the highest quality of life compatible with the daily demands of diabetes management
• In children, achieve normal growth and physical development and psychological maturation
• Establish realistic goals adapted to each individual’s circumstances
Goals of T1DM Management
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DCCT and EDIC Findings• Intensive treatment reduced the risks of retinopathy,
nephropathy, and neuropathy by 35% to 90% compared with conventional treatment
• Absolute risks of retinopathy and nephropathy were proportional to the A1C
• Intensive treatment was most effective when begun early, before complications were detectable
• Risk reductions achieved at a median A1C 7.3% for intensive treatment (vs 9.1% for conventional)
• Benefits of 6.5 years of intensive treatment extended well beyond the period of most intensive implementation(“metabolic memory”)
DCCT/EDIC Research Group. JAMA. 2002;15;287:2563-2569.
Intensive treatment should be started as soon as is safely possible after the onset of T1DM and maintained thereafter
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Principles for Good Glycaemic Control
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• Paedaitric Endocrinologist• Diabetes Nurse Educator / Nurse Practitioner• Dietician• Social Worker• Psychologist
• Age-appropriate clinics
ISPAD Clinical Practice Consensus Guidelines 2006–2007
The Multidisciplinary Team Approach
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ISPAD Clinical Practice Consensus Guidelines 2006–2007
• Education for parents / child (age appropriate)
• Correct insulin regimen• Contact in between clinics for adjustments• Good relationship with GP
Contributors to good glycaemic control
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Rapid (Humalog, Novorapid, Apidra)
Hours
Long (glargine)
Short (Humalin R, Actrapid)
Intermediate (NPH, Protaphane)
Long (detemir)
InsulinLevel
0 2 4 6 8 10 12 14 16 18 20 22 24
N Engl J Med. 2005;352:174-183.
Pharmacokinetics of insulin Products
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Pre-mix
Twice-daily
MDI
IncreasedComplexity
Better control
Less Hypoglycaemia
CSII
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INSULIN DOSING CARDEzy-BICC
SMART-METERAccu-Chek Aviva Expert
INSULIN DOSING APPInsulin Pro
Insulin dosing advice
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DKA
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Risk factors for DKA at diagnosis of T1DM
• Younger age• Ethnic minority• No first degree relative• Low SES/poor medical access/uninsured• Lack of community health screening• Lower weight SDS at diagnosis
Rates of DKA inversely related to prevalence of T1DM
Diabet Med 2013. doi: 10.1111/dme.12252Pediatr Clin N Am 2011; 58 : 1301–1315
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• Hyperglycemia BG > 11 mmol/l (young or partially treated children, pregnant adolescents may
present with “euglycemic ketoacidosis”)
• Venous pH <7.3 and/or bicarbonate <15 mmol/L– mild DKA pH <7.3 bicarbonate <15 – moderate pH <7.2 bicarbonate <10– severe pH <7.1 bicarbonate < 5
• Glucosuria and ketonuria/ketonemia (β-HOB)
ISPAD Clinical Practice Consensus Guidelines 2006–2007
DKA criteria
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ISPAD Clinical Practice Consensus Guidelines 2006–2007
Pathophysiology of DKA
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• Feeling unwell for a short period, often less than 24 hours
• Polyuria, polydipsia and increased thirst, nocturia• Polyphagia • Weight loss • Nausea and vomiting, vomitus can have coffee-
ground colour due to haemorrhagic gastritis• Abdominal pain, due to dehydration and acidosis• Weakness
ISPAD Clinical Practice Consensus Guidelines 2006–2007
DKA Clinical Manifestations 1
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• Neurologic signs: restlessness, agitation,lethargy and drowsiness, coma. Increased
• Osmolality is the main factor that contributes to altered mental status
• Visual disturbances due to hyperglycaemia • Deep and rapid breathing, known as Kussmaul
breathing, may have acetone odour on breath.
ISPAD Clinical Practice Consensus Guidelines 2006–2007
DKA Clinical Manifestations 2
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• Signs of dehydration due to fluid loss through polyuria, vomiting and breathing: reduced skin turgor, dry mucous membranes
• Signs of hypovolaemia: tachycardia, hypotension, postural hypotension
ISPAD Clinical Practice Consensus Guidelines 2006–2007
DKA Clinical Manifestations 3
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• Mild hypothermia due to acidosis-induced peripheral vasodilation, warm dry skin.
• Fevers are rare despite infection. Severe hypothermia is a poor prognostic sign
ISPAD Clinical Practice Consensus Guidelines 2006–2007
DKA Clinical Manifestations 4
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Measurement of Ketone bodies
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Hypoglycaemia
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Hypoglycaemia 1
• Diaphoresis• Tachycardia/
Palpitations• Shakiness• Tingling• Pallor
Adrenergic
• Confusion• Irritability• Behavoural changes• Difficulties concentrating• Headache• Visual disturbance• Slurred speech• Altered consciousness• Seizures
Neuroglycopenic
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Hypoglycaemia 2• Check BGL if symptoms: <4.0mmol/L• To increase BGL by 3-4mmol/L:
<30kg child use 10g≥30kg child use 15g
• Re-check BGL every 10-15 mins and repeat treatment if necessary
ISPAD GuidelinesPediatric Diabetes 2009: 10(Suppl. 12): 134–145
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Hypoglycaemia 3• Check 20-30 mins after resolution to
ensure BGL maintained• Solid food should be avoided until BGL ≥
4mmol/L (impairs absorption of fast-acting CHO)
• Severe hypoglycaemia: IM Glucagon – 0.5mg in <12 years; 1.0mg in ≥ 12 years
ISPAD GuidelinesPediatric Diabetes 2009: 10(Suppl. 12): 134–145
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Cognitive Effects of Hypoglycemia in Children
• Repeated and early exposure to severe hypoglycemia has been reported to reduce long-term spatial memory in children with type 1 diabetes
• Early exposure to hypoglycemia may be more damaging to cognitive function than later exposure
Diabetes Care. 2005;28:2372-2377.
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Incidence of Severe Hypoglycemia: T1DM Exchange
Garg S, et al. Presented at 5th International Conference on Advanced Technologies & Treatment for Diabetes, Barcelona, 2012.
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J Pediatr. 2002;141:490-495.
Causes of Hypoglycemia in Toddlers and Preschoolers
• Unpredictable food intake and physical activity
• Imprecise administration of low doses of insulin
• Frequent viral infections• Inability to convey the symptoms of low
blood sugar
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Glucose Variability and Health Outcomes: Direct and Indirect
Pathways
Health Psychol. 1992;11:135-138Diabetes Care. 1996;19:876-879;
Diabetes Technol Ther. 2008;10:69-80.
Glucose variability
Reluctance to intensify therapy
High A1C
ComplicationsMorbidity Mortality
Quality of life
Fear of hypoglycemia
Severe hypoglycemia
Controversial
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DEXCOM MEDTRONIC
HYPOMON
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Sick Day Management
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STRESS
COUNTER-REGULATORY
HORMONE
INSULINRESISTANCE KETOSISHYPERGLYCAEMIA
Also hypoglycaemia with ketosis eg gastroenteritis
Sick Day Management 1
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Sick day management 2• Regular BGL and ketone monitoring• Additional insulin: 10-20% of total daily
insulin as regular corrections• Encourage oral fluids
IV fluids necessary if unable to maintain BGL to sustain additional required insulin
Paediatric Diabetes 2009; 10 (Suppl. 12): 134-145
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Sick day management 3
Insulin pump:• Check pump / line / site• Subcutaneous injection may be
appropriate• Increase basal rate: 150-200% • Regular correction boluses
Paediatric Diabetes 2009; 10 (Suppl. 12): 134-145
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Who and when to call
• Concerns regarding early presentation of T1DM
• New diagnosis• Existing patients – issues while reviewing
at GP surgery
0466 655 068