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Diabetes in Childhood and Adolescence - Coggle Diagram
Diabetes in Childhood and Adolescence
ADA Classification
Type 1
Autoimmune, idiopathic
Type 2
Insuline resistance + relative insulin deficiency, insulin secretory defect
Type 3
Range of different type of diabetes including defects of β-cell function, defects insulin action, disease of exocrine pancrea
Type 4
Gestational
T1DM
Epidemiology
Most common metabolic disease
50% diagnoses before 15yr
Rapidly fatal without insulin admin
Abrupt onsent, short hx
Life long condition
Ass short term and long term complications
Highest incidence in Europe - lowest in asia
90% of childhood and adolescent diabetes
Mimodal distribution in IRE 5-6 yrs and 12-14yrs
Pathogenesis
Genetic Susceptibility
HLA 50% of genetic risk
Protective allese
Concordance in monozygotic twins <50%
Environmental factors
Possible Harmful
Enterovirus
Possibly antibitocs
Obesity
High birth weight
COVID-19
Gluten
Rotavirus
Possible Protective
Breast milk
Probiotics
Vit D
Omega-3
Gut microbiome
Immune system - Autoimmune
T cell mediated pancreatic islet β cell destruction
Process begins months /yrs before presentation with clinical symptoms
Clinically symptomatic when 90% of β cell destroyed
Pancreatic beta cell loss
Stages
Stage 1 and 2 Preclinical Diabetes
Months or yrs prior to presentation
Antibody positive
Islet cell
Insulin
Glutamic Acid Decarboxylase
ZnT8
Abnormal Glucose tolerance
Stage 3 Clinical Presentation
Partial Remission - Honeymoon Phase
80% of cases transient decrease in insulin requirements
Duration weeks - months
Important to inform parents that the phase is transient
Stage 4 Chronic Phase
Lifelong insulin therapy
Clinical Feature
Polyuria
Polydipsia
Weight loss
Lethargy
+/- Eneuresis
+/- Constipation
Short duration 2-3 wks
Diagnosis
Symptoms
Random BG >11.1 mmol/L
Rare: Oral Glucose tolerance test
Fasting BG of >7.0
2hr post prandial dugar >11.1
HbA1c >6.5%
Baseline Investigations
Plasma glucose
Urine for ketones + glucose
Blood ketones
VBG
Electrolytes
Infection screen if require
HbA1c
Autoantibodies
ICA
IAA
GAD
IA2
ZnT8
Evidence of other Autoimmune disease
Management
Urgent same day referal to MDT paeds diabetes team
Admission
Acute mangement and stabilisation - DKA / non DKA
Insulin admin
Education and training with MDT
+/- psychology
Glucose Homeostatsis
Fed
↑BG ↑ Insulin
↑ Glycogen synthesis
↑ Lipid synthesis
↑ Protein synthesis
↓Gluconeogenesis
Fasting
↓BG ↓Insulin
↑ Glycogenolysis
↑ Gluconeogenesis
↑ Protein catabolism
↑Lipolysis
↑Free fatty acids
↑ Ketone bodies
Uncontrolled Diabetes
Hyperglycaemia
Increased Fatty acid oxidation + ketone body production
Ketosis, acetonuria, acidosis, coma, death
Diabetic Ketoacidosis DKA
Acute metaboloc decompensation - potentially fatal
Clinical Hx
Polyuria
Ploydipsia
Weight loss
Abdominal pain
Weakness
Vomiting confusion
Stupor
Coma
Clinical Signs
Dehydration
Smell of ketones
Lethargy
Drowsiness
Kussmaul breathing
Biochemical Findings
Ketones (blood/urine)
Hyperglycaemia (>11)
Acidosis
Other electrolyte abnormalities
Management
ABC
Admid ICU / HDU
IV acess x2
Oxygen
Management according to strict paediatric DKA protocol
Fluid resus / iv insulin / K+
Electrolyte monitoring - K+
Close monitoring
Sepsis/ infx
Neurological deterioration
Cerebral oedema
Treatment Options
Insulin
Sites of Admin
Abdomen
Thighs
Buttocks
Preperations
Ultrarapid
Fiasp
Rapid
Novorapid
Lispor
Short
Actrapid
Humulin S
Intermedite
Insultard
Humulin I
Long
Glargine
Determir
Ultralong
Degludec
Regime
BD regime
Multiple daily injections
Insulin pump therapy
Continous subcut insulin infusion
Sensor augmented pump therapy
Hybrid closed loop
Continous Management
Education
• Diet (Healthy Eating, CHO counting)
• Monitoring glycaemic control (HbA1C), targets
• Exercise
• Smoking / Alcohol / Substance misuse
• Management of Intercurrent illness (sick days)
• Management of Hypoglycaemic episodes – Avoidance, detection, management
• Management in school
• Insulin Regime – choice and training
Diabetes MDT
Child
Parents and other family
Paediatric endocrinologist and medical diabetes team
Diabetic Nurse Specialists
Dietitian
Psychology
Social Worker
Ophthalmology
Chiropody
GP
Targets and Follow-up
Aims
Aim for frequent blood sugar monitoring (usually 4 BM’s daily – fingerprick or
continuous/flash glucose monitoring)
Aim for pre-prandial sugar: 4 – 8 mmol/L initially
Aim for post-prandial sugar: < 10mmol/L initially
Target Time in Range > 70%, Hypoglycaemia <4%
Target HbA1c 7% : 53 mmol/mo
Follow up
Adjust insulin doses accordingly
Liaise with diabetic team (phone / clinic)
Monitor sugars more often during intercurrent illness – risk of DKA
If surgery reqd need careful glucose monitoring
Clinical Visits
Monitor growth (height, weight, BMI, BP)
Metabolic control: HbA1C (< 7% : 53 mmol/mol) Time in range
Psychosocial wellbeing
Pubertal development
Check injection sites
Review foot care
Life style – promote healthy lifestyle
Annual screening
Constant re-education through life
Dietary education CHO counting
Associated Conditions
Growth and pubertal development, often CDGP
Obesity (excessive exogenous insulin assoc with high energy intake)
Autoimmune conditions:
Hypothyroidism, Hyperthyroidism, Coeliac Disease
Adrenal insufficiency (Addison’s Disease)
Issues and Complications
Short Term / Ongoing
– Hypoglycaemia
– DKA
– Sick days (management)
– Lipohypertrophy (48%)
– Psychological
Long Term
Microvascular
– Retinopathy (early intervention, laser Tx to protect vision)
– Nephropathy (Microalbuminuria, Blood Pressure, ESRD)
– Neuropathy
Macrovascular
Lipids
BP
Weight
BMI
Exercise
DDX
Neonatal DM
Very rare
Requiring insulin in first 3-6 months of life
Ass w/ IUGR
50% transient
Permanent ass with pancreatic aplasia and single gene defects
Monogenic Dabetes MODY
Single gene disorder causing β cell dysfunction
Autosomal dominant fhx
Antibody negatve
Slim build, no insulin resistance
Less insulin than T1DM
Endogenous insuline secretion - persisting stimulated C peptide
Not prone to ketoacidosis
Family screening
Drug Related
– Neurosurgery (Dexamethasone)
– Oncology (chemotherapy)
T2DM
Cystic Fibrosis Related Diabetes (CFRD)
Insulin deficiency and resistnce
Cirrhosis contributes to resistance
Onset is a poor prognostic indicator
Poor control promotes catabolism
Screening - OGTT
Insulin doses smaller than in T1DM
Can develop T1DM
Stress hyperglycaemia
– Reported in up to 5% attendances to A&E
– Acute illness, trauma, post seizure, fever
– Recheck blood sugar series when well
