Diabetes mellitus in children By Henry Cummings MBBS, FMCPaed Delsuth, Oghara
Transcript
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Diabetes mellitus in children By Henry Cummings MBBS, FMCPaed
Delsuth, Oghara
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Pre-test 1. Dm is the commonest endocrine disorder in children
2. Only type 1 dm occurs in children 3. TIDm is a non progressive
low-insulin catabolic state 4. Exogenous insulin replacement
remains the only form of replacement therapy 5. In managing DKA,
always add kcl to the initial rehydrating fluid.
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Childhood Diabetes mellitus Definition Types Patho physiology
Clinical features Modalities of management Complications, short
term, long term Recent advancements Conclusion
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DEFINITION BY WHO: DM is a metabolic disorder of multiple
aetiologies characterised by chronic disturbances of carbohydrate,
fat & protein metabolism, resulting from defects in insulin
secretion, insulin action or both. DM is the commonest endocrine
disease in childhood & adolescence.
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MAGNITUDE OF THE PROBLEM Overall incidence 1 to 2 per 1000
school age children. Estimated prevalence of childhood DM in 2003
were: 430,000 globally 250,000 live developing countries. 63,000
live in 58 poorest countries(least developed countries).
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TYPES OF DM Type 1 DM(IDDM) Beta cell autoimmune destruction
Absolute insulin deficiency Requires insulin for survival Accounts
for over 90% of childhood DM Peak age incidence 10-12 years Slight
male predominance Prone to ketosis
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Type 2 DM (NIDDM) Insulin resistance with relative deficiency
OR Secretory defect with or without resistance Does not require
insulin for survival Strong genetic component Not prone to ketosis
Acanthosis nigrans may be present No islet cell antibodies
Associated with overweight teenagers
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Maturity onset diabetes of the youth (MODY) Early onset of
dominantly inherited type 2 DM Non- obese children No islet cell
antibodies Family history in several generation Identified genetic
mutations e.g mutations of glucokinase or hepatic nuclear factor 1
& 2 genes Non- ketotic Two (or at least one)family member
diagnosed before age of 25 years
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Neonatal Diabetes hyperglycemia requiring insulin in the first
3months of life Rare condition 1:400,000 Associated with IUGR 50%
of cases are transient Associated with paternal isodomy & other
imprinting defects of Chr 6 In transient NND permanent DM may
appear later in life
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Secondary diabetes mellitus May be associated with cystic
fibrosis, hemochromatosis, drugs such as L- Asparaginase
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Criteria for diagnosis Symptoms of DM and casual plasma glucose
conc > 11.1mmol/L(200mg/dl) (10 for venous) FPG >
7.0mmol/L(126mg/dl) (6.3 for venous and cap) 2hr post load of
glucose >11.1mmol/L during an OGTT
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blood sugars blood sugars Normal RPG: 70 140mg/dl Normal FBS:70
100mg/dl Hypoglycemia: Mild40 70mg/dl Severe40mg/dl Neonatal
Pathophysiology Insulin essential to process CHO, fat, protein
It blood glucose levels by glucose uptake into muscle cells and fat
cells stimulates glycogenesis inhibits glycogenolysis the breakdown
of fat to triglycerides, free fatty acids, and ketones.
(lipolysis)
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Pathophysiology Lack of Insulin glucose oxidation in muscle
& fat cells Proteolysis & amino acid release Glycogenolysis
& gluconeogenesis all result in Hyperglycaemia Glucose intake
still continues
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Pathophysiology The kidneys cannot reabsorb the excess glucose
load, causing glycosuria, osmotic diuresis(polyuria), thirst, and
dehydration. Untreated pt excrete high glucose load causing
polyphagia Increased fat and protein breakdown leads to ketone
production and weight loss.
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Pathophysiology contd Acidosis result from ketosis Acidosis
leads to renal excretion of K + and Po 4 Na + loss is due to
osmotic diuresis & vomiting Hypokalemia is due to vomiting,
osmotic diuresis & hyperaldosteronism Coma likely due to
ketosis, acidosis, dehydration & hyperosmolality
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Absolute insulin deficiency OR Stress, infection or
insufficient insulin intake Counter-regulatory hormones: Glucagon,
Cortisol, Catecholamines, GH Lipolysis FFA to liver Ketogenesis
Alkali reserve Acidosis Lactate Glucose utilization Proteolysis
Protein synthesis Glycogenolysis Gluconeogenic substrates
Gluconeogenesis Hyperglycemia Glucosuria (osmotic diuresis) Loss of
water and electrolytes Dehydration Impaired renal function
Hyperosmolarity
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Phases of T1DM 1. Preclinical diabetes 2. Presentation of DM 3.
Partial remission or honeymoon phase 4. Chronic phase of lifelong
dependency on administered insulin
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Preclinical DM Occurs months to years preceding the clinical
presentation of T1DM Antibodies can be detected as markers of beta
cell auto immunity:- GAD, IA,ICA, IA2 etc IVGTT
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T1DM: a slowly progressive T-cell mediated autoimmune illness
Genetic susceptibility Islet Cell Mass 100% 50% 0% Inciting
Event(s)Diabetes I II III Time (years) Silent Cell Loss Diabetes
Onset cell Mass?? Is cell loss exclusively immune mediated?
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Clinical presentation Vary from non-emergency px( polydipsia,
polyuria, weight loss, enuresis) to severe dehydration, shock and
DKA Onset may be acute, precipitated by an acute illness, or more
chronic and insidious over weeks or even months.
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Lab Investigations Glucose levels E & U Ketones C peptides
Islets cell antibodies
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Other Lab Investigations Lipids Microalbumin Thyroid fxn test
Hb A1c fructosamine
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Modalities of management requires Multidisciplinary team
Insulin therapy Diabetic education Exercise Diet Psychological care
Monitoring Others:- sick day mx, adjusting to school
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Insulin therapy Exogenous insulin replacement remains the only
form of replacement therapy
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The Basal/bolus Insulin Concept Basal Insulin - Suppresses
glucose production btw meals and overnight -40% to 50% of daily
needs Bolus Insulin (meal time) -Limits hyperglycaemia after meals
-Immediate rise and sharp peak at 1 hour -50% -60% total daily
insulin requirement for meals
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Basal/bolus therapy regimens Intensive management : MDI
Multiple Dose Insulin Once-daily IA or LA insulin usually given at
night and 3-ce daily SA or VA before each meal Mixed preps e.g.
Mixtard, humulin 70/30 CSII Continuous Subcutaneous Insulin
Infusion (Insulin pump therapy)
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INSULIN THERAPY contd. Twice daily regimen: Split dose regimen
(2/3 morning, 1/3 evening; 2/3 intermediate acting, 1/3 soluble).
Aim at maintaining blood glucose within 80-150mg/dl, with the
occurrence of as few hypoglycaemic episodes as possible.
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Twice a day insulin Soluble insulin Intermediate- acting
insulin Insulin 60 0 20 40 Endogenous insulin
BreakfastLunchSupper
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DIET Complex carbohydrates (CBHs) are preferred to simple
refined CBHs. Dietary regimen should be adjusted according to
convenience of the family and school timings to ensure better
compliance. Total CBH content of the meal &snacks should be
kept constant.
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EXERCISE Encourage regular exercise. Insulin requirement may be
lower, metabolic control improved and self- esteem & body image
better in physically fit child.
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SELF- CARE EDUCATION Should include nature of illness, acute
& chronic complications, insulin action, duration and timing,
injection techniques, nutrition information, self blood glucose
monitoring and urine ketone checks. Education must be appropriate
to childs age & family educational background.
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Monitoring Monitoring of growth & development: the use of
percentile charts is a crucial element in the care of children
& adolescents with DM Poor gain of height & weight,
hepatomegaly and delayed puberty might be seen in children with
persistently poorly controlled DM
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Monitoring HbA1c at least twice a year Screening for long term
complications
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Partial remission (honeymoon) phase Defined as when the patient
requires < 0.5units of insulin/kg/day and has an HbA1c
TREATMENT contd Maintain IV insulin until DKA resolves: pH >
7.3, bicarbonate > 15mmol/L, stable serum Na+ 135 145mmol/L, No
emesis; then switch to SC insulin (maintain IV insulin 30min after
SC) Ketones may take longer to clear
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HYPOKALEMIC = give with initial resuscitation 20mmol/l
EUKALEMIC = at the time of insulin intro HYPERKALEMIC = when
patient makes urine POTASSIUM
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Max dose 0.5mmol/kg/hr If hypokalemia persist then reduce
insulin infusion rate! ECG monitoring helps! Potassium
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Is given cautiously only if pH < 6.9 HCO3 < 5mmol/l 1
2mmol/kg over one hour! Acidosis
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Hourly monitoring and charting of Blood pressure Respiratory
rate Heart rate Level of consciousness Blood sugar Blood ketones
Electrolyte and urea(Ca,PO4,Mg) Input /output Insulin given
Monitoring/charting
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Inadequate rehydration Hypoglycemia Hypokalemia
hypophosphatemia Cerebral edema Complications of therapy
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Management of DKA Follow up
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PG >33.3 mmol/L (600 mg/dL) Arterial pH >7.30 Serum
bicarbonate >15 mmol/L Small ketonuria, absent to low ketonemia
Effective serum osmolality >320 mOsm/kg Stupor or coma HHS
(Hyperglycemic hyperosmolar state)
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Long-term complications Retinopathy Cataracts Hypertension
Progressive renal failure Early coronary artery disease Peripheral
vascular disease Neuropathy, both peripheral and autonomic
Increased risk of infection Injection-site hypertrophy Growth
failure. Delayed puberty
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Recent advancements Whole pancreas transplantation Islet cell
transplantation Engineered stem cells manipulated genetically to
produce insulin Techniques to protect b cells from autoimmune
attack Immunotherapy Alternate non invasive routes for insulin
administration Chemical alteration of insulin molecule Artificial
pancreas Adding c peptide to insulin Implantable insulin pumps New
blood glucose meters
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Conclusion DM (particularly T1DM), a common and potentially
life threatening endocrine disorder in children is often
misdiagnosed or poorly managed Having a regularly updated
management protocol in our Paediatric units will greatly improve
the level and quality of care these children receive. Thank you for
listening.
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Post test 1. Dm is the commonest endocrine disorder in children
2. Only type 1 dm occurs in children 3. TIDm is a non progressive
low-insulin catabolic state 4. Exogenous insulin replacement
remains the only form of replacement therapy 5. In managing DKA,
always add kcl to the initial rehydrating fluid.