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Diabetes Mellitus in Children

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  • DM can be defined as a chronic metabolic disorder of multiple aetiologies characterized by chronic hyperglycemia with disturbances of CHO, fat, & protein metabolism resulting from defects in insulin secretion, action, or both.

  • Type 1 - neonatal transient, neonatal permanent, & autoimmune
  • Type 2 – classically associated with obesity, MODY (genetic, types 1-6)
  • Secondary Forms (cystic fibrosis, haemochromatosis, Cushing's syndrome, acromegaly, phaeochromatoma, hyperthyroidism)

  • TDM in the newborn has onset in 1st weeks of life.
  • Persists several weeks to months.
  • Occurs most often in SGA.
  • Low/absent insulin response to glucose.
  • Characterized by hyperglycemia, glycosuria β†’ severe dehydration Β± metabolic acidosis.
  • Minimal or no ketonemia or ketonuria.
  • Insulin is mandatory during active phase. (1-2U/kg/day in 2 doses).
  • Resolves spontaneously.
  • Improvement, accelerated growth & weight gain.
  • Prognosis – Excellent.
  • DD- pancreatic agenesis.

  • Previously known as Adult-onset, NIDDM, MODY.
  • Increase incidence because of increase childhood obesity.
  • Not Insulin-Dependent (except during stress, etc., for symptomatic hyperglycemia).
  • Not ketosis-prone (severe infections, stress).
  • Insidious presentation usually - (routine medical exam or for other problems).
  • Minority of all DM patients in pediatric years (10-20%).
  • Inherited nature – stronger than T1DM, polygenic but strong family history.
  • No known HLA or association with autoimmune markers or diagnosis.

  • Uncommon but distinct entity.
  • Presentation < 25 years, often teenager.
  • Probably A-D without skipping.
  • Associated with mutations of glucokinase gene in chromosome 7.

Epidemiology

  • Accounts for more than 90% of Childhood & Adolescent DM.
  • 100,000 children < 15 years develop T1DM annually with wide global variations in incidence.
  • Finland (highest), Korea (low), few data from Africa.
  • Seasonal onset - winter.
  • Can manifest at any age (approximately 50% at > 18 years).
  • Bimodal peak age distribution: 5-7 years & puberty.
  • No sex predilection.
  • Autoimmune antibodies in > 90% of patients, associated with thyroiditis.

Risk Factors

  • Chronic autoimmune disease – vast majority (HLA DR3 & 4, B8, BW15 on chr 6).
  • T-cell mediated autoimmune destruction of pancreatic Ξ²-cells in genetically predisposed individuals. (Islet AB, Insulin AB).
  • Idiopathic – few.
  • Seasonal factors - new cases more common in winter/autumn.
  • No evidence yet with commercial infant formula that contains cow’s milk protein.

Pathophysiology

Pathophysiology
  • Insulinopenia β†’ decreased glucose utilization (muscle, fat).
  • β†’ postprandial hyperglycemia, at lower insulin levels β†’ increased hepatic glycogenolysis/gluconeogenesis β†’ fasting hyperglycemia β†’ osmotic diuresis.
  • β†’ glucosuria β†’ calorie & energy loss β†’ dehydration.
Pathophysiology

Clinical Manifestations

Symptoms develop when about 90% of Ξ² cells are destroyed:

  • Polyuria, nocturia,
  • Bedwetting,
  • Excessive thirst,
  • Weight loss,
  • Fatigue,
  • Polyphagia or depressed appetite,
  • Persistent mycotic infection.

Ketosis Β± Acidosis:

  • Abdominal pain,
  • Nausea, vomiting,
  • Tachypnea and deep respiration,
  • β€œKetone smell”,
  • Lethargy, obtundation, coma.

Asymptomatic:

  • Fortuitous discovery of glycosuria (beware of renal diabetes).

Diagnosis of Diabetes - ADA Expert Committee


NORMAL IMPAIRED DIABETES
FASTING < 100 mg%
(5.5mmol/L)		 100-125 β‰₯ 126 mg%
(7mmol/L)
ORAL GTT
(2 hours)		 < 140 mg%
(7.8mmol/L)		 140-199 β‰₯ 200 mg%
(11.1mmol/L)

Diabetic Ketoacidosis (DKA)

  • Stage of severe metabolic decompensation as a result of severe deficiency of insulin or its effectiveness.
  • Most serious metabolic disturbance of T1DM.
  • DKA & its complications – Most common cause of morbidity and mortality in individuals with T1DM.
  • Manifestations:
    • Hyperglycemia – BG > 200mg% (11.1mmol/l).
    • Metabolic acidosis from overproduction of ketone acids. pH < 7.30, plasma HCO3 < 15mEq/l.

DKA: Lab Features

  • Ketonuria
  • Ketoacidosis
  • Increased anion gap
  • Decreased Serum HCO3, pH
  • Increased serum osmolality
  • Hypertonic dehydration

Risk Factors for DKA

  • Young age < 5 years, lower socioeconomic status
  • In established T1D: Higher Hb A1C
  • Adolescents (especially females)
  • Infections, longer duration
  • Psychiatric disorders
  • Precipitating factors: poor metabolic control & frequently missed insulin injections, infections, trauma, psychological & emotional stress especially in adolescents

DKA: Pathogenesis

  • Increased counter regulatory hormones β†’ Glycogenolysis & gluconeogenesis BG > 250mg/dl > renal threshold β†’ glycosuria β†’ osmotic diuresis + decreased intake & vomiting β†’ dehydration (decreased GFR) β†’ increased BG β†’ electrolyte disturbance (activation of RAS-aldosterone axis β†’ serum K+ loss β†’ risk of C.Oedema).
  • Increased catabolism & cellular loss β†’ loss of Na, K, PO4.
  • Formation of buffers β†’ depletion of buffers β†’ metabolic acidosis.

DKA: Management

  • Rehydration: Initial fluid is normal saline.
    • If in shock, give 30ml/kg over 1-2hrs.
    • Calculate deficit and replace over 48hrs.
  • Insulin: Regular insulin 0.05units/kg/hr as continuous infusion (infusion pump or soluset).
  • Potassium: Add to IVF once urine output is adequate.
  • Determine & treat precipitating factors e.g. fever - blood culture, urine mcs; Avoid urethral catheter - condom drainage of urine.
  • Rehydration phase: (deficit: Minimal - 30-50mls/kg, Moderate - 50-90mls/kg, Severe - 100mls/kg. Give - 50% in 12hrs, rest in 24hrs, use infusion pump.
  • Maintenance: 100mls/kg, 1st 10kg, 50ml/kg - 11-20kg, 20ml/kg - >20kg OR 1.5-2 L/m2/day. 10% for fever/hyperventilation.

Electrolytes in DKA

  • K loss - 6-7 mEq/kg. Urinary loss + increased Aldosterone secondary to dehydration.
  • Serum K may be normal or increased because of shift to extracellular space, BUT total body K - depleted, serum K - unreliable. Insulin & fluids will also lower K. Give K as long as IVF.
  • Replace after initial fluid bolus & child making urine.
  • Options: KCL - hyperchloremic acidosis (worsens acidosis), K acetate - metabolized in liver to HCO3.
  • KPO4 - if PO4 low (contributes to buffer) but risk of decrease of Ca & Mg; thus use ≀ 1.5mEq/kg/day. Use KPO4 + K acetate.

Others

  • Monitoring:
    • Hourly serum glucose
    • Serum Na, K, PO4, HCO3, Cl, urea, creatinine, calcium, pH, ketones
    • Urinalysis; ketones, glucose
    • Neurological signs for cerebral edema

Complications

  • Mortality in DKA – 0.15-0.31% (UK, North America)
  • Cerebral edema – 60-90% of deaths - leading cause
  • Other causes of death - aspiration pneumonia (NGT if vomiting or unconscious), Multi-organ failure
  • Occasionally cerebral thrombosis, infarct, hemorrhage
  • Hypoglycemia, congestive heart failure
  • Renal failure

Cerebral Edema

  • Complication of DKA & its treatment
  • Occurs primarily in children
  • Incidence of clinically significant cerebral edema – low (1-2%)
  • No single etiology – rapid shift in extracellular fluid (ECF) & intracellular fluid (ICF) osmolality, CNS acidosis, Excess fluid administration, cerebral hypoxia. Final step - through cytokines

Risk factors of cerebral edema

  • Younger children (below 5 years use 0.05 units/kg/h of insulin)
  • Children with newly diagnosed T1DM
  • Failure of Na to rise as predicted
  • Use of bicarbonate therapy
  • A greater degree of acidosis and hypovolemia

Signs & Treatment of Cerebral Edema

  • Usually 4 to 12 hours after initiation of therapy
  • Headache, decreased consciousness, Hypertension, bradycardia, pupil abnormalities, papilloedema, decorticate posturing
  • Reduce rate of fluid administration and give mannitol (1 g/kg iv over 20 min)

Outpatient Management

  • Insulin: T1DM depend on insulin to live.
  • Nutrition: Require CHO, protein & fat to grow.
  • Exercise
  • Psychological support: Child and family.
  • Blood sugar monitoring & HbA1C

  • Dreadful disease, requires team support: paediatrician, nurse educator, dietician, mental health professional, social worker, peer discussion group, summer camps, role models, support groups
  • Aims of therapy:
    • Provide normal growth, puberty, psychomotor development, & well-being
    • Exercise is an integral component of growth & dev. No sport is excluded.
    • Nutrition - one of cornerstone of mx
    • No sp nutrition required other than for optimal growth & dev. Same food type as for gen populatn
    • Regular eating pattern for Insulin regimen
    • Individual nutritional reqment & meal plan based on age, sex, wt, activity, preferences
    • Meal plan: 50% CHO- 70% as Complex eg starch to prolong digestion & absorption for slow rise of BG
    • Avoid refined sugars, give high fiber diet eg veg, legumes, whole-meal bread, cereals diet & sugar-free carbonated drinks,
    • Lipids-30%- limit cholesterol
    • 20% protein (plant)- limit egg-yolk, give fish, poultry, lean-cut meat
    • Variable daytime fractioning adapted to insulin regimen, age phy activity, life-style etc
    • 3 meals, 2 snacks. Night tx snack essential to avoid nocturnal hypoglycemia
    • BG target: fasting/preprandial – 70-130mg/dl
    • After meals < 180mg/dl
    • Night: not < 60mg/dl (early morning headache- suggestive of hypoglycemia in the night)
    • Standardized Hb A1c < 7.7%; 6-9-good metab control, 9-12-fair, > 12 poor
    • Avoid severe or frequent hypoglycemia especially- < 5 years ( HbA1c objectives are higher: > 7.5 & < 8.5%; BG: 100- 200mg/dl)
    • Hb A1c- glycosylated Hb -A reliable index of long-term glycemic control
    • Represents fraction of Hb to which glucose has been non-enzymatically & irreversibly bound. Occurs throughout the life-span of RBC (3/12)
    • Allows estimation & duration of hypoglycemia & initial value to compare treatment
    • Hb A1c is affected by RBC survival eg haemoglobinopathy
    • Recurrent hypoglycaemia-depresses overall average
    • For such cases use fructosamine assay- non-covalent glycation of serum proteins over 2 weeks

Serial Blood Glucose Monitoring

  • Ideally - 4 times: before breakfast, lunch, supper & bedtime & if symptoms are present.
  • Many types of glucometer for home use. Some can store data with time & date.
  • Detect factitious glucose log books.

Treatment: Insulin

  1. Simplest Insulin regimen - split mixed regimen – short + intermediate (regular & NPH). Disadvantage - restriction to specific routine & meals.
  2. Frequent injection of short-acting Insulin - mimics endogenous Insulin secretion. Advantage - more flexibility & improved metabolic control.
  3. Lispro injection – used before each meal + longer-acting Insulin more sophisticated.
  4. Insulin pump (CSII) - increasingly popular – external device - continuous infusion through silicone tubing. Delivers preset amount titrated boluses to meal.
  5. Whichever regimen must match lifestyle of child & family.
  1. Short-acting
    • Regular/semilente – onset - 30mins, peak - 2-4hrs, duration – 4-6hrs
  2. Intermediate-acting
    • NPH (pork)
    • NPH (human) - onset - 2-4hrs, peak - 6-12hrs, duration - 10-20hrs
    • Lente
  3. Long-acting
    • Ultralente - onset - 12-18hrs, duration - 18-20hrs

Split-mixed: regular + intermediate 2x/day

  • 2/3 before breakfast
  • 1/3 before supper
  • 1/3 regular + 2/3 NPH
  • 1/2 regular + 1/2 NPH

Metabolic Response

  • Dawn phenomenon - normal physiology due to overnight GH secretion & increased Insulin clearance.
  • In T1DM - no compensation with increased insulin output β†’ increased early morning glucose levels. Usually recurrent.
  • Somogyi - High morning glucose due to a rebound from late night or early morning hypoglycemia β†’ exaggerated counter regulatory response. (hypoglycemia begetting hyperglycemia). But most children remain hypoglycemic. Hence rare in children.
  • Brittle diabetes - wide fluctuations in BG despite large & frequent adjustment of insulin doses. Recurrent DKA. Usually adolescent female. May be due to psychological problems, eating disorders.
  • Honeymoon phase - A transient decrease in insulin requirement associated with improved residual Ξ² cell function. (Thought to be due to Islet cell regeneration).
  • Younger children have no or limited H phase. Older children & adolescents - longer.
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