Diabetes Mellitus in Pediatric: Dr. Wasnaa Hadi Abdullah

Diabetes Mellitus in Pediatric
Dr. Wasnaa Hadi Abdullah

MBChB, FIBMS(Ped),
FIBMS(Ped.Endocrine)
Lecturer, Pediatric Endocrinologist
Formerly called insulin-dependent diabetes mellitus (IDDM) ,T1DM is characterized by low or absent levels of
endogenously produced insulin .
The natural history includes 4 distinct stages:

(1) preclinical β -cell autoimmunity with progressive defect of insulin secretion,
(2) onset of clinical diabetes,
(3) transient remission honeymoon period,
(4) established diabetes.
T1DM is due to chronic T cell–mediated autoimmune process; autoantibodies can be detected months to
years prior to clinical onset of T1DM.
85% of newly diagnosed type 1 diabetic patients do not have a family member with T1DM.
Clinical Manifestations:
Polyuria (including nocturia & nocturnal enuresis), polydipsia, polyphagia (↑ appetite), &
weight loss.
Patients presenting with more advanced disease will exhibit signs of DKA including dehydration,
nausea, vomiting, abdominal pain, lethargy, altered mental status, and in extreme cases, coma.
Investigations:
Initial tests for DM include:-
1. Random & Fasting glucose levels.
2. GUE, especially for glucose & ketone bodies.
3. Serum electrolytes.
4. Baseline HbA1c.
5. Search for other autoimmune diseases e.g. celiac disease,
hypothyroidism.
Honeymoon Period
some residual β-cell function may improve after insulin Rx when the
child recovers from the effects of hyperglycemia ,this may
necessitate reduction in the initial total SC insulin dose.
Honeymoon period usually starts shortly after starting insulin

therapy & fades within few months.
Diabetic Ketoacidosis
Etiology: DKA usually occur in 3 main conditions:-

1. 20–40% of children with new-onset diabetes.
2. Children with known diabetes who omit insulin doses.
3. Children who do not successfully manage an intercurrent illness.
Time Therapy Comments
1st hr 10 mL/kg IV bolus 0.9% Bolus fluid may be
normal saline repeated. NPO. Monitor
I/O, neurologic status.
Insulin drip at 0.05 to 0.1 Use flow sheet. Have
unit/kg/hr mannitol at bedside;
1 g/kg IV push for
cerebral edema
2nd hr until DKA Still 0.9% normal saline, 85ml/kg
resolution but when blood glucose (deficit)+Maintenance –
decrease to < 250 mg/dl, Boluses
add 5% glucose solution
to the fluid , If glucose If K <3 mEq/L, give 0.5-
further decrease, lower 1 mEq/kg as oral K
the infusion rate of solution or
insulin but never stop it. increase IV K to 80
mEq/L
Variable Oral intake with No emesis; CO2 ≥16
subcutaneous insulin mEq/L; normal
electrolytes
Note that the initial IV bolus is considered part of the total fluid allowed in the 1st
24 hr and is subtracted before calculating the IV rate.
Maintenance (24 hr) = 100 mL/kg (for the first 10 kg) + 50 mL/kg (for the second
10 kg) + 25 mL/kg (for all remaining kg)
e.g. calculation for a 30-kg child:
1st hr. = 300 mL IV bolus 0.9% NaCl

Rx of DKA:
1. Flow chart.
2. Blood tests for glucose, K, Na, & pH
3. Fluid therapy: nothing by mouth with shoots of fluids for severe dehydration by NS 10 ml/kg .
4. Insulin therapy: It should be given by infusion (not bolus) in rate 0.05-0.1 Unit/kg/hr.
5. Subsequent fluid & insulin therapy: Fluid in the next hours should be replaced with 0.9% NS (85 ml/kg +
Maintenance – Boluses).
6. When blood glucose decrease to < 250 mg/dl, add 5% glucose solution to the fluid (or change the fluid
to G.S. 1/5). If glucose further decrease, lower the infusion rate of insulin but never stop it.
7. Potassium: K is always depleted in DKA. Thus it should be added to the IV fluids after patient pass urine.
8. Sodium: Serum Na should be steadily ↑ with therapy by ≈ 1.6 mmol/L for each 100 mg/dl ↓ of glucose.
If Na level is high (>150 mmol/L), it mean severe hypernatremic dehydration which require slower fluid
replacement (>36 hr), whereas if Na is declining rapidly, it may indicate excessive free water
accumulation with risk of cerebral edema.
9. Osmolality: A rapid decline, or slow decline to subnormal range, may indicate excess of free water with
risk of cerebral edema. Therefore, patient should not be allowed oral hypotonic fluids .
10. Ketoacidosis: Production of ketone bodies ↓ after insulin therapy. Β- Hydroxy-butyrate (which is not
detected by dipstick of urine) is converted to acetoacetate (which can be detected); therefore, urinary
ketone level is not a useful indicator of the adequacy of therapy.
Bicarbonate therapy should be avoided (because of ↑ risk of cerebral edema) except in severe acidosis (pH
<7.0) that results in hemodynamic instability.
Persistent acidosis may indicate inadequate insulin or fluid therapy, infection, or rarely lactic acidosis.
11. Transitional phase: When DKA essentially resolved by following criteria:-

o Clinical: Kussmaul respirations abate abdominal pain resolve, & no emesis.
o Laboratory: pH >7.30, CO2>15 mEq/L, Na stable between 135-145 mEq/L.
Age Total daily insulin
(unit/kg/day)
Pre-pubertal 0.75–1
Pubertal 1-1.2
Post-pubertal 0.8-1
Complications of DKA:
➢ Cerebral edema;
➢ Intracranial thrombosis or infarction;
➢ ARF (due to severe dehydration);
➢ Pancreatitis (with ↑ serum amylase & lipase);
➢ Arrhythmias (due to electrolyte abnormalities);
➢ Pulmonary edema;
➢ and Bowel ischemia.
Cerebral Edema (CE)
Etiology: It remains incompletely understood, but baseline acidosis and abnormalities of
Na, K, & urea concentrations; as well as early bolus administration of insulin and high
volumes of fluid, & bicarbonate therapy are identified as risk factors.
Clinical manifestations: CE involves signs of ↑ ICP e.g., sudden severe headache,

vomiting, ↓consciousness, seizure, Cushing triad (bradycardia, hypertension, apnea),
pupillary changes, & papillodema.
Rx. Immediate interventions include elevation of the head of the bed, reduction in IV fluid
rate, and the administration of IV Mannitol 1g/kg over 20 min.
3 yrs old boy with history of polyuria and excessive thirst
for 1 week, presented with abdominal pain and repeated
vomiting.
Q1: What is your dx?

Q2: What type of fluid you start with?
Q3: After few hours of starting management, your patient
develop severe headache, what do you want to check now?
management?
Rx of T1DM
• Excellent diabetes control involves many goals: to maintain blood glucose and HbA1c levels as close
to normal without causing hypoglycemia, to eliminate polyuria and nocturia, to prevent ketoacidosis,
to permit normal growth and development, and avoid development of diabetes related complications.
• SC insulin is the standard therapy for T1DM. It has many types include
Starting Doses of SC Insulin (without DKA):

Age Total daily insulin (unit/kg/day)
Prepubertal 0.25–0.5
Pubertal 0.5-0.75
Postpubertal 0.25–0.5
Insulin Regimens
✓ 4-injection regimen involves basal dose of long-acting insulin e.g. glargine, these are
typically calculated to provide 50% of the total daily dose at bed time; the remainder 50%
provided with bolus doses of short-acting insulin e.g. Lispro, aspart at mealtimes.
✓ 2-injection regimen involves use of premixed insulin preparations that include both
rapid- and intermediate-acting insulin (in ratio e.g. 70/30). 70% of the total daily dose is
typically provided with breakfast and 30% with dinner.
Insulin Pump Therapy
Continuous SC insulin infusion via

battery-powered pumps provides a closer
approximation of normal insulin profiles
and increased flexibility regarding timing
of meals and snacks compared with
conventional insulin injection regimens.
Education & Monitoring in DM
The physician should educate the patient & his family about:-
✓ How to measure blood glucose .
✓ How to prepare & inject insulin .
✓ How to recognize & treat Cxs e.g. hypoglycemia.
Blood glucose should be checked frequently at least 4 times daily (before

each meal & at bed time) & the dose of insulin is adjusted accordingly. If
blood glucose is high in any given time, it usually indicates insufficient
insulin dose given in the previous period & vice-versa.
Nutritional therapy
✓ Carbohydrate (55%); it should be mainly of complex sugar e.g. starch.
✓ Fat (30%); unsaturated is better .
✓ Protein (15%).
✓ Fibers are useful in improving control of blood glucose.
HbA1c: Its measurement can give the average blood glucose in the preceding 2-3 mo.
Hypoglycemic Reactions in DM
Hypoglycemia is the major limitation against control of glucose levels because it is dangerous
for young children that may → permanent decrease in cognitive function.
C.M.
• Catecholamine release → pallor, sweating, tremor,

tachycardia, hunger, irritability.
• Cerebral glucopenia → drowsiness, personality

changes, mental confusion. If severe, it can cause
seizures or coma.
Prolonged severe hypoglycemia can result stroke-like focal motor
deficits that persist after resolution of hypoglycemia.
Treatment:
Administer 10 to 20 g of a rapidly-absorbed carbohydrate. May repeat
in 10 to 15 minutes such as Sweetened fruit juice , soda , Honey, table
sugar.
Altered mental status, unable to swallow, or does not respond to oral

glucose administration after 2 trials : Give glucagon IM.
Then if no response give an initial IV bolus of glucose in hospital of
10% dextrose solution.
Morning hyperglycemia in DM is either due to:-
✓ Dawn phenomenon; it is a common cause due to taking too little insulin at bed time combined with ↑
secretion of GH overnight.
✓ Somogyi phenomenon; it is due to taking too much insulin at bed time → hypoglycemia → ↑
counter-regulatory hormones → hyperglycemia.
To differentiate between the 2 conditions above, check blood glucose at 3:00 am & adjust the dose of insulin
accordingly.
Infection in patient with DM need frequent checking of blood
glucose (every 1-2 hr) & ketone in urine (every void or every other
void) at home with adjustment of insulin dose accordingly; but if
fail to control blood glucose or development of DKA, refer to
hospital.
Long-Term Complications of DM
• Diabetic Retinopathy; it needs screening by an ophthalmologist within 3-5 yr after the onset of T1DM
(but not before age 10 yr).
• Diabetic Nephropathy; it needs screening at same times as retinopathy; it starts as microalbuminuria,

then progress to frank albuminuria, then may progress to the end stage renal disease (ESRD).
Rx. Control of DM, restriction of protein intake, control of hypertension, & use of ACE inhibitors.
• Diabetic Neuropathy; DM can affect both peripheral & autonomic nervous systems. Early signs are
sensory loss, loss of sense in reaction to hypoglycemia.
Rx. Control of DM, use of anticonvulsants for neuropathic pain, topical analgesics.
Mauriac syndrome is a syndrome due to
chronic underinsulinization that results in
dwarfism, proximal muscle wasting, moon
face, protuberant abdomen, and enlarged
liver (due to fat & glycogen infiltration).
LJM
Syndrome
TYPE 2 DIABETES MELLITUS
It considered a polygenic (multifactorial) disease, usually
occur in older children & adolescents who are obese & have
+ve family hx of T2DM.
Insulin resistance with relative insulin deficiency. Presentation
with DKA occurs in up to 10% of cases.
C.M. Markers of insulin resistance include; Acanthosis

nigricans (a dark pigmentation on the neck & other flexural
areas), central obesity, Hrt, & hyperlipidemia.
Rx.
• ↓sedentary lifestyle by improving exercise & physical activity.
• Nutritional education with weight loss.
• Insulin Rx may be required for patients who present with DKA or markedly
↑ HbA1c (>9.0%).
• Oral hypoglycemic agents are the standard Rx for T2DM mainly in

adolescents .
The only FDA-approved oral agent for the treatment of T2DM in children and
adolescents is metformin.
All adolescents with T2DM should be screened for hypertension and lipid
abnormalities as well as microalbuminuria and retinopathy at diagnosis. Fatty
liver disease is being diagnosed with increasing frequency in T2DM.

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Diabetes Mellitus in Pediatric

Dr. Wasnaa Hadi Abdullah

The natural history includes 4 distinct stages:

Honeymoon period usually starts shortly after starting insulin

Etiology: DKA usually occur in 3 main conditions:-

e.g. calculation for a 30-kg child:

1st hr. = 300 mL IV bolus 0.9% NaCl

11. Transitional phase: When DKA essentially resolved by following criteria:-

Clinical manifestations: CE involves signs of ↑ ICP e.g., sudden severe headache,

Q1: What is your dx?

Starting Doses of SC Insulin (without DKA):

Continuous SC insulin infusion via

Blood glucose should be checked frequently at least 4 times daily (before

• Catecholamine release → pallor, sweating, tremor,

• Cerebral glucopenia → drowsiness, personality

Altered mental status, unable to swallow, or does not respond to oral

• Diabetic Nephropathy; it needs screening at same times as retinopathy; it starts as microalbuminuria,

C.M. Markers of insulin resistance include; Acanthosis

• Oral hypoglycemic agents are the standard Rx for T2DM mainly in

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