CHILDHOOD DIABETES

MELLITUS
By- Dr. Mesafint M.
Objectives
• Define DM
• List types of DM

• Analyze the clinical manifestation of DM

• List complication of DM

• Recall the management principle of DM

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 Diabetic Mellitus(DM)

• DM is a common, chronic metabolic syndrome

characterized by hyperglycemia as a cardinal biochemical
feature.

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 ETIOLOGIC CLASSIFICATIONS
OF DM
• The major forms of DM are classified according to those
caused by deficiency of insulin secretion due to pancreatic
β-cell damage (type 1 DM(T1DM) or IDDM) and

• Those that are a consequence of insulin resistance

occurring at the level of: skeletal muscle, liver, and adipose
tissue, with various degrees of β-cell impairment(type2
DM (T2DM)).

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 • Other specific types
• Genetic defects of β-cell function
• Genetic defects in insulin action
• Diseases of the exocrine pancreas
• Endocrinopathies
• Drug- or chemical-induced
• Infections
• Uncommon forms of immune-mediated diabetes
• Other genetic syndromes sometimes associated
with diabetes
• Gestational diabetes mellitus
• Neonatal diabetes mellitus

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 Incidence
• IDDM(Insulin dependent diabetes mellitus) is the most
common endocrine disorder in children.
• Peak age of presentation is 5-7yrs and at the time of
puberty.
• Affects 1/500 children < 18 yrs.

• with prevalence in siblings approaching 6% while the

prevalence in the general population in the USA is only
0.4%.
• Risk increase if parents or siblings have diabetes.

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 Type 2 DM
• The children and adolescents with this type of diabetes
are usually obese but are not insulin dependent and
infrequently develop ketosis
• The presentation of T2DM is typically more insidious.
• T2DM has a strong genetic component.
• The genetic basis for T2DM is complex and incompletely
defined; no single identified defect predominates as does
the HLA association with T1DM.
• The specific etiology is not known, do not have
autoimmune destruction of β cells.

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 Type 1 DM
• T1DM is characterized by autoimmune destruction of
pancreatic islet β cells.
• Both genetic susceptibility and environmental factors
contribute to the pathogenesis.
• Susceptibility to T1DM is genetically controlled by alleles
of the major histocompatibility complex (MHC) class II
genes expressing human leukocyte antigens (HLAs).
• It is also associated with autoantibodies to islet cell
cytoplasm (ICA), insulin (IAA), antibodies to glutamic acid
decarboxylase (GADA or GAD65), and ICA512 (IA2).

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Pathophysiology
 Natural History of Type 1 DM
1. Initiation of autoimmunity
2. Preclinical autoimmunity with progressive loss
of β-cell function

3. Onset of clinical disease

4. Transient remission

5. Established disease
6. Development of complications
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 C/F
• Diabetes is more acute in onset in children than adult.
• Onset is usually preceded by infection.

• Polyuria, polydipsia, polyphagia and rapid loss of weight.

• Nocturia maybe an early symptom in a child who was dry

at night.

• Often diabetic coma is the first manifestation.

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 Dx
• Classic Sx of polyuria, polydipsia and weight loss are
suggestive.

• A Dx of DM can be made if Sx presents with :

FBG* is > 126mg/dl or

2 hr postprandial serum glucose is >200mg/dl on two

separate occasions or

RBG > 200mg/dl at any time

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 IMPAIRED GLUCOSE
TOLERANCE (IGT) DIABETES MELLITUS (DM)

Symptoms of DM plus random

Fasting glucose 100-125 mg/dL (5.6- plasma glucose ≥200 mg/dL (11.1
7 mmol/L) mmol/L)

or

Fasting plasma glucose ≥126 mg/dL

2-hr plasma glucose during the OGTT (7 mmol/L)
≥140 mg/dL, but <200 mg/dL 11.1 or
mmol/L) 2-hr plasma glucose during the
OGTT ≥200 mg/dL

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 Lab

1. Urine –Glycosuria, ketonuria

2. Blood sugar RBG and FBG;HbA1c

3. serum electrolyte: hyponatremia, hypokalemia,

hypochloremia

4. Acid base: Bicarbonate base deficit , PH is low

5. Blood(CBC) :increased Hct due to dehydration,
leukocytosis.

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 Mg’t

• The goal of chronic mg’t include adequate nutrition for

normal growth and development and active life.

• Exogenous insulin sufficient to avoid acute clinical

manifestations and metabolic control sufficient to
minimize long term complications.

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  1. Insulin Therapy
• Most children with new-onset diabetes have some residual
β-cell function which reduces exogenous insulin needs.
• Children with long-standing diabetes and no insulin reserve
require about: - 0.7 U/kg/d if prepubertal
- 1.0 U/kg/d at midpuberty and
-1.2 U/kg/d by the end of puberty
• Dose in the newly diagnosed child, is about 60–70% of the
full replacement dose for age.

• The optimal insulin dose can only be determined

empirically, with frequent self-monitored blood glucose
levels and insulin adjustment.

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 • However, early in the course of the disease, the
requirement may be less than 0.5 u/kg/dy especially
during the honeymoon’s or remission phase of IDDM.
• The total daily dose is divided b/n short acting regular
insulin (1/3rd of total dose) and intermittent acting (NPH)
insulin (2/3rd of the total dose).
• It is conventional to give 2/3rd of daily dose before break
fast and 1/3rd of total dose before evening meal.
• Further adjustment is made depending on the result of
blood or urine sugar.
• The goal of Rx is to maintain FBG b/n
80-120mg/dl and PPBG<200mg/dl.

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 2. Diet: children with IDDM requires nutritionally
balanced diet; with adequate calories and nutrient for
normal growth.

• The recommended diet should contain 55%

carbohydrate, 30% fat and 15% protein.
• Mostly CHO and the fat should contain low level of
cholesterol and saturated fat.

3. Exercise: regular exercise is recommended.

• With exercise insulin requirements are lowered and
metabolic control is improved.
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 4. Monitoring: 2- 4 record is needed a day to provide
enough information to calculate daily dose and during a
period of metabolic instability and infection more record
is needed.

5. Patient/parents education:

• About principles of home mg’t
• Insulin storage and administration
• Pathogenesis, adherence, follow up and
prognosis.

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 • Complication
• Diabetic Ketoacidosis
• hypoglycemia (RBG<60mg/dl): characterized by
behavior changes, weakness, pallor, diplopia, sweating,
nausea, vomiting, tachycardia, palpitation and hunger.

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 • Long-Term Cxs: Related to Glycemic Control

• Can be divided into 3 major categories:

1) Microvascular complications, retinopathy
and nephropathy;
2) Macrovascular complications, particularly accelerated
coronary artery disease, cerebrovascular disease, and
peripheral vascular disease; and
3) Neuropathies, both peripheral and autonomic,
affecting a variety of organs and systems.

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 Diabetic Ketoacidosis (DKA)
• Is the end result of metabolic abnormalities resulting
from severe insulin deficiency or ineffectiveness.

• In 20-40% is the first manifestation of DM.

• Is the most common cause of morbidity & mortality in

diabetic children.

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Diagnostic criteria of DKA

• Hyperglycemia (>200mg/dl)

• Ketonemia
• Acidosis

• Glucosuria and
• Ketonuria

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 CLASSIFICATION OF DIABETIC
KETOACIDOSIS
Normal mild moderate severe

Co2 (meq/l) 20-28 16-20 10-15 <10

PH 7.35–7.45 7.25-7.35 7.15-7.25 <7.15

% wt loss - 3-5 5-9 >=10

BP - normal decreased Much

decreased

Behaviour Clinically normal irritable Lethargic/

stable Coma
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Risk factors for DKA
<5 years
Poor compliance/previous hx of DKA
Poor access to medical care

Lower income and parental education

Infections

Psychiatric disorders
Acute stress

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 What are the presenting
complaints?
• Gastro-enteritis*
• Vomiting-but no diarrhea
• Dehydration-but excessive urine output!

• Respiratory distress* but no lung findings

History and PE= 95% of diagnosis take the history

listen to the history”

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Physical exam

• Vital signs-including weight

• Pattern of respiration
• Hydration

• Mental status
• Evidence for complications
• Evidence for insulin resistance

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 Ix
- Glucose* - Venous pH
- Ketones* - BUN
- Sodium - Serum osmolality
- Potassium - Phosphorus
- Chloride - Calcium
- HCO3

*Always perform in all child

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Treatment
• Volume depletion and cerebral edema are major causes
of mortality and morbidity.

• Always balance b/n dehydration & cerebral edema.

• CVP and arterial pressure monitoring are required to

guide fluid management in very ill patients.

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DKA: treatment
• Treatment is divided in to 3 phases:
- treatment of ketoacidosis

- transition period

- continuing phase and guidance

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Treatment of ketoacidosis
Goals of treatment of DKA

• Intravascular volume expansion

• Correction of deficits in fluids, electrolytes, and acid-base status

• Initiation of insulin therapy to correct catabolism, acidosis

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Treatment of dehydration
• Bolus=20ml/kg/hr
• Do not give more than 40 ml/kg as bolus

• Fluid volume(required)= deficit + maintenance

• Deficit=85ml/kg (8.5% loss)
• Maintenance=based on the wt of the child

• Total fluid rate= deficit+ maintenance-bolus

23hr
• Goal is to replace deficits based on severity over 24-36
hours
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 Electrolyte replacement
• Potassium add when k < 5 and with urination
• K > 5.5 no potassium in IVF
• K 4.5-5.5 20 meq/L kcl (k2PO4 is prefered)*
• K < 4.5 40meq/L kcl
• Sodium replaced as hydration proceeds
• Phosphate-the controversy!
• Bicarbonate-almost never needed
• Hco3 combines with H+ and dissociated to co2 and H2O
whereas bicarbonate passes the blood-brain barrier
slowly, co2 diffuses freely, thereby exacerbating cerebral
acidosis and cerebral depression.

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 Initiation of insulin
• Do not give initial bolus of insulin
• May be started immediately or after 1 hr
• Iv insulin drip at 0.1 unit/kg/hour
• May decrease to 0.05 u/kg/hr if BG decreasing too
quickly
• Target RBS =80-180mg/dI
• When RBS<=250 add 5% D/W; don’t D/C insulin, if sns of
acidosis persists it is not to treat hyperglycemia.
• Expected RBS drop= 50-80mg/hr

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 Mg’t of insulin in our setup

• Initially regular insulin 1IU/kg of which half IV and half

IM

• Then 0.5 IU/kg SC every 6 hrly until patient is out of DKA

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Monitoring
Follow with flow sheet
• Clinical status & vital signs

• Neurological asst. every hourly

- consciousness, respiration, apnea, PR, headache,
pupil size, Sz, posturing

• Labs. U/A, RBS

• Rates of insulin, fluids, dextrose

• Caution with meds. that may alter mental status

• Assess, reassess and then assess again
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 • Transition off IV insulin
• PH>7.30 and HCO3 >15 -18
• Patient able to eat (conscious)
• No emesis

• Subcutaneous insulin:
• give sc injection; D/C insulin/IV dextrose feed child

• known diabetes patient

• Previous dosing
• New patient age dependent adjustment

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Complications

• Cerebral Edema
• Hypokalemia/Hyperkalemia

• Hypoglycemia
• Hypovolemia

• Infections
• shock

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 Cerebral Edema
• Major cause of death in childhood DKA
• At risk:
• Initial PH < 7.1(severe acidosis)
• Baseline mental status abnormal
• Newly diagnosed DM
• Younger children (<5 years old)
• Rapid rehydration(> 50cc/kg in first 4 hrs)
• Hypernatremia/ persistent hyponatremia
• Increased blood urea nitrogen, which may
represent a greater degree of hypovolemia
• The use of bicarbonate therapy for correction of
the acidosis in DKA

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Treatment of cerebral edema

• Elevate the head of the bed

• Mannitol:1 gram/kg IV over 30 minutes

• Decrease IVF rate and insulin infusion rate

• Pediatric ICU management

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 Thank You!
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