DIABETES IN CHILDHOOD AND ADOLESCENCE (1)

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�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

DEFINITION

• Diabetes mellitus (DM) is a group of metabolic diseases
• Characterized by chronic hyperglycaemia
• Resulting from defects in insulin secretion, insulin action, or both.

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

DIABETES MELLITUS

WORLDWIDE:

2000: 170 million (2.8%)

2030: 366 million (4.4%)

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» will more than double (+ obesity ↑)

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MOST RAPID GROWTH:

• Urban centres
• Low- / Middle income economies

GREATEST HUMAN EPIDEMIC EVER!

How frequently does diabetes occur?

About 50% of diabetics � go undiagnosed

17

16,5

23,5

10

95

12

1

In million people

DIABETICS (2000 & 2030)

Issues

• Most common is Type 1 DM?
• Prevalence not really known
• Poor access to insulin
• Poor glucose home monitoring - Poor access to meters and reagent strips
• Poor glyceamic control
• Complex diet
• Camps
• Developing States/ Regional/ National Clubs
• Research
• Poverty
• Education

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Future

• Create awareness
• DIP
• Research
• Central Laboratory of Excellence – Regional/National
• Team
• Create Children, Adolescents With Diabetes and Parents Club - CADAP
• Advocacy
• Poverty Alleviation plan – Rotary, Lion etc
• Generation of Fund- N100/ person/year; N25000/corporate body/biannually
• Camps

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�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Classification
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Classification of Diabetes�

MM/october 2005

Type 1 (juvenile or insulin-dependent diabetes)

(beta-cell destruction, usually leading to absolute insulin deficiency)

• Autoimmune

• Idiopathic

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Type 2 ( non-insulin dependent diabetes)

(may range from predominantly insulin resistance with relative insulin

deficiency to a predominantly secretory defect with or without insulin

resistance)

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Other specific types

Neonatal Diabetes

Maturity onset Diabetes of the Young

Diseases of exocrine pancreas

Drugs and Chemical induced,

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�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Etiology of T1Diabetes

MM/october 2005

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Pancreas

• The pancreas functions as both an exocrine and an endocrine gland
• Exocrine function is associated with the digestive system because it produces and secretes digestive enzymes
• Endocrine Function: produces two important hormones in Islets of Langerhans, insulin and glucagon
• They work together to maintain a steady level of glucose, or sugar, in the blood and to keep the body supplied with fuel to produce and maintain stores of energy.

Pancreatic Hormones

• Insulin (beta cells)
• stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose � 
• Glucagon (alpha cells)
• stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose�
• Glucagon and insulin work together to regulate & maintain blood sugar levels

• Glycogen
• Polysaccharide consisting of numerous monosaccharide glucoses linked together. Stored as an energy source in liver & muscles

Insulin works antagonistically with glucagon to control blood sugar levels.

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Functions of insulin

• Enables glucose to be transported into cells for energy for the body
• Glucose is the preferred fuel of the body cells and the only fuel that the brain can use
• Converts glucose to glycogen to be stored in muscles and the liver
• Facilitates conversion of excess glucose to fat
• Prevents the breakdown of �body protein for energy
• Summary
• Stimulating the uptake of glucose by the tissues
• Converting glucose to glycogen in the liver
• Increasing the production of fats and proteins

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Diabetes Mellitus

• After a meal, blood glucose levels rise, prompting the release of insulin
• Causes cells to take up glucose, and liver & skeletal muscle cells to form the glycogen thus decreasing blood glucose
• As glucose levels in the blood fall, further insulin production is inhibited
• Glucagon production is stimulated when blood glucose levels fall
• Glucagon causes the breakdown of glycogen into glucose, which in turn is released into the blood to maintain glucose levels within a homeostatic range
• Glucagon is inhibited when blood glucose levels rise
• Diabetes Mellitus results from inadequate levels of insulin

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• Meal 🡪 ↑glucose levels 🡪 insulin released 🡪 cells take up glucose🡪 convert to glycogen (liver & skeletal cells)🡪 ↓glucose level in the blood🡪 insulin production ceases; Glucagon 🡪 converts glycogen into glucose 🡪 return to normal blood glucose levels

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Natural History of Type 1 Diabetes

CELLULAR (T CELL) AUTOIMMUNITY

LOSS OF FIRST PHASE

INSULIN RESPONSE

(IVGTT)

GLUCOSE INTOLERANCE

(OGTT)

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

HLA haplotypes

HLA B 8 DR3 DQ2

B 15 DR4 DQ8

Risk 1/100 1/47

Only 11% lack either DQ 2 or DQ 8

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However: 75 % DM1 population have either (or both) these alleles

But some HLA types are protected

DQ6

Do not acquire diabetes

Before the age of 10

Genetic Risk of T1D

• Siblings: 5 – 6 %

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• Mother: 3 – 4 %
• Father: 6 %

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• Monozygotic Twins: 30 – 50 %

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• General Population: 0,4 %

MM/october 2005

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Phases of Diabetes type 1

• Preclinical diabetes.

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• Presentation of diabetes.

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• Partial remission or honeymoon phase.

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• Chronic phase of lifelong dependency on administered insulin.

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MM/october 2005

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Modes of Presentation of T1D�

• Polyuria, nocturia,

bed wetting

• Excessive thirst
• Weight loss
• Fatigue
• Polyphagia or depressed appetite
• Persistent mycotic infection

MM/october 2005

Modes of presentations of T1D�

• Ketosis ± Acidosis
• Abdominal pain
• Nausea, vomiting
• Tachypnea and deep respiration
• “Ketone smell”
• Lethargy, obtundation, coma
• Asymptomatic
• Fortuitous discovery of glycosuria (beware of renal diabetes)

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MM/october 2005

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Type 2 Diabetes Mellitus in Children and Adolescents

T2DM in the Pediatric Population

• T2DM is considered to account for only 2-3% of cases of DM in this population
• The incidence has increased by almost ten fold over the last decade
• Incidence
• <0.5/100,000/yr in1983.
• 0.7-1.2/100,000/yr in 1993.
• 7.2/100,000/yr in 2OO3.

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Risk Factors Associated WITH T2DM

• Obesity

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• Gender and Race

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• Age and Pubertal Status

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• Positive Family History

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Risk Factor 1 {Obesity}

• The most prominent clinical risk for T2 DM children and adolescents is severe obesity�
• The average body mass index (BMI) ranges between 35-39 kg/m² (NR 15-25 kg/m²)�
• 1/3 had a BMI > 40 kg/m² {morbid obesity}

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• 17% had BMI > 45 kg/m².

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Risk Factor 2 {Ethnicity}

• In an individual case, ethnicity is not a useful predictive parameter.
• 2/3 of the adolescents with type 2 diabetes � in an American study are African-American� ��

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Risk Factor 3 {Gender}

• Females appear to be more susceptible to development of T2DM, with an overall female to male ratio of 1.7/1 irrespective of race.

Risk Factor 4 {Age & Puberty}

• The mean age of adolescents with T2DM ranged between 12 to 14 years�
• All patients were in puberty (Tanner stage III or greater)

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• Females present 1 year earlier than males �
• Rare cases of T2DM among kids as young as 5 years have been reported�

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Risk Factor 5 {Positive Family History}

• Elevated levels of C-peptide and proinsulin, both of which are associated with high-risk for T2DM.
• 60% to 80% of patients had a family history of

T2DM in one first degree relative.

• Once a young proband has been identified, other family members should be screened for insulin resistance and/or overt diabetes.

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Clinical Presentation

• 20% of adolescent patients have polyuria, polydipsia, and weight loss
• The remaining present with obesity, dysuria, and enuresis
• 25% of females have vaginal moniliasis
• Hypertension in 20-30% of patients with T2DM
• Acanthosis nigricans is present in 60-90%.

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Acanthosis nigricans

• �

Maturity onset Diabetes of the Young (MODY)

Dr Seeletso Nchingane

Professor Robert Tattersal

• British endocrinologist

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• He first identied MODY in 1974

Introduction - MODY

• Monogenic diabetes of the youth

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• Autosomal dominant
• +ve F/Hx often in successive generations

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• Onset before 25 yrs
• Some have mild fastin hyperglycaemia for yrs
• Some have varying degrees of glucose tolerance for yrs b4 persistant fasting hyperGl
• Mild hyperG may not cause classic diabetes symptoms, hence late Dx
• In most patients, Dx is in childhood or adolescence
• In some, there may be rapid progression to asymptomatic/ symptomatic hyperGl, nessessitating OHA or insulin
• Majority of known MODY gene mutations will develop diabetes, with exception of glucokinase mutations

Characteristics

• Non-ketotic, non-insulin dependent

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• Usually lean

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• Overall incidence of MODY is ~ 1 - 5% of all DM

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• ~2.4% of diabetes incidence in children < 15years

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• Several clinical characteristics distinguish patients with MODY from type 2 DM

Clinical presentation

• Mild asymptomatic hyperglycaemia
• Non-obese
• Positive family history of diabetes
• Some have mild fasting hyperglycaemia for years without symptoms

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• Mostly incidental finding

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DIAGNOSTIC CRITERIA

• Fasting blood glucose level
• Diabetic
• Plasma >7.0 mmol
• Capillary >6.0 mmol
• IGT
• Plasma 6.0-6.9 mmol
• Capillary 5.6-6.0 mmol

• 2 hours after glucose load

(Plasma or capillary BS)

• IGT
• 7.8-11.0
• Diabetic level
• > 11.1 (200 mg)

Diagnosis of Diabetes�ADA Expert Committee

MM/october 2005

Diabetes Care 2004, 27: S5-S10

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

DIABETIC KETOACIDOSIS 1

• Accelerated catabolic state
• Increased glucose production � (via glycogenolysis and gluconeogenesis)
• Impaired peripheral glucose utilization (hyperglycemia and hyperosmolality)
• Increased lipolysis and ketogenesis � (ketonemia and metabolic acidosis)

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Diabetic Ketoacidosis�

• Risk Factors
• As initial presentation:
• Young age: < 5 years
• Low socioeconomic background
• In established T1D
• Higher HbA1c
• Adolescents, in particular females
• Psychiatric disorders
• Longer duration of diabetes

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MM/october 2005

Edge et al. Arch Dis Child 2001; Rewers,A. et al JAMA 2002

Diabetic Ketoacidosis�

• Precipitating factors
• Poor metabolic control and frequently missed insulin injections
• Infections
• Medications

MM/october 2005

Diabetic Ketoacidosis

• Hyperglycemia, blood glucose > 200 mg % (11 mmol/ l) AND
• Metabolic acidosis, venous pH < 7.30 and/or plasma bicarbonate < 15 mEq/l
• Ketonemia and ketonuria
• Kussmaul respiration
• Nausea, vomiting, Dehydration,
• Abdominal pain, Loss of weight
• Acetone smell, Impaired sensorium
• Shock

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MM/october 2005

Diabetes Ketoacidosis & Type 2 Diabetes

• 42% of Afro-American patients presented with ketonuria�
• 25% presented with diabetic ketoacidosis (DKA) traditionally considered the hallmark of type 1 diabetes

GRADING OF DKA

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• Mild ketoacidosis Venous pH < 7.3 or bicarbonate < 15 mmol/L

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• Moderate ketoacidosis Venous pH < 7.2 or bicarbonate < 10 mmol/L

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• Severe ketoacidosis Venous pH < 7.1 or bicarbonate < 5 mmol/L

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Frequency of DKA

At disease onset

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15-70% at onset of diabetes

Inversely correlate with the regional incidence of T1DM

<5 yr of age

Families which do not have ready access to medical care for social or economic reasons

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Children with established diabetes

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Poor metabolic control or previous episodes of DKA

Peripubertal and adolescent girls

Psychiatric disorders

Difficult or unstable family circumstances

Children who omit insulin Children with limited access to medical services

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Management of DKA�

• Perform a clinical evaluation to confirm the diagnosis and determine its cause
• Weigh the patient and measure the height or length to determine surface area

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Assess clinical severity of dehydration

• Usually 5-10%: prolonged capillary refill time
• hyperpnea
• dry mucus membranes
• sunken eyes
• absent tears
• weak pulses
• cool extremities

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Assess clinical severity of dehydration

≥ 10%: weak or impalpable peripheral pulses

• hypotension
• oliguria
• shock

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• Assess level of consciousness with Glasgow Coma Scale (GCS)

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Take Critical Blood Sample

• Laboratory measurement:
• Glucose, E U C, Ca, P, Mg, b-Hydroxybutyr
• Hemoglobin and complete blood count
• Venous pH, pCO2, Osmolality
• HbA1c
• Urinalysis for ketones
• Serum free insulin concentration
• Specimens for culture (blood, urine, throat)
• Electrocardiogram (ECG)

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ABC Supportive measures 1�

• Secure the airway
• Oxygen to patients with severe circulatory impairment or shock
• Cardiac monitor
• Peripheral intravenous (IV) catheter
• Arterial catheter (critically ill patients managed in an intensive care unit

ABC Supportive measures 2�

• Empty the stomach by continuous nasogastric suction to prevent pulmonary aspiration in the unconscious or severely obtunded patient
• Catheterization of the bladder

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�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Goals of therapy

• Correct dehydration
• Correct acidosis and reverse ketosis
• Restore blood glucose to near normal
• Avoid complications of therapy
• Identify and treat any precipitating event?Antibiotics

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Fluids and salt

Patients with DKA have a deficit in ECF volume that usually is in the range 5–10%.

Begin with replacement of fluid before insulin therapy. (FBI)

Initiate treatment with isotonic 0.9% saline:

1st hour: 10–20 ml/kg body weight (Bolus)

Use crystalloid not colloid

And then 2^nd to 24^th hour calculate and give (Deficit +Maintenace) – (Bolus)

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Oral fluids

• Oral fluids should be introduced only when substantial clinical improvement has occurred
• When oral fluid is tolerated, IV fluid should be reduced

Sodium Correction

• The sodium content of the fluid may need to be increased if measured serum sodium is low and does not rise appropriately as the plasma glucose concentration falls
• Corrected sodium =
• measured Na⁺ + 2 x [(glucose – 5.6)/5.6)] mmol/L

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Osmolality Correction

• Calculation of effective osmolality = �[2x(Na⁺ + K⁺) + plasma glucose] mOsm/kg

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Insulin therapy

• DKA is caused by either relative or absolute insulin deficiency
• Begin with 0.1 U/kg/h 1–2 h AFTER starting fluid replacement therapy
• An IV bolus is unnecessary, may increase the risk of cerebral edema and should not be used at the start of therapy
• The dose of insulin should usually remain at 0.1 U/kg/h at least until resolution of DKA

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Potassium replacement 1

• Even with normal or high levels of serum potassium at presentation, there is always a total body deficit of potassium (3-6 mmol/kg).
• 20 mmol/l KCl+20 mmol/l K phosph = 40 mmol/l

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Potassium replacement 2

• Hypokalemic

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• Normal K⁺ concentration

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• Hyperkalemic

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• Start potassium replacement at the time of initial volume expansion and before starting insulin therapy.

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• Start after initial volume expansion and concurrent with starting insulin therapy

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• Defer potassium replacement

therapy until urine output is documented

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Acidosis

• Severe acidosis is reversible by fluid and insulin replacement
• There is no evidence that bicarbonate is either necessary or safe in DKA:
• paradoxical CNS acidosis
• hypokalemia

Acidosis 2�Cautious alkali therapy for:�

• pH < 6.9
• 🢥 decreased cardiac contractility and peripheral vasodilatation
• 🢥 life-threatening hyperkalemia
• If bicarbonate is considered necessary,
• 1–2 mmol/kg over 60 min

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Practically�

• Maintain rate of fluids administration constant and vary rate of insulin administration
• Maintain IV insulin until pH > 7.3, bicarbonate > 16, then switch to SC insulin (maintain IV insulin for at least 30 min after commencing SC)
• Ketones may take longer to clear

MM/october 2005

Practically�

• Use a flow sheet to follow Neurological status, vital signs, in and out
• Blood glucose, chemistry: BUN, Hct, electrolytes, acid base status, ketonuria
• Therapy: insulin, fluids, electrolytes

MM/october 2005

PROTOCOL FOR DKA

Complications of DKA�

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• DKA and its complications are the most common cause of mortality and morbidity in children with T1D
• Initial Manifestation of T1D: 15- 67 % in Europe and USA
• Mortality: 0,15 to 0,31 % (North America and UK)
• Cerebral Edema (60 to 90 % of deaths); other causes: aspiration pneumonia, MOF…do not forget to place a nasogastric tube if vomiting and unconscious

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MM/october 2005

Cerebral Edema�

• Pathophysiology: mechanisms hypothetical
• Risk factors
• Younger children (below 5 years use 0,05 units/kg/h of insulin
• Children with newly diagnosed T1D
• Failure of Na to rise as predicted
• Use of bicarbonate therapy
• A greater degree of acidosis and hypovolemia

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MM/october 2005

Cerebral edema�

• Usually 4 to 12 h after initiation of therapy
• Headache, decreased consciousness, HT, bradycardia, pupil abnormalities, decorticate posturing
• Reduce rate of fluid administration and give mannitol IV 0,25 to 1 g/ kg IV over 20 min.

MM/october 2005

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

SC insulin injections�

• Change to SC insulin just before a mealtime
• First SC injection should be given � 15–30 min (with rapidacting insulin) � 1–2 h (with regular insulin) � before stopping the insulin infusion
• After transitioning to SC insulin, frequent blood glucose monitoring is required to avoid marked hyperglycemia and hypoglycemia

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Daily Treatment�

• Insulin: regimen varies with age, acceptance by patient , stages of diabetes, doctor’s preferences and economical considerations
• Diet: ± 50 % of CHO, ± 30 % of lipids, ± 20 % of proteins of RDC. Day time fractioning varies according to insulin regimen
• Exercise should be regular
• Psychological support

MM/october 2005

Exercise

Diet

Insulin

Aims of Therapy in childhood T1D�

• Provide normal growth, puberty, psychomotor development and well being
• BG target levels:
• Fasting or preprandial: 70 to 130 mg %
• After meals: < 180 mg %
• Night : not below 60 mg %
• Standardized HbA1c < 7,5 %
• Avoid severe or frequent hypoglycemia in particular < 5 years where BG and HbA1c objectives are higher (100-200 mg % and > 7,5 and < 8,5%).

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MM/october 2005

Insulin Types 1

• Insulin can be classified according to duration of action into
• Very short acting types; these have an onset of action within 5 to 15 minutes peak of action within 30-180 mins and duration of action of 3 to 5 Hrs
• aspart,(Novorapid), lispro (Humalog), Glulisine(Apidra).
• Short-acting; starts working within 30 minutes and is active for about 5 to 8 hours
• Regular insulin, Actrapid, Humulin R.

NB For high carbohydrate meals, these analogues are best given 15-30 minutes before the meal

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Insulin Types 2

• Intermediate-acting; starts working in 2 to 4 hours and is active 10 to 18 hours.
•  NPH (Neutral Protamine Hagedon)
• Insulatard
• Humulin N
• Long-acting, such as ultralente insulin – starts working in 4 to 6 hours, and is active well beyond 32 hours.

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Insulin Types 3

• Very Long Acting Insulin
• start working within 1 to 2 hours and continue to be active, without major peaks or dips, for about 24 hours
• Are not mixed with any other insulin in the same syringe.
• Insulin Determir
• Insulin Glargine

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Insulin therapy : Pharmocokinetics�

MM/october 2005

���Natural Artificial

Mixing of Insulin

• This can be
• Manually in the Syringe
• Intermediate + Short acting
• Regular + Protamin based
• Fixed Ratio Combination
• Mixtard = 30%Actrapid + 70% Insulatard
• Novomix = 30%Aspart + 70% Pratamine aspart

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Insulin Regimen

• ‘Fixed regimen’
• Practically simple
• Tailored to the ‘average day’
• Insulin matched with “Diabetes Diet”
• Alter daily dose and split dose on results:
• Cumulative BG’s
• HbA_1c
• Growth
• Symptoms

“Conventional Insulin Regimen”

• 2 injections per day
• Pre-breakfast and Pre-evening meal
• Self-Titrated Insulin
• Fast acting (20-50%)
• Isophane Preparation (80-50%)
• Pre-Mixed Insulin
• 3 injection per day
• Split evening dose
• Rapid Acting Analogue before tea
• Lispro®; Novorapid®

Insulin Formulations and Syringes

• Insulin is available in most countries as U-100. This means it contains 100 units / ml
• In some countries insulin is still available as U-40, which means 40unit/ml
• Insulin syringes are also manufactured as both U-100 and U-40

Insulin Pens

Self Blood Glucose Monitoring�

• Ideally 4 blood glucose measurements per day, but…

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MM/october 2005

Self-management education is the cornerstone of diabetes treatment

And what about urine tests?�

• Still helpful for diagnosis
• To evaluate the presence of ketosis
• Helpful when blood glucose monitoring not available or not accepted
• Not helpful for diagnosing hypoglycemia (renal threshold 180 mg %)

MM/october 2005

�Childhood Diabetes Mellitus��

• Definition
• Epidemiology
• Types and causes
• Aetiology
• Natural History
• Genetics
• Phases
• Presentation modes
• Diabetic Ketoacidosis
• Treatment
• Insulin Regimen
• Metabolic and long term complications

MM/october 2005

Complications�

• Death (in many developing countries)
• Hypoglycemia
• Weight Gain
• Skin Conditions
• Psychological dysfunction
• Growth & Puberty
• Autoimmune diseases
• Microvascular complications
• Retinopathy
• Microalbuminuria
• Neuropathy
• Macrovascular complications

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MM/october 2005

Complications�

• Weight gain and obesity
• Proportional to the drop in HbA1c with improvement of diabetes control
• Particularly problematic in adolescent girls
• May be due to abnormal eating behavior
• Skin: lipoatrophy and lipohypertrophy

MM/october 2005

Complications�

• Growth & Puberty
• Autoimmune diseases
• Thyroid
• TAAB: 20-30 %
• Hypothyroidism: ~3- 5 %
• Thyrotoxicosis
• Coeliac Disease: ~ 3-5 %
• Addison: ~ 1 %

MM/october 2005

Hypoglycemia�

• Most frequent complication of T1D
• Severe prolonged hypoglycemia may cause permanent CNS damage, particularly in young children (< 6 years)
• may be symptomatic or asymptomatic : “Hypoglycemic unawareness”
• Important limiting factor to achieve near-normal hypoglycemia

MM/october 2005

Hypoglycemia: recommendations�

• T1D children should always have an immediate source of sugar
• Children, family and school teachers should receive education on the recognition and treatment of hypoglycemia
• Children should wear some identification or warning of their diabetes
• Glucagon should be readily accessible

MM/october 2005

Other Complications 1

• Limited Joint Mobility (LJM) with Prayer sign

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Other Complications 2

• Mauriac Syndrome

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Mauriac syndrome

• Dwarfism
• Obesity
• Hepatomegaly
• Cushingoid facies
• Elevate transaminases
• Associated with poor control T1DM
• Reversible with good glycaemic control.

Summary

• Diabetes Melitus is a common disorder of glucose metabolism that is increasingly recognised in children and adolescents
• It needs to be identified early and management commenced promptly and continuously for life
• It is associated with complications that could be debilitating