DR Badi AlEnaziConsultant pediatric endocrinology and

diabetologest

Polyuria causesDMDiabetes inspidusHypokalemiaCerbral salt wasting Psychotic polydepsiaChronic Renal diseaseHypercalcaemia

What investigations needed?GlucoseSerum KSerum caSerum creteninSerum osmolalityUrin osmolalityUrine sp gravityWater deprivation testMRI brain

What Diabetes is NOTDiabetes is NOT “a touch of sugar”

It is a serious chronic disease that can lead to complications such as heart attack, stroke, blindness, amputation, kidney disease, and nerve damage

Diabetes MellitusDiagnosis 2011

Diabetes MellitusFasting Glucose > 125 mg/dl

2 Hour PP Glucose > 200 mg/dl A1C >6.5%

Pre-DiabetesFasting Glucose: 100-125 mg/dl

2 Hour PP Glucose: 140-200 mg/dl A1C: 5.7-6.4% (underestimates DM)*

*

The Worldwide Epidemic:Diabetes Trends

30

135177

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300

370

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1985 1995 2000 2010 2025 2030

Diabetes Mellitus26-28 Million Americans in 2010

Leading US CauseMyocardial Infarction

Kidney FailureAmputations

Blindness

Type 2 DM Type 1 DM

~4,300 New Cases Every Day >1,000,000 New Cases Every Year

5%

95 %

20051990

Prevalence in Saudi Arabia

ObesityObesity

Diabetes

45%15%

7.5% 23%

Diabetes

Type 1 diabetes mellitus

most common form of diabetes mellitus in children and adolescents(90% of cases).

It is an autoimmune disorder characterized by T-cell mediated destruction and progressive loss of pancreatic B-cells leading to eventual insulin deficiency and hyperglycemia.

EpidemiologyThe incidence of Type 1 diabetes mellitus

(T1DM) has been increasing, but shows marked geographical variation. In Europe the highest incidence rates are seen in (Finland, Sweden).

During childhood there are two peaks in presentation, one between ages 5 and 7yrs and before or at the onset of puberty.

seen in the winter months.

Etiology

The cause of T1DM involves both genetic and environmental factors.

Pathophysiology

T1DM is a chronic autoimmune condition. Immune tolerance is broken and antibodies

against specifi c B-cell autoantigens are generated (e.g. anti-islet cell; anti-insulin; anti-GluAD; anti-IA2 antibodies).

PathophysiologyT-cell activation leads to B-cell

inflammation (‘insulitis’) and to subsequent cell loss through apotosis.

The rate of B-cell loss varies (months–years) and the timing and presentation of symptomatic diabetes may depend on factors that

increase insulin requirements (e.g. puberty).

Clinical presentation

The onset of symptoms evolves over a period of weeks. Symptoms are a reflection of insulin deficiency resulting in increased catabolism and hyperglycaemia.

In the majority, first presentation is usually made in the early symptomatic phase with:

weight loss; polyuria/polydipsia;nocturia/nocturnal enuresis.Other less common symptoms include:candida infection (e.g. oral thrush, vulovaginitis)skin infections.

Clinical presentationFailure to recognize these symptoms will

result in delayed or late diagnosis And presentation with DKA

Assessment of new patient

History: duration of symptoms.Family history: of diabetes/other autoimmune

disease.Examination: weight/BMI; signs of DKA

Diagnosis and investigations

The diagnosis is readily established in a symptomatic child with a random blood glucose level >11.1mmol/L. Other investigations:

U&E.Blood pH (to exclude DKA). Diabetes-related autoantibodies: islet cell

antibody (ICA)/anti-insulinantibody (IAA)/anti-GluAD antibody (GluAD)/anti-

IA-2. Other autoimmune disease screen: thyroid

function test/thyroid antibodies; coeliac disease antibody screen.

Type 1 diabetes mellitus: management

All newly diagnosed patients must start insulin therapy as soon as possible.

An intensive programme of education and support is needed for the child and parents. The aims of management of T1DM are:

• education of child and family about diabetes;

• insulin therapy;• nutritional management;• monitoring of glycaemic control;

avoidance and management of hypoglycaemia;

• management of acute illness and avoidance of DKA

• screening for development of associated illness

• screening for diabetes-related microvascular complications

• prevention and treatment of microvascular complications

Education, counselling, and support

An intensive programme of education and counselling is needed in the first few days/weeks to cover the fundamental principles about T1DM andits management.

• Basic pathophyisology of T1DM.• Insulin therapy:• actions of insulin;• SC injection techniques;• dose adjustment principles, including

carbohydrate counting Tchniques.• Home/self blood glucose monitoring.

Education, counselling, and supportAcute complications:• avoidance, symptom recognition, and treatment

of hypoglycaemiaand diabetic ketoacidosis • ‘sick day rules’ during illness to prevent DKA • Diet:• healthy, low-fat;• high complex carbohydrate.• Long-term complications: risk factors and

avoidance.• Psychological issues.

Nutritional management

Diet and insulin regimen need to be matched to optimize glycaemic control.

Instruction on and application of carbohydrate counting techniques

are required. A healthy diet is recommended with a high complex carbohydrate

and relatively low fat content.

Blood glucose monitoring

• Regular daily blood glucose monitoring and testing when blood levels are suspected to be low or high is recommended.

• Home blood glucose monitoring is normally carried out using a portable glucose meter and finger-pricking device.

.

Blood glucose monitoring• Regular testing is required to assist with

insulin dose-adjustment decisions, and to learn and predict how changes in lifestyle, food, and

exercise affect glycaemic control.• A minimal testing frequency of 4 times per

day should be encouraged.• SC continuous glucose monitoring (CGM)

devices are also now available and in certain select situations may offer some advantages

and benefi ts to patients

Insulin type

Insulin regimens

The daily requirement for insulin varies with age:

• at diagnosis, 0.5U/kg/day;• childhood/prepubertal, 0.5–1.0U/kg/day;• puberty, 1.2–2.0U/kg/day;• post-puberty, 0.7–1.2U/kg/day.Insulin is administered SC, usually as a bolus

injection.

A number of patients receive insulin in the form of a continuous SC insulin infusion (CSII) delivered by a pump device.

Insulin regimensInsulin injection sites include the SC tissues

of the upper arm, the anterior and lateral thigh, the abdomen, and buttocks.

The choice of regime is a compromise between achieving optimal therapy

and minimizing psychosocial development. The patient and family must have input into the choice.

Insulin regimens

Two dose regimen The simplest regimen. Two injections per day. Each injection is a mix

of short/rapid-acting insulin plus an intermediate-acting insulin.

Traditionally 2/3 of the total daily dose is given at breakfast and 1/3 given before/at

the evening meal.

Disadvantages• Need to mix insulins.• Peak action of insulin does not correspond with timing of main meals.• Increased frequency of between meal and nocturnal hypoglycaemia.• Between meal snacks required to minimize hypoglycaemia.Note: Less hypoglycaemia with rapid analogue insulin use.

Three-dose regimen Improvement and intensification of the two-dose

regimen:• Basal insulin: once a day intermediate- or long-acting

insulin(traditionally at bedtime).• Fast-acting insulin: At meal times (i.e. 3 per day) and with

betweenmeal snacks.Advantages• Increased flexibility with meal times/exercise planning.• Insulin dose adjustment— carbohydrate (CHO) counting.Disadvantages• Need for more injections.• Need more frequent blood glucose monitoring.

Hypoglycaemia

All children with T1DM will experience an episode of hypoglycaemia.

Symptoms develop when blood glucose <3.5mmol/L. The frequency of hypoglycaemia is higher with more intensive insulin regimens and in young

children. Symptoms and signs include:• feeling of hunger;• sweatiness;• feeling faint/dizzy;• irritability/confusion.• pallor.

Hypoglycaemia

Hypoglycaemia: managementAcute episodes of mild to moderate

symptomatic hypoglycaemia can be managed with oral glucose (glucose tablets or sugary drink). Oral glucose

gels applied to the buccal mucosa can be used in the child who is unwilling or unable to cooperate to eat. Severe hypoglycaemia can be managed in

the home with an intramuscular injection of glucagon 1mg

Macrovascular Microvascular

Stroke

Heart disease and hypertension

Ulcers and amputation

Diabetic eye disease(retinopathy and cataracts)

Renal disease (Kidney)

Neuropathy

Foot problems

Peripheral vascular disease

Diabetes Complications

Type 2 diabetes mellitus

T2DM is a multifactorial and heterogeneous condition in which the balance between insulin sensitivity and insulin secretion is impaired.

is characterized by hyperinsulinaemia; however, there is relative insulin insufficiency to overcome underlying concomitant tissue insulin resistance.

Epidemiology

T2DM is emerging as a significant health problem with increasing incidence in most developing countries.

The increasing frequency of T2DM parallels the upward trend in childhood obesity in

these populations. T2DM now accounts for up to 45% of the new

cases of diabetes diagnosed in childhood in USA

Calorie Difference: 257 calories

590 calories

CHEESEBURGER

20 Years Ago Today

333 calories

Aetiology

T2DM is not an autoimmune disease.

a strong genetic basis, which is thought tobe polygenic.

risk factors for the development of T2DM areas follows.• Obesity.• Family history of T2DM.• Ethnic origin:• Asian;• Polycystic ovarian syndrome.• Small for gestational age (SGA).

Clinical features

Clinical presentation ranges from mild incidental hyperglycaemia to the typical manifestations of insulin deficiency.

Presentation with DKA may occasionally be seen.

acanthosis nigricans.

Diagnosis

Current diagnostic prerequisites for T2DM are:• presence of T2DM risk factors • lack of absolute/persistent insulin defi ciency;• absence of pancreatic autoantibodies.

Management

All patients with T2DM require the same type and degree of educational support and clinical follow-up as for patients with T1DM.

Specific treatment goals should in addition include the following:

• aim to improve insulin sensitivity and insulin secretion;

• manage obesity and its comorbidities via lifestyle changes;

• screening and management of T2DM comorbidities such as hyperlipdaemia and hypertension.

ManagementMild (incidental) T2DM should initially be

managed with lifestyle interventionsaimed at lowering caloric intake (low fat; reduced

CHO diet)and increasing physical activity. Where these

interventions fail, pharmacologicaltherapy is added. In children, the oral insulin

sensitizing agentmetformin is added as a fi rst step; however, if

glycaemic targets remaindiffi cult to achieve insulin therapy should be

included.

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