Diabetes melitus (DM) – is an endocrine-metabolic disease. Absolute or relative insulin insufficiency takes place in pathogenesis of this disease. It causes violations of carbohydrate, protein and

“Diabetes melitus”

Diabetes melitus (DM) – is an endocrine-metabolic disease. Absolute or relative insulin insufficiency takes place in pathogenesis of this disease. It causes violations of carbohydrate, protein and lipid exchange.
Urgency. Nowadays 1 of 10 persons has evident or latent form of DM. By the data of UOHP there is around 120 mln people that have DM. Children’s type of DM can occur in all the age groups and it is 20% of the total amount DM patients.

Etiology:

nAlimentary factor (increased usage of sugar food and products rich of carbohydrates, that are easy to digest);

nHypodynamia;

nStress of sociological and physical character (2 age periods- 6-7 and 10-12 years);

nInfluence of Я-cytotropic viruses (measles, rubella, parotitis, virus of hepatitis B and infectious mononucleosis);

nInfluence of antigens on pancreatic islet apparatus (90% of children at the beginning of disease have auto- antibodies in the blood serum);

nInherited susceptibility (autosomal- recessive type of inheritance).

Pathogenesis:

nIncreased resistance to insulin

nCompensatory increase of insulin secretion

nRelative insulin insufficiency (insulin is used not enough effectively)

nProgression of diabetes

nDecompensation of metabolism

nCompensatory increase of secretion of hormones-antagonists (glucagon, somatostatin, glucocorticoids, somatotropic hormone, catecholamines)

nIncrement of metabolism violations and hemostasis changes

nDisruptive activity of compensatory factors

Chart of pathogenesis by Fisher:

nGenetic susceptibility.

nDamaging influence of various factors of environment on Я-cells of pancreatic islet apparatus.

nActive auto-immune process.

nProgressive reduction of the 1^st phase of insulin secretion.

nPresent DM (damaging of more than 90% of cells).

nTotal destruction of Я-cells.

Pathogenesis of clinical and metabolic changes:

nInsulin deficit;

nInsufficient usage of glucose by insulin- dependent tissues;

nIncrease of glucagon activity;

nIntensification of glucagon disintegration in liver;

nHyperglycemia, glycosuria;

nHypertonic dehydration;

nPolyuria, polydypsia;

nElectrolytes loss;

nPolyphagy;

nViolations of protein exchange, lipolysis;

nKetonemia (acidosis), ketonuria.

Clinical manifestations

Before beginning of the evident clinical manifestations of DM:

-Persistent eczemas;

-Furunculosis;

-Itch of genital organs and other body areas;

-Headache;

-Bleach;

-Hyperhidrosis;

-General weakness, especially after physical load;

-Thirst for sweets.

Clinical manifestations:

Acute beginning, aggressive clinical behavior and severecourse of disease are characterized.

Main symptoms:

-polydipsia (in case of 80% of children with PD, around 6 liters per day, thirst at night);

-polyphagia, distortion of taste;

-polyuria (as result of hyperglycemia), nycturia;

-loosing of the body weight;

From the skin and skeletal system side:

-dryness of skin, panaritium, pyoderma, furunculosis;

-bones osteoporosis;

Clinical manifestations:

Respiratory system:

-inclination to lungs tuberculosis, acute pneumonias;

Cardiovascular system:

-diabetic cardiopathy;

Organs of gastrointestinal tract:

-parodontosis, caries, gingivitis;

-chronic gastritis;

-diabetic enteropathy;

-fatty hepatosis of liver;

Urinary system:

-acute and chronic kidney insufficiency (at 10-30%)

Clinical classification:

By the form:

-insulin- dependent

-insulin-independent

Degrees of severity:

-mild

-moderate

-severe

Phases:

-compensation

-subcompensation

-decompensation

Complications:

-early

-late

Forms of DM

І. Manifestal DM (there is clinical and laboratory signs of DM):

-Mild degree (I level) – there is no complications, compensation is achieved by keeping to a diet and small doses of insulin till 0,5 UA (Unit of Action)/kg/day;

-Moderate degree of difficulty (II level) – daily need in insulin is 0,5-1 UA/kg, stable disease course, there is no hard complications, ketosis is easily eliminated by rise of insulin doses;

- Severe degree (III level) – labile disease course, high hyperglycemia, inclination to ketosis and ketoacidosis, presence of complications.

Forms of DM:

Compensate form:

-glycemia is not higher than 11 mmol/l, sugar fasting 4,4-6,1 mmol/l, after food- 4,4-8,8 mmol/l;

-there is no hypoglycemia;

-there is no ketone bodies in blood;

-there is no acetone in urine;

-glucosuria is not higher than 5 % of sugar value of food (including all carbohydrates and 50% of proteins);

-physical and emotional conditions are not damaged;

-arterial pressure is lower than 130/85 mm of mercury column;

-glycolized hemoglobin is lower than 6,5 %;

-index of body weight is 19-25;

-triglycerides are 1,7 mmol/l;

-cholesterol is lower than 5,2 mmol/l.

Forms of DM

Decompensate form of DM:

-high hyperglycemia and glucosuria;

-ketoacidosis, present complications;

-it needs high doses of insulin.

Forms of DM

ІІ. Classes of statistic risk:

There is no clinical manifestations, but there is conditions and inclination to DM. It is necessary to do glucose tolerant test (in case of relative or absolute risk).

Criteria of absolute risk:

-one of twins is sick;

-both parents are sick;

-mother is sick, father has sick relatives or vice versa.

Forms of DM

Criteria of relative risk:

-obesity;

-diseases of pancreatic gland;

-lasting usage of glucocorticoids;

-periodic hyperglycemia.

ІІІ. Violations of glucose tolerance – latent violations of carbohydrate exchange.

Diagnostics

Objective criteria of disease: hyperglycemia (N= 3,3-5,5 mmol/l) is higher than 8,8 mmol/l + glucosuria. Hyperglycemia fasting is higher than 7 mmol/l at the repeated definition + clinical signs of DM – there is no need in glucose tolerant test (GTT – glucose load is 1,75 g/kg).

Criteria of negative GTT:

-Maximal level of sugar in 30-60min is higher than starting level for not more than 50-80%;

-In 120 min maximal sugar level has to decrease down to starting ones;

-There is no glucosuria ever.

Laboratory diagnostics

Cortisone (50 mg)- and prednisolone- glucose (10 mg) probes. Diabetic results:

-blood sugar in 1 hour after load is 11,1 mmol/l, in 2 hours – 8,3 mmol/l;

-ketone bodies in blood and urine.

Additional criteria at DM diagnosis:

-rise titer of antibodies to antigens of pancreatic islet apparatus;

-increased content of glycolized hemoglobin (N=4-6 % of the total hemoglobin);

-insulin-dependent DM in anamnesis.

Early complications of DM (comae)

nHypoglycemic coma. At children hypoglycemia causes irreversible changes of brain, its effects are prolonged. Often “biochemical” hypoglycemia develops (in case of reduced glucose level in blood there is no clinical manifestations), that is why hypoglycemia is condition when glucose level in blood is lower than 4 mmol/l (at the lowest bound at healthy child- 3,5 mmol/l).

Provocative factors:

-sudden loads;

-missed eating;

-overdose of insulin.

Early complications of DM (comae)

nHypoglycemic coma.

Clinical and diagnostic criteria:

-sudden beginning, rapid course;

-weakness, vertigo, paleness, hyperhydrosis, sense of hunger, irritation, tearfulness, inadequate behavior, later- convulsions, loss of consciousness.

-tone of eyeballs, breathing, body temperature- are not violated, some times –bradycardia, daily diuresis is normal;

-smell of acetone from moth is absent;

-there is no acetonuria, hyperketonemia, exicosis and glucosuria;

-osmolarity of blood serum is 310 mosm/l, рН of blood is 7,38-7,45;

-level of lactic acid is 0,4-1,4 mmol/l.

Early complications of DM (comae)

nHypoglycemic coma.

Classification and therapy.

-mild – is blocked by using of 20 g of rapid-soluble carbohydrates (candy, piece of chocolate, sugar, honey, fruits);

-moderate – needs therapy measures in case of small children, in case of older – it needs outside help;

-severe – needs urgent hospitalization and parenteral introduction of glucagon (for children younger than 5 years - by 0,5 mg, older than 5 years- by 1 mg) or 20 % solution of glucose by 1 mg/kg.

The best method for preventing of hypoglycemia is conversion to plural insulin introduction in comparison with decreased dose in case of its one time introduction.

Early complications of DM (comae)

2. Diabetic ketoacidosis (DKA) or ketoacidotic coma. It occurs at 23% of children sick with DM and 40% of children younger than 4 years. At 1% of cases DKA is complicated by brain edema (that is the main reason of children’s death in case of DM).

DKA is decompensation of DM that causes hyperglycemia, acidosis, ketones presence.

Risk factors of DKA:

- Diabetes that was diagnosed not long ago (especially at newborns);

-emotions, stress;

-infections (viral and bacterial);

-missed injections of insulin;

-at teenagers – not enough dose of insulin, violated schedule of eating, alcohol usage.

Early complications of DM (comae)

2. Diabetic ketoacidosis (DKA). Clinics.

-gradual beginning (during 3-5 days- only weakness, than- emesis, thirst, dryness in mouth cavity, dryness of skin and mucous layers, sleepiness;

-hypotension of muscles, there is no convulsions;

-decreased tone of eyeballs;

-smell of acetone from mouth;

-stomach ache;

-breathing by the Cussmaul type;

-decreased arterial pressure, tachycardia;

-hypothermia;

-dehydration, expressed exicosis;

-polyuria- oliguria- anuria.

Early complications of DM (comae)

2. Diabetic ketoacidosis (DKA).

Laboratory criteria:

-hyperglycemia is 20-30 mmol/l, glucosuria is higher than 2 %;

-level of lactic acid is 0,4-1,4 mmol/l;

-level of ketone bodies in blood is 3,3-17 mkmol/l (N=1,7);

-level of ketone bodies in urine is ++++;

-osmolarity of blood serum is not higher than 320 mosm/l;

-decreased level of blood рН down to 6,8 (N=7,38-7,45);

-increase of level of hemoglobin and hematocrit;

-decreased level of potasium of blood serum (N=4.0-5.5 mmol/l) and erythrocytes (N=80-100 mmol/l);

-decreased level of sodium of blood serum (N=135-145 mmol/l) and erythrocytes (N=12-25 mmol/l);

-increased level of urea of blood (N=4,2-7,5 mmol/l).

Early complications of DM (comae)

2. Diabetic ketoacedosis (DKA).

Stages of DKA depending on CNS damaging:

1 stage (starting coma) – sleepiness, flaccidity, headache, impairment of consciousness in 20% of cases, loss of consciousness- at 10% of cases.

2 stage (general coma) – flaccidity, hypotension, suppression of reflexes are increased, consciousness by the sopor type.

3 stage (terminal coma) – consciousness absence during 6-8 hours.

Early complications of DM (comae)

2. Diabetic ketoacidosis (DKA).

Main principles of therapy:

1. Provision and supporting of breathing;

-therapy of shock - 4,5 % albumin - 10 ml/kg, very rapid injection;

2. Renewal of loss liquid (V of liquid - 10 % of body weight; content- physiological saline: solution of Ringer-Lock: 5 % solution of glucose as 1:1:1). Deficit of liquid is renewed slowly and evenly during 24 hours. If blood glucose decreases down to 12 mmol/l – 0,45% physiological saline (5% dextrose) 2 mmol/kg.

Early complications of DM (comae)

2. Diabetic ketoacidosis (DKA).

Main principles of therapy:

3. Insulin- therapy:

-uninterrupted intravenously injection of small dose of insulin 0,1 UA/kg/hour;

-right after beginning of insulin- therapy KCl or panangin are added;

-Sodium bicarbonate is prescribed only if рН of blood is lower than 6,9 or after absence of improvement of circulation after introduction of 4% albumin – 5ml/kg;

4. Preventing of complications (hypokalemia, brain edema).

Early complications of DM (comae)

3. Hyperosmolar coma. Main reason is insulin insufficiency. It occurs on the background of rapid dehydration (emesis, diarrhea, hemorrhage, over urination), usage of diuretics and glucocorticoids.

Clinical and diagnostic criteria:

-slow beginning during 10-12 days;

-glucose level in blood is 50-100 mmol/l, glucosuria;

-there is no ketone bodies in blood and urine;

-lactic acid level in blood is 0,4- 1,4 mmol/l;

-osmolarity of blood serum increases up to 500 mosm/l;

-рН of blood is 7,38-7,45;

-symptoms of dehydration, expressed exicosis;

Early complications of DM (comae)

3. Hyperosmolar coma.

Clinical and diagnostic criteria:

-weakness, flaccidity, often convulsions;

-frequent, surface breath;

-Рs is frequent, arterial pressure is normal or collapse;

-dry skin;

-expressed neurologic symptoms (pathologic reflex of Babinskiy, nystagmus, hypertone, absence of tendinous reflex);

-prolonged polyuria, then- oliguria;

-lethality is 50 %.

Early complications of DM (comae)

4. Hyperlactatacidotic coma (lactic acid coma). It is the main reason of accumulation of lactic acid in blood. Often it occurs at children in case of DM combination with VVS, pneumonia, difficult anemia.

Clinical and diagnostic criteria:

-hyperglycemia is not higher than 30 mmol/l, glucosuria;

-there is no ketonemia and ketonuria;

-often there is oliguria and anuria;

-level of lactic acid in blood is higher than 1,4 mmol/l;

-osmolarity of blood serum is 310 mosm/l;

-рН of blood 7,2-6,8.

Early complications of DM (comae)

4. Hyperlactatacidotic coma.

Clinical and diagnostic criteria:

-often it is on the background of hypoxia;

-moderately expressed exicosis, expressed acidosis;

-nausea, emesis;

-ache behind breast bone, muscles ache;

-Kussmaul’s breathing;

-Ps is frequent, arterial pressure is normal or decreased;

-skin is dry.

Late complications of DM (angiopathies)

І. Diabetic retinopathy is the main reason of blindness.

3 stages:

-not proliferative;

-simple;

-proliferative.

Patients with DM often have cataract.

ІІ. Diabetic nephropathy is the main reason of death and disability of patients with DM. It is necessary to detect the early criteria of kidney injury – microalbuminuria (prenephrotic stage). If child with DM has microalbuminuria during 6-12 month – blockers of APF are prescribed, even if arterial pressure is normal.

Late complications of DM (angiopathies)

ІІІ. Neuropathies.

nCentral (increased irritability or depression, decrease of memory, violations of sleep).

nPeripheral (injury of lower limbs, ache of shins and feet, paresthesia, convulsions).

Syndrome of Moriak – retardation of growth, sexual development, hepatomegalia, accumulation of fat at face, chest, at the area of VII cervix vertebra, depression, osteoporosis, ascites.

Therapy of DM

3 Principles:

І. Insulin-therapy. Main method of PD treatment.

1.Individual schedule. The following criteria is taken in account:

-age;

-DM duration;

-regime of child at school and at home;

-level of education;

-ability to change the insulin dose;

-physical activity;

-social and economic conditions, support of family.

Principles of treatment of DM

І. Insulin therapy.

2. To take in account the influence of factors on the absorption and activity duration of various preparations of insulin.

They include:

-state and size of subcutaneous adiposities layer;

-place of insulin injection (in case of injection in the area of stomach – it acts faster and less continuous than injection in the area of hip);

-deepness of injection;

-insulin dose.

Principles of therapy of DM

І. Insulin therapy.

By the duration of action insulin preparations are divided into:

-preparations of short action (simple insulin, SU- insulin, actrapid, insulrap)- effect appears in 30 min, maximal action is 2-4 hours.

-medium duration (monotard, protofan, insulong)- effect appears in 60 min, action- 8-10 hours.

-prolonged action (ultratard, ultralong)- effect appears in 3 hours, maximal action – 12-24 hours.

Principles of therapy of DM

І. Insulin therapy.

Main demands to insulin therapy:

-selection of insulin dose is holding in hospital;

-in case of early diagnostics – insulin dose is minimal (at the 1^st year of disease – 0,3-0,5 UA/kg/day, later – 0,7- 0,8 UA/kg/day);

-proportion of daily and night dose is 2:1;

-in case of decompensation and for intravenously injection insulin of short action is used;

-in case of children only highly purified insulin preparations are used;

-preference is given to basic- bolus method.

Principles of therapy of DM

Assessment of effectiveness of insulin therapy:

-permanent support of compensation state;

-assessment of glycemic and glucosuric profile (it is necessary to achieve normoglycemia fasting).

In case of children of the 1^st year of life on the background of insulin therapy glucosuria till 1% and level of blood glucose 8-10 mmol/l are acceptable.

Principles of therapy of DM

ІІ. Diet therapy.

Main demands:

-calorie level is detected efficiently (energetic demand of the 1 year old child is 1000-1100 ccal, every year + 100 ccal), caloric value at PD is physiologic;

-50 % of calorie level is supported by carbohydrates (source is vegetables, fruits, berries, corn, fabaceous);

-daily control of eating (taking food not less than 5 times a day, every food taking at the same time);

-preference is given to products that include cellulose;

-exclusion from the ration of semolina, bananas, grape, ebony, sugar and products with sugar, products with white flour, high-heat fat;

-proportion of proteins: fat: carbohydrates is 1:0,8:3, norm is 1:1:4.

ІІІ. Adequate physical load.

DM prophylaxis

nPrimary:

-rational balanced food;

-control of body weight;

-strife against hypodynamia;

-proved usage of “diabetogenic” medical preparations (glucocorticoides, hypotensive preparations);

-children that have absolute or related risk criteria of PD development need necessary GTT 1 time a year.

2.Secondary:

-early definition of disease;

-support of compensation;

-preventing of complications.

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