Diabetes Mellitus, Diabetes Insipidus and Diabetic Ketoacidosis in Children
Pediatrics diabetic mellitus
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Transcript of Pediatrics diabetic mellitus
DIABETUS MELLITUS
DIABETES MELLITUS (DM) Is a common, chronic, metabolic syndrome
characterized by hyperglycemia as a cardinal biochemical feature.
The major forms of diabetes are classified according to those caused by deficiency of insulin secretion due to pancreatic β-cell damage (type 1 DM, or T1DM) 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 (type 2 DM, or T2DM).
ETIOLOGIC CLASSIFICATIONS OF DM Type I diabetes (β-cell destruction, usually leading to absolute insulin
deficiency) Immune mediated , Idiopathic
Type 2 diabetes (may range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance)
Other specific types
- Genetic defects of β-cell function (MODY 1-6)
- Genetic Defects in insulin action
-Pancreatitis, Drug-or chemical-induced, Trauma, pancreatectomy
DIABETES MELLITUS
Infections Congenital rubella, coxackie virus Cytomegalovirus Other genetic syndromes associated with
diabetes Down syndrome Klinefelter syndrome Turner syndrome prader will syndrome
DIABETES MELLITUS Gestational diabetes mellitus Neonatal diabetes mellitus Transient—without recurrence Transient—recurrence 7–20 yr later Permanent from onset
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,”
and4.established diabetes associated with acute
and chronic complications and decreased life expectancy.
IMPAIRED GLUCOSE TOLERANCE. The term impaired glucose tolerance (IGT) refers
to a metabolic stage that is intermediate between normal glucose homeostasis and diabetes.
A fasting glucose concentration of 99 mg/dL is the upper limit of “normal.”
This choice is near the level above which acute-phase insulin secretion is lost in response to IV administration of glucose and is associated with a progressively greater risk of the development of microvascular and macrovascular complications.
PATHOGENESIS The autoimmune attack on the pancreatic islets
leads to a gradual and progressive destruction of β cells, with loss of insulin secretion.
It is estimated that, at the onset of clinical diabetes, 80–90% of the pancreatic islets are destroyed.
PATHOGENESIS
Regeneration of new islets has been detected at
onset of T1DM, and it is thought to be
responsible for the honeymoon phase (a
transient decrease in insulin requirement
associated with improved β-cell function).
PATHOPHYSIOLOGY
Insulin is our most important anabolic hormone! Saving , storing and up building of carbohydrate , protein
and fat. Carbohydrate -Insulin stimulates the insulin receptor on
the cell surface Glut 4 , a glucose transporter, is sent to the cell surface of the muscle to pick up glucose by endocytosis. The more insulin the more transporter!!
Glucose is phosphorylated and ready for either storing as glycogen or glycolysis and energy production (ATP)
PATHOPHYSIOLOGY
Fat -Insulin preservs the fat stores (It antagonizes
the adrenaline sensitive lipase in fat tissue)
Protein -Aminoacid uptake in the cells is
stimulated and breakdown of protein is reduced.
PATHOPHYSIOLOGY.
Insulin levels must be lowered to then mobilize
stored energy during the fasted state.
Thus, in normal metabolism, there are regular
swings between the postprandial, high-insulin
anabolic state and the fasted, low-insulin
catabolic state that affect liver, muscle, and
adipose tissue .
PATHOPHYSIOLOGY.
T1DM is a progressive low-insulin catabolic state in which feeding does not reverse but rather exaggerates these catabolic processes.
With moderate insulinopenia, glucose utilization by muscle and fat decreases and postprandial hyperglycemia appears
At even lower insulin levels, the liver produces excessive glucose via glycogenolysis and gluconeogenesis, and fasting hyperglycemia begins.
Postprandial hyperglycemia then fasting hyperglycemia will occur
PATHOPHYSIOLOGY. Hyperglycemia produces an osmotic diuresis
(glycosuria) when the renal threshold is exceeded (180 mg/dL; 10 mmol/L).
The resulting loss of calories and electrolytes, as well as the persistent dehydration, produce a physiologic stress with hypersecretion of stress hormones (epinephrine, cortisol, growth hormone, and glucagon).
These hormones, in turn, contribute to the metabolic decompensation by further impairing insulin secretion (epinephrine),
by antagonizing its action (epinephrine, cortisol, growth hormone), a
by promoting glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis (glucagon, epinephrine, growth hormone, and cortisol)
Impairing insulin secretion , antagonizing insulin
action , decrease glucose utilization , increase
glucosneogenesis and ketogenesis
PATHOPHYSIOLOGY
CLINICAL PRESENTATION
Childhood type 1 diabetes can present in several different ways.
Classic new onset Diabetic ketoacidosis Silent (asymptomatic) incidental discovery
Classic new onset - Hyperglycemia without acidosis is the most common presentation of childhood type 1 diabetes. Symptoms are caused by hyperglycemia and include polyuria, polydipsia, weight loss despite increased appetite initially (polyphagia), and lethargy.
DIABETIC KETOACIDOSIS As an initial presentation or in a known case of
DM when they omit their insulin or when there is infection or stress.
Can be classified as mild,moderate and severe DKA
Normal Mild Moderate Severe
CO 2 meq/l(venous)
20-28 16-20 10-15 <10
PH(venous) 7.35-7.45 7.25-7.35 7.15-7.25 <7.15
Clinical No change Alert but fatigued
Kussmal breathing ,sleepy
comatous
DIABETIC KETOACIDOSIS
When extremely low insulin levels are reached, keto acids accumulate. Keto acids produce abdominal discomfort, nausea, and emesis.
Dehydration accelerates, causing weakness and polyuria persists. As in any hyperosmotic state, the degree of dehydration may be clinically underestimated
Ketoacidosis exacerbates prior symptoms and leads to Kussmaul respirations (deep, heavy, rapid breathing), fruity breath odor (acetone), diminished neurocognitive function, and possible coma.
DIAGNOSIS Fasting plasma glucose ≥ 126 mg/dL (7 mmol/L)
on two occasions Symptoms of hyperglycemia and
a random venous plasma glucose ≥ 200 mg/dL (11.1 mmol/L)
Abnormal oral glucose tolerance test (OGTT) defined as a plasma glucose ≥ 200 mg/dL (11.1 mmol/L) measured two hours after a glucose load of 1.75 g/kg (maximum dose of 75 g)
Most children and adolescents are symptomatic and have plasma glucose concentrations well above ≥ 200 mg/dL (11.1 mmol/L); thus, OGTT is seldom necessary to diagnose type 1 diabetes.
CHALLENGES IN PEDIATRICS DM
There are unique challenges in caring for children and adolescents with diabetes that differentiate pediatric from adult care.
These include the obvious differences in the size of the patients, developmental issues such as the unpredictability of a toddler's dietary intake and activity level, and medical issues such as the increased risk of hypoglycemia and diabetic ketoacidosis.
Because of these considerations, the management of a child with type 1 diabetes must take into account the age and developmental maturity of the child.
GOALS Successful management of children with
diabetes includes the following : Balancing strict glycemic control, which
reduces the risk of long-term sequelae, and avoidance of severe hypoglycemia, which is more likely with stricter control.
In children, targeted glycemic goals define what is thought to be the best balance between these long- and short-term complications.
GOALS Maintaining normal growth, development, and
emotional maturation. Increasing self-independent management as the
child grows is an ongoing goal. Training the patient and family to provide
appropriate daily diabetes care in order to attain glucose control within the range of predetermined goals, and to recognize and treat hypoglycemia.
DKA MANAGEMENT1.Volume expansion 10-20 ml/kg R/L or N/S over 1 hour2.Insulin therapy and K+ replacement - 0.1u /kg/hr continuous insulin mxt -0.5 u/kg/ every 4-6 hourly intermittent insulin mxt -K + 20-40 meq/L of fluid3. Fluid mxt 85 ml/kg + maintenance fluid –bolus/23
hrs(0.45 % N/S and when glucose is < 250 mg/dl change the fluid to 5 % D/W
DKA MXT RISKS Hypoglycemia Cerebral edema Hypokalemia So we need to follow the child with V/S,
frequent glucose and electrolyte measurement to act accordingly.
Bed side mannitol 1gm/kg is important
Treatment Insulin Therapy. 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
Basic education – about the insulin injection , meal planning ,exercise, about symptoms of hypo/hyperglycemia and importance of SMBG and the impact of poor control of DM.
EXERCISE No form of exercise, including competitive
sports, should be forbidden to the diabetic child. But the risk of hypoglycemia is there during or
within hours after exercise so BG measurement is important .
They have to take candy or carbonated juice to take immediately if there are symptoms of hypoglycemia
Onset of action
30-60 minutes
5-15 minutes
1-2 hours
1-3 hours
0.5-1 hours
Peak of action
2-4 hours
1-2 hours
5-7 hours
4-8 hours
dual
Duration of action
6-8 hours
4-5 hours
13-18 hours
13-20 hours
10-16 hours
Insulin
Soluble - Regular
Lispro- Aspart
NPH
Glargine-Detemir
Combinations
Insulin PreparationsKinetics following s.c. injection
T2DM MANAGEMENT
Weight loss and physical exercise are said to
be the main strategies in controlling glucose
level in T2DM patients
Oral hypoglycemic agents like metiformin
can be tried
Insulin if they have ketonuria
Long term complications of DM-Micro vascular
complications( Retinopathy, nephropathy)
-Macro vascular complication-Growth failure and delayed puberty
INJECTION MODELSRepeted injections
Future intelligent pumps with reliable sensors for glucose levels= mechanical pancreas