Treatment DM and DKA and complications s

Diabetes mellitus (DM) is a common, chronic,
metabolic disease characterized by hyperglycemia as
A cardinal biochemical feature.
The major forms of diabetes are:-
1-Type 1 diabetes mellitus (T1DM) results from
deficiency of insulin secretion because of pancreatic β-
cell damage, most common childhood and
adolescence.
2-Type 2 diabetes mellitus (T2DM) is a
consequence of insulin resistance occurring at the

level of skeletal muscle, liver, and adipose tissue,
with various degrees of β-cell impairment.

TYPE 1 DIABETES MELLITUS
Called insulin-dependent diabetes
mellitus (IDDM) or juvenile diabetes,
T1DM is T1DM is characterized by low or
absent levels of endogenously produced
insulin and by dependence on exogenous
insulin to prevent development of
ketoacidosis, an acute life-threatening
complication of T1DM. The onset occurs
predominantly in childhood, with a median
age of 7-15 yr, but it may present at any age.

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,”
(4) established diabetes during which there
may occur acute and/or chronic complications
and decreased life expectancy(Established
disease and Development of complications).
.

CLINICAL MANIFESTATIONS
The classic clinical manifestations of new
onset diabetes in children reflect the
hyperglycemic and catabolic physiologic state
and include polyuria, polydipsia, polyphagia,
and weight loss. Other common symptoms
include fatigue, weakness, and a general
feeling of malaise. Patients presenting with
more advanced disease will exhibit signs of
DKA including dehydration, nausea,
vomiting, lethargy, altered mental status,

and in extreme cases, coma. If the diagnosis is
not recognized, the progression of symptoms
follows a predictable course from early
intermittent polyuria, to sustained polyuria
and weight loss, followed by development of
DKA. In most cases, this initial progression
occurs over a period of weeks rather than
months. Approximately 20–40% of children
with new-onset diabetes progress to DKA
before diagnosis.

Female patients may develop vulvovaginal
candidiasis from the chronic glycosuria.
Eventually, daily losses of water and glucose
may be as high as 5 L and 250 g, respectively,
representing 1,000 calories, or 50%, of the
average daily caloric intake. These losses
trigger compensatory polydipsia and
polyphagia; however progressive dehydration
and weight loss will inevitably ensue unless
treatment is initiated.

Diagnostic Criteria for Diabetes
Mellitus
Fasting (at least 8 hr) plasma glucose ≥ 126 mg/dL
(7.0 mmol/L) Or
2 hr plasma glucose during OGTT ≥ 200 mg/dL
(11.1 mmol/L) Or
Hemoglobin A1c ≥ 6.5% (48 mmol/mol) Or
Symptoms* of diabetes mellitus plus random or
casual plasma glucose ≥ 200 mg/dL (11.1 mmol/L)
*(Symptoms include polyuria, polydipsia, and
unexplained weight loss with glucosuria and
ketonuria).

Glycosylated Hemoglobin (HbA1c)
A baseline hemoglobin A1c (HbA1c) will be
confirmatory and allows an estimate of the
duration of hyperglycemia and provides an
initial value by which to compare the
effectiveness of subsequent therapy. Falsely
low HbA1c levels are noted in hemolytic
anemias, pure red cell aplasia, blood
transfusions, and anemias associated with
hemorrhage, cirrhosis, myelodysplasias, or
renal disease treated with erythropoietin.

Baseline HbA1c may be higher in African
Americans than whites.
In non diabetic individuals, the HbA1c
fraction is usually less than 6%;
In diabetics, values of 6-7.9% represent
good metabolic control, values of 8.0-9.9%,
fair control, and values of 10% or higher, poor
control.

Differential diagnosis
1-UTI, compulsive water drinking diabetes
insipidus (for polyuria).
2-Pneumonia, Acute abdomen (DKA).
3-Meningitis(diabetic coma).
4-Salicylate poisoning( acidosis).
5-Hyperthyroidism…the polyuria polydipsia
are result from hyper dynamic state with
increased blood flow to the kidney.

Management
1-Insulin replacement.
2-Education .
3-Monitoring and follow up.
4-psychological support.
5-Management of complication.

Insulin THERAPY
Insulin therapy is initiated at the time of diagnosis for
all patients with T1DM.
Excellent diabetes control involves many goals:
1-to maintain blood glucose and HbA1c levels as
close to normal without causing hypoglycemia,
2-to eliminate polyuria and nocturia,
3-to prevent ketoacidosis,
4-to permit normal growth and development and
avoid development of diabetes related complications

Insulin regimen
Conventional insulin therapy: consist of
rapid or short acting insulin mixed with an
intermediate acting insulin preparation given
twice a day before breakfast and before
dinner...
Morning dose consist of approximately tow-
third intermediate acting insulin and one
third short or rapid acting preparations.
Pre dinner dose is usually half intermediate
acting and half short or rapid acting type.

Basal-bolus regimens can be accomplished with
multiple daily injections (MDIs), where a slow-onset,
long-duration background insulin is given once or
twice daily for between-meal glucose control (basal)
and a rapid-onset insulin is given with meals to
provide carbohydrate coverage and correct
hyperglycemia. Alternatively, an insulin pump can
be used, where a rapid-onset insulin is used to
provide both basal (via continuous infusion) and
bolus (at mealtimes and as needed for
hyperglycemia) coverage.

The doses of short-acting insulin include 2
components: carbohydrate ratio (typically
expressed as 1 unit of insulin for a set number
of grams of carbohydrates) and insulin
sensitivity factor (ISF, also referred to as
“correction factor,” and typically expressed as
1 unit of insulin will decrease blood sugar by a
set number of mg/ dL).

Insulin Pump Therapy Continuous
subcutaneous insulin infusion (CSII) via battery-
powered pumps provides a closer approximation of
normal plasma insulin profiles and increased
flexibility regarding timing of meals and snacks
comparedwith conventional insulin injection
regimens. Insulin pump models can be programmed
with a patient’s personal insulin dose algorithms,
including the insulin to carbohydrate ratio and the
ISF (also called the correction factor)

for pre meal glucose levels. At mealtimes, the
patient enters the blood glucose level (or it is
automatically transmitted from a linked glucometer)
and the carbohydrate content of the meal, and the
pump computer will calculate the proper insulin
bolus dose. The degree of glycemic control is mainly
dependent on how closely patients adhere to the
principles of diabetes self-care, regardless of the
type of intensive insulin regimen. One benefit of
pump therapy may be a reduction in severe
hypoglycemia and associated seizures.

Education the family
1-Instruct the group about insulin
administration (all family members),time
dose , site of injection, Storage of insulin.
2-Educate the family about the symptoms of
hypoglycemia. The child may show pallor,
sweating, hunger, tremor, and tachycardia .
As glucose levels decline further, cerebral
glucopenia occurs with drowsiness,
personality changes, mental confusion.
3-Adjustment of the dose according to blood
glucose level, illnesses, exercise.

Monitoring
Self-monitoring of blood glucose (SMBG) is
an essential component of managing diabetes.
Monitoring often also needs to include
insulin dose, unusual physical activity, dietary
changes, hypoglycemia, intercurrent illness…
Ideally, the blood glucose concentration
should range from approximately 80 mg/dL
in the fasting state to 140 mg/dL after meals.
In practice, however, a range of 60-220
mg/dL is acceptable.

TYPE 2 DIABETES MELLITUS
known as adult-onset diabetes mellitus
or non– insulin dependent diabetes
mellitus, T2DM develops as a result of
insulin resistance and progressive non-
autoimmune β-cell failure. Pediatric T2DM
may account for up to 80% of the new cases of
diabetes in high-risk populations such as
obese adolescents of African or Hispanic
population ancestry .

It is now apparent that childhood onset T2DM
differs from adult disease in that it is
associated with a more rapid decline in β-cell
function and the earlier development of
T2DM-related complications.

The presentation of T2DM is typically more
insidious than that with T1DM. In contrast to
patients with T1DM who are usually ill at the
time of diagnosis and whose presentation
rarely spans more than a few weeks, children
with T2DM often seek medical care because of
excessive weight gain and fatigue as a result of
insulin resistance and/or the incidental
finding of glycosuria during routine physical
examination.

A history of polyuria and polydipsia is not
always a cardinal clinical feature in these
patients. Acanthosis nigricans (dark
pigmentation of skin creases in the nape of
the neck especially), a sign of insulin
resistance, is present in the majority of
patients with T2DM and is accompanied by a
relative hyperinsulinemia at the time of the
diagnosis.

TREATMENT
Lifestyle modification (diet and exercise)
is an essential part of the treatment regimen.
Adding insulin when hypoglycemic oral
agent failure occurs.
Oral hypoglycemic agents be introduced
at the time of diagnosis.
Patients who present with DKA or with
markedly elevated HbA1c (9.0%) will
require treatment with insulin using protocols
similar to those used for treating T1DM.

Once blood glucose levels are under control,
most cases can be managed with oral
hypoglycemic agents and lifestyle
interventions, but some patients will continue
to require insulin therapy. The most commonly
used and the only FDA-approved oral agent
for the treatment of T2DM in children and
adolescents is metformin.

Renal function must be assessed before starting
metformin as impaired renal function has been
associated with potentially fatal lactic acidosis.
Significant hepatic dysfunction is also a
contraindication to metformin use, although mild
elevations in liver enzymes may not be an absolute
contraindication. The usual starting dose is 500 mg
once daily, with dinner to minimize the potential for
side effects.


This may be increased to a maximum dose of
2,000 mg/day. Abdominal symptoms are common
early in the course of treatment, but in most cases
they will resolve with time. Other agents such as
thiazolidinediones, sulfonylureas, acarbose,
pramlintide, incretin mimetics, and sodium-glucose
transport protein inhibitors are being used routinely
in adults but are not used as commonly in
pediatrics.

Diabetic Ketoacidosis
Diabetic Ketoacidosis ,Severe insulinopenia
(or lack of effective insulin action) results in a
physiologic cascade of events in 3 general
pathways:
1. Excessive glucose production coupled with
reduced glucose utilization raises serum
glucose. This produces an osmotic diuresis,
with loss of fluid and electrolytes,
dehydration, and activation of the renin–
angiotensin–aldosterone axis with accelerated
potassium loss.

When glucose elevation and dehydration are
severe and persist for several hours, the risk
of cerebral edema increases.
2. Increased catabolic processes result in
cellular losses of sodium, potassium, and
phosphate.
3. Increased release of free fatty acids from
peripheral fat stores supplies substrate for
hepatic ketoacid production. When ketoacids
accumulate, buffer systems are depleted, and
a metabolic acidosis ensues.

Therapy must address both the initiating
event in this cascade (insulinopenia) and the
subsequent physiologic disruptions. Reversal
of DKA is associated with inherent risks that
include hypoglycemia, hypokalemia, and
cerebral edema. Any protocol must be used
with caution and close monitoring of the
patient.

Treatment DM and DKA and complications s

Treatment DM and DKA and complications s

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