DM Part 2

TREATMENT
• Therapy depends on the degree of insulinopenia at presentation and
weather it is new onset DM or previously diagnosed.
• Most children with new diabetes (60–80%) have mild to moderate
symptoms, have minimal dehydration with no history of emesis, and
have not progressed to ketoacidosis. ( ie: classical presentation or non
ketotic onset)
• Once DKA has resolved in the newly diagnosed child, therapy is
transitioned to that described for children with non ketotic onset.
• ➢ Children with previously diagnosed diabetes who develop DKA are
usually transitioned to their previous insulin regimen.
• New-Onset Diabetes Without Ketoacidosis
• Excellent diabetes control involves many goals:
1. to maintain a balance between tight glucose control and avoiding
hypoglycemia
2. to eliminate polyuria and nocturia
3. to prevent ketoacidosis
4. to permit normal growth and development with minimal effect on
lifestyle.
Insulin Therapy
• Insulin Therapy New recommendation regarding starting dose of
insulin ( unit /kg/ day) as in the table below:
Notes
• The optimal insulin dose can only be determined empirically, with
frequent self-monitored blood glucose levels and insulin adjustment
by the diabetes team.
• Residual β-cell function usually fades within a few months and is
reflected as a steady increase in insulin requirements.
Types of insulin and their regimens used are
• Actrapid (soluble) , monotard (lente), & mixtard ( 30/70)
Two doses regimen
• Actrapid 1/3 and monotard 2/3 or
• Mixtard only with 2/3 of the daily dose in the morning and 1/3 in the
evening, ( sometimes we personalize the dose and the % of the
combination).
• However, such a schedule would provide poor coverage for lunch and
early morning, and would increase the risk of hypoglycemia at
midmorning and early night.
Two doses regimen
Basal bolus regimen
• Insulin analogs (Lispro (L) and aspart) which are absorbed much
quicker because they do not form hexamers.
• Their action started within 10 minutes with duration of action of 2
hours without peak.
• The long-acting analog glargine (G) creates a much flatter 24-hr
profile, making it easier to predict the combined effect of a rapid
bolus (L or A) on top of the basal insulin, producing a more
physiologic pattern of insulin effect.
Notes
• The basal insulin glargine should be 25–30% of the total dose in
toddlers and 40–50% in older children.
• The remaining portion of the total daily dose is divided evenly as
bolus injections for the 3 meals
• Postprandial glucose elevations are better controlled, and between-
meal and night time hypoglycemia are reduced.
• Frequent blood glucose monitoring and insulin adjustment are
necessary in the 1st weeks as the child returns to routine activities
and adapts to a new nutritional schedule, and as the total daily
insulin requirements are determined.
• Insulin Pump Therapy : increased use now a day and it needs daily
calibration and determination of the insulin dose according to the
diet and exersice…….etc
• Inhaled Insulin: Pre prandial inhaled insulin is being evaluated in
adults with T1DM and T2DM (no more use because of pulmonary
fibrosis)
• Pre-meal oral insulin (Oralin) has been evaluated in comparison with
oral hypoglycemic agents, mostly in patients with T2DM. The clinical
data appear promising, but further evaluation of efficacy in T1DM is
needed
Manegmant of diabetic Ketoacidosis
• Reversal of DKA is associated with inherent risks that include
hypoglycemia, hypokalemia, and cerebral edema. so any protocol
must be used with caution and close monitoring of the patient
• Hyperglycemia and Dehydration: Insulin (0.1 unit/ kg/ hour) IV or IM
must be given at the beginning of therapy to accelerate movement of
glucose into cells, to stop hepatic glucose production, and to halt the
movement of fatty acids from the periphery to the liver. Rehydration
also lowers glucose levels by improving renal perfusion and enhancing
renal excretion.
Hyperglycemia and Dehydration
• The combination of these therapies usually causes a rapid initial
decline in serum glucose levels. Once glucose goes below 180 mg/dL
(10 mmol/L), the osmotic diuresis stops and rehydration accelerates
without further increase in the infusion rate.
• Repair of hyperglycemia occurs well before correction of acidosis.
Therefore, insulin is still needed to control fatty acid release after
normal glucose levels are reached.
Hyperglycemia and Dehydration
• To continue the insulin infusion without causing hypoglycemia,
glucose must be added to the infusion, usually as a 5% solution.
Glucose should be added when the serum glucose has decreased to
about 250 mg/dL (14 mmol/L) so that there is sufficient time to
adjust the infusion before the serum glucose falls further.
Hyperglycemia and Dehydration
• The insulin infusion can also be lowered from the initial maximal rate
once hyperglycemia has resolved.
• During repair of fluid deficits we must take in consideration the
potential risk of cerebral edema. All fluid intake and output should be
closely monitored.
• Limited ice chips may be given as a minimal oral intake.
Potassium
• Although patients with DKA have a total body potassium deficit, the
initial serum level is often normal or elevated.
• This is due to the movement of potassium from the intracellular
space to the serum, both as part of the ketoacid buffering process
and as part of the catabolic shift. Potassium can be added to the IV
fluid infusion after ensuring urine output in a dose ranging from 20 –
40 meq / L and sometimes may reach 60 meq / L. Mildly elevated
creatinine or BUN is not a reason to withhold potassium therapy if
good urinary output is present.
Bicarbonate therapy for ketoacidosis
• Low insulin infusion rates (0.02–0.05 units/kg/h) are usually sufficient
to stop peripheral release of fatty acids, thereby eliminate the
production of ketone bodies
• Bicarbonate buffers, regenerated by the distal renal tubule and by
metabolism of ketone bodies, and their excretion in the urine steadily
repair the acidosis once keto acid production is controlled.
Bicarbonate therapy for ketoacidosis
• Bicarbonate therapy is rarely necessary and may even increase the
risk of hypokalemia and cerebral edema. (only indicated in case of
sever acidosis , ie :when the blood PH < 7.1) Persistent acidosis may
indicate inadequate insulin or fluid therapy, infection, or rarely lactic
acidosis.
• Urine ketones may be positive long after ketoacidosis has resolved ,
Therefore, persistent ketonuria may not accurately reflect the
degree of clinical improvement and should not be relied upon as an
indicator of therapeutic failure.
Manegmant of cerebral edema
• For all patient with DKA , frequent neurologic checks for any signs of
increasing intracranial pressure, such as a change of consciousness,
depressed respiration, worsening headache, bradycardia, apnea,
pupillary changes, papilledema, posturing, and seizures.
• Mannitol 10% (10gm /100ml) must be readily available for use at the
earliest sign of cerebral edema.
•All patients with DKA should be
checked for initiating events in
order to avoid them to prevent the
recurrence of DK
Management of DKA (summary)
1. Admission to the emergency unit.
2. ABC if the patient is comatosed and O2 to be delivered via mask.
3. IV LINE and Aspiration of blood for RBS, B.urea, S.Cr, S.K, S.Na, S.Cl,
CBP, B.C/S ,ASTRUP , Urine for ketone, sugar, pus cell.
Management of DKA (summary)
• 4. Calculation of the deficit and maintenance of the fluids ; to be
replaced over 36- 48 hours (hyperosmotic dehydration) Oral fluid is
stopped and only sucking of chips of ice is allowed.
Management of DKA (summary)
• 5. IV fluid (0.9%N/S or RL bolus 10 - 20ml / kg /1st hour) and then
rate of fluid replacement from the 2nd hour till resolution of DKA
• Calculated according to the following formula : ( 85× Bwt +
maintenance – bolus / 23 hours= rate / hour ).
• Change the type of the fluid from N/S to 5% GW or G/S (1/3,1/5)
when RBS is less than 250 mg/dl . WHY?
Management of DKA (summary)
• 6 KCl: the patient is hypokalemic even if S.K was normal .WHY? 20 - 40
meq/L (1 ml = 2 meq) and sometimes increased to 60 meq/L .
• 7. INSULIN : either IV continuous infusion via a separate IV line
started at time zero OR interrupted IM or IV dose started after one
hour (the dose in both ways is 0.1 unit /kg/h) Changed to SC insulin
and start oral fluid when there are no emesis, or acidosis with
normal electrolytes. HOW?
Management of DKA (summary)
• 8. Sod. Bicarbonate : only used in sever acidosis (PH less than 7.1) in a
dose of 20-40 meq ( 1 ml = 1 meq) with the fluid. WHY?
• 9. Mannitol :10% if signs of cerebral oedema appear in a dose of 1 gm
/ kg IV infusion.
• 10. Antibiotic : if infection is present.
• 11. checking for the initiating events should be done and treated &
avoid to be repeated
Preperation of insulin infusion
• Put 50 unit of soluble (actrapid) insulin in one pint (500 cc) NS = 0.1
u/cc & use EVAC to control the rate of infusion
• OR use micro-drip (burette) & put 10 unit of soluble insulin for every
100 cc NS.
• In either ways you must flush 1cc/ Kg rapidly to saturate the insulin
receptors & then the rate will be: 1CC /Kg /hour = 60 micro drops /kg
/60 min = one micro drop /kg/min. The rate should be reduced to 1/2
if RBS is below 150 mg/dl
EXTRA SLIDE
• IV infusion sets come in different types, with different drop factors.
• A micro-drip set, which is often used in pediatric patients because it
delivers fluid more slowly and precisely, has a drop factor of 60
• Meaning 1cc of fluid is equivalent to 60 micro drops.
• So when we say 60 micro drops/kg/60 minutes, we're essentially
saying the same thing as 1cc/kg/hour, but in a different unit of
measurement.
• 60 micro drops /kg /60 min = one micro drop /kg/min.
NEVER FORGET THE FLOW SHEET FOR
DIABETIC KETOACIDOSIS
• (name, age, date, time, BWt & SA, PR, BP,PH, RBS , S.electrolyte, Fluid
input, output, insulin dose, signs of cerebral oedema, and notes)
Treatment of T1DM is not only the use of
insulin but it include other important issues
Basic Education: therapy consists not only of initiation and adjustment
of insulin dose but also of education of the patient and family.
In the acute phase, the family must learn the “basics,” which includes:

▪ monitoring the child's blood glucose and urine ketones,

▪ preparing and injecting the correct insulin dose subcutaneously at the
proper time,
▪ recognizing and treating low blood glucose reactions, and
▪ having a basic meal plan
Note
• Most families are trying to adjust psychologically to the new diagnosis
of diabetes in their child and thus have a limited ability to retain new
information. Written materials covering these basic topics help the
family during the 1st few days.
Nutritional Management
• Nutrition plays an essential role in the management of patients with
T1DM. This is of critical importance during childhood and
adolescence, when appropriate dietary intake is required to meet the
needs for energy, growth, and pubertal development.
• The caloric mixture should comprise approximately:
55% carbohydrate, 30% fat, and 15% protein.
Some mindless notes
• Approximately 70% of the carbohydrate content should be derived
from complex carbohydrates such as starch; intake of sucrose and
highly refined sugars should be limited.
• Carbohydrate counting has become a mainstay in the nutrition
education and management of patients with DM. Each carbohydrate
exchange unit ( need one unit of insulin) is variable and must be
calculated for each patient but roughly it is about 15 g of CHO
Other mindless notes
• Patients and their families are provided with information regarding
the carbohydrate contents of different foods and food label reading.
• The total daily caloric intake is divided to provide 20% at breakfast,
20% at lunch, and 30% at dinner, leaving 10% for each of the
midmorning, midafternoon, and evening snacks, if they are desired
• Emphasis should be placed on regularity of food intake and on
constancy of carbohydrate intake.
Monitoring
• Success in the daily management of the diabetic child can be
measured by the ability of the family, and subsequently the child, in
assuming responsibility for daily “diabetic care.”
• Monitoring often include : insulin dose, unusual physical activity,
dietary changes, hypoglycemia, intercurrent illness, and other items
that may influence the blood glucose
Monitoring
• Self-monitoring of blood glucose (SMBG) is an essential component of
managing diabetes.
• Accu check devices to measure the B. glucose within one minute.
Parents and patients should be taught to use these devices and
measure blood glucose at least 4 times daily—before breakfast,
lunch, and supper and at bedtime
• The records the results and other notes in special notebook to be
reviewed with doctor during follow up visit. (Ideally, the blood
glucose concentration should range from approximately 80 mg/dL in
the fasting state to 140 mg/dL after
HbA1C
• A reliable index of long-term glycemic control is provided by
measurement of glycosylated hemoglobin.
• HbA1C represents the fraction of hemoglobin to which glucose has
been nonenzymatically attached in the bloodstream.
• HbA1C measurement reflects the average blood glucose
concentration from the preceding 2–3 mo.
HbA1C
• It is recommended that HbA1C measurements be obtained 3 to 4
times per year to obtain a profile of long-term glycemic control.
the HbA1C fraction: in nondiabetic individuals, is usually:
• less than 6%. in diabetics
• 6–7.9% represent good metabolic control
• 8.0–9.9%, fair control
• 10.0% or higher, poor control.
Exercise:
• No form of exercise, including competitive sports, should be
forbidden to the diabetic child.
• A major complication of exercise in diabetic patients is the presence
of a hypoglycemic reaction during or within hours after exercise.
glucoregulation is likely to be improved through the increased
utilization of glucose by muscles
• The major contributing factor to hypoglycemia with exercise is an
increased rate of absorption of insulin from its injection site. Regular
exercise also improves glucoregulation by increasing insulin receptor
number.
• In patients who are in poor metabolic control, vigorous exercise may
precipitate ketoacidosis because of the exercise-induced increase in
the counterregulatory hormones.
• In anticipation of vigorous exercise, one additional carbohydrate
exchange may be taken before exercise, or the total dose of insulin
may be reduced by about 10–15% on the day of the scheduled
exercise.
• It is also important to watch for delayed hypoglycemia several hours
after exercise.
Management During Infections
• Although infections are no more common in diabetic children than in
nondiabetic ones, they can often disrupt glucose control and may
precipitate DKA.
• In addition, the diabetic child is at increased risk of dehydration if
hyperglycemia causes an osmotic diuresis or if ketosis causes emesis.
• Counter-regulatory hormones associated with stress blunt insulin
action and elevate glucose levels. If anorexia occurs, however, lack of
caloric intake increases the risk of hypoglycemia.
Management During Infections
• Although children younger than 3 yr tend to become hypoglycemic
and older children tend toward hyperglycemia, the overall effect is
unpredictable. Therefore, frequent blood glucose monitoring and
adjustment of insulin doses are essential elements of sick day
guidelines.
• One regimen is to add 10 -20% of the total daily dose as actrapid
before each meal in addition to the usual daily dose if hyperglycemia
developed ( two doses daily regimen).
• The overall goals are to maintain hydration, control glucose levels,
and avoid ketoacidosis.
complications of the management
• Hypoglycemic Reactions: Hypoglycemia is the major limitation to tight
control of glucose levels.
• Most children with T1DM can expect mild hypoglycemia each week,
moderate hypoglycemia a few times each year, and severe
hypoglycemia every few years.
• These episodes are usually not predictable, although exercise,
delayed meals or snacks, wrong dose and wide swings in glucose
levels increase the risk.
Hypoglycemia
• Hypoglycemia can occur at any time of day or night.
• Early symptoms and signs (mild hypoglycemia) may occur with a
sudden decrease in blood glucose to levels that do not meet standard
criteria for hypoglycemia in non diabetic children.
• The child may show pallor, sweating, apprehension , hunger, tremor,
and tachycardia, all due to the surge in catecholamines as the body
attempts to counter the excessive insulin effect. Behavioral changes
such as irritability, and aggression are more prevalent in children.
Hypoglycemia
• As glucose levels decline further, cerebral glucopenia occurs with
drowsiness, personality changes, mental confusion, and impaired
judgment (moderate hypoglycemia),
• Progressing to inability to seek help and seizures or coma (severe
hypoglycemia). Prolonged severe hypoglycemia can result in a
depressed sensorium or stroke-like focal motor deficits that persist
after the hypoglycemia has resolved.
Hypoglycemia
• Although permanent squale are rare, severe hypoglycemia is
frightening for the child and family and can result in significant
reluctance to attempt even moderate glycemic control afterward.
• Important counter-regulatory hormones in children include growth
hormone, cortisol, epinephrine, and glucagon.
• The latter two seem more critical in the older child. Many older
patients with long-standing T1DM lose their ability to secrete
glucagon in response to hypoglycemia. In the young adult,
epinephrine deficiency may also develop as part of a general
autonomic neuropathy .
Hypoglycemia
• This substantially increases the risk of hypoglycemia because the early
warning signals of a declining glucose level are due to catecholamine
release.
• Recurrent hypoglycemic episodes associated with tight metabolic
control may aggravate partial counter-regulatory deficiencies,
producing a syndrome of hypoglycemia unawareness and reduced
ability to restore euglycemia (hypoglycemia-associated autonomic
failure). Avoidance of hypoglycemia allows some recovery from this
unawareness syndrome.
Management of hypoglycemia
The most important factors in the management of hypoglycemia are:
• An understanding by the patient and family of the symptoms and
signs of the reaction and an anticipation of known precipitating
factors such as sports activities. Tighter glucose control increases the
risk.
• A source of emergency glucose should be available at all times and
places, including at school and during visits to friends.
Management of hypoglycemia
• If possible, it is initially important to document the hypoglycemia
before treating, because some symptoms may not always be due to
hypoglycemia.
• Any child suspected of having a moderate to severe hypoglycemic
episode should be treated before testing.
• It is important not to give too much glucose; 5–10 g should be given
as juice or a sugar-containing carbonated beverage or candy and the
blood glucose checked 15–20 minutes later.
Management of hypoglycemia
• Patients, parents, and teachers should also be instructed in the
administration of glucagon when the child cannot take glucose
orally. An injection kit should be kept at home and school. The
intramuscular dose is 0.5 mg if the child weighs less than 20 kg and
1.0 mg if more than 20 kg. This produces a brief release of glucose
from the liver.
• Parents must then be prepared to take the child to the hospital for IV
glucose administration, if necessary.
Somogyi Phenomenon, Dawn Phenomenon,
and Brittle Diabetes
• In both dawn and somogyi phenomena , there is increase in blood
glucose levels with ketosis in the early morning hours before
breakfast.
• The dawn phenomenon is thought to be due mainly to overnight
growth hormone secretion and increased insulin clearance. It is a
normal physiologic process seen in most non diabetic adolescents,
who compensate with more insulin output. A child with T1DM cannot
compensate so we need to increase the evening lente insulin.
Somogyi Phenomenon
• the Somogyi phenomenon, a theoretical rebound from late night or
early morning hypoglycemia, thought to be due to an exaggerated
counterregulatory response. so we need to decrease the evening
insulin dose. Continuous glucose monitoring systems may help clarify
the cause of the elevated morning glucose levels.
Brittle Diabetes
• The term brittle diabetes has been used to describe the child, usually
an adolescent female, with unexplained wide fluctuations in blood
glucose, often with recurrent DKA, who is taking large doses of insulin
(no physiological abnormality but usually psychological cause)
None adherance
• Family conflict, denial, and feelings of anxiety find expression in non
adherence to instructions regarding nutritional and insulin therapy
and in noncompliance with self-monitorin.

FEAR OF SELF-INJECTING AND SELF-TESTING:

• Extreme fear of self-injecting insulin (injection phobia) is likely to
compromise glycemic control as well as emotional well-being.
Lipohypertrophy
• Lipohypertrophy at sites of insulin injection.
• Children and adolescents may refuse to rotate their injection sites
because repeated injection in the same site is associated with less
pain sensation.
• Failure to rotate injection sites results in subcutaneous scar formation
(lipohypertrophy).
• Insulin injection into the lipohypertrophic skin is usually associated
with poor insulin absorption and/or insulin leakage with resultant
suboptimal glycemic control.
LONG-TERM COMPLICATIONS
• The increasingly prolonged survival of the diabetic child is associated
with an increasing prevalence of complications.
• Limited joint mobility (LJM) highly correlated with micro vascular
complication of DM and can be used as rapid screening test in
outpatient clinic.
• Complications of DM can be divided into 3 major categories—
• (1) microvascular complications, specifically, retinopathy and
nephropathy
• (2) macrovascular complications, particularly accelerated coronary
artery disease, cerebrovascular disease, and peripheral vascular
disease
• (3) neuropathies, both peripheral and autonomic, affecting a variety
of organs and systems. In addition, cataract may occur more
frequently.