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diabetes mellitus
chronic disorder of metabolism characterized by a partial or complete deficiency of insulin hormone
most common metabolic disease in childhood
normal carbohydrate metabolism
insulin builds bridge for sugar in bloodstream from external and internal sources to enter cells so they can create energy
carbohydrate metabolism in type 1 diabetes
no insulin to shut off internal sugar production or manage external sugar sources or build bridge for cells to use sugar for energy
classification of type 1 diabetes
diagnosed in children and young adults
previously known as juvenile diabetes
insulin dependent
body does not produce insulin (autoimmune destruction of pancreatic beta cells)
rarely overweight
rarely has family history
classification of type 2 diabetes
typically diagnosed in adulthood
non-insulin dependent
body fails to produce and properly use insulin
commonly overwight
common familial tendency
treatment is weight maintenance/loss, exercise, insulin, and oral agents
clinical manifestations of type 1 DM
hyperglycemia and acidosis
weight loss
polyphagia
polydipsia
polyuria
enuresis
irritability
unusual fatigue
abdominal pain
risk factors of type 2 DM
overweight
family history
inactivity
low HDL and high triglycerides
certain ethnic races
hispanics
african americans
clinical manifestations of type 2 DM
3 P’s (polyphagia, polydipsia, polyuria)
fatigue
extreme hunger but loss of weight
blurred vision
frequent infections
acanthosis nigrocans
leathery skin appearance that feels rough
diabetes medical management
medical nutrition therapy
medication administration
insulin
oral agents
developmental issues
glucose/urine monitoring
hypoglycemia management
hyperglycemia management
sick-day management
medical nutrition therapy
carbs main food sources that increases blood sugar
fat can increase blood sugar later
develop CHO goals
conventional - consistent CHO intake
intensive - insulin to CHO ration (most frequent)
objectives of nutritional management
appropriate meal and snack planning
dietary balance of carbs, fats, and proteins
extra food during increased exercise
consistent meal times
avoid high sugar
develop appropriate insulin regimen and physical activity program
increase insulin with extra food
decrease insulin need with strenuous exercise (can be difficult to know, typically just increase food intake)
carbohydrate sources
breads, grains, cereals, pastries, rice, pasta
milk, dairy
fruits
vegetables
carb-free foods
meat
cheese
sugar-free jello
goal of insulin therapy
provide for physiologic needs
rapid acting insulin
aspart (novolog)/lispro (humalog)
short-acting insulin
regular insulin
intermediate acting insulin
NPH/Lente
long-acting insulin
glargine (Lantus)/detemir (Levemir)
rapid acting onset, peak, and duration
onset - 15 minutes
peak - 1 hours
duration - 3-4 hours
short acting onset, peak, and duration
onset - 30 minutes
peak - 3 hours
duration - 6-8 hours
intermediate acting onset, peak, and duration
onset - 1-2 hours
peak - 6-8 hours
duration - 12-18 hours
long acting onset, peak, and duration
onset - 4-6 hours
peak - 8-20 hours
duration - 24 hours
conventional insulin therapy
BID or TID dosing
intensive insulin therapy
basal/bolus insulin dosing
management tools for intensive therapy
insulin pens
blood glucose meters
sub-q ports (changed every 7-10 days)
insulin pumps
only gives short acting insulin; delivers steady amount and can program boluses but can stop working and are very expensive
blood glucose monitoring
monitored at least 4 times a day - before meals and at bedtimes
also should be checked anytime child feels/displays symptoms of hypoglycemia
check before recess/PE class
urine ketone monitoring
any time BG >240 mg/dl on two separate occasions
during illness
pump therapy - blood glucose levels >240 mg/dl on any occasion
management tools for intensive insulin therapy
rapid acting insulin
basal rate
bolus - match insulin dose to actual CHO intake
correction factor - correct for blood sugars above desired level
pump emergency kit
know insulin dosing calculations
examples on canvas
toddler developmental issues with diabetes management
parents must differentiate misbehavior from hypoglycemia
encourage child to report funny feelings
expect food jags
give choices regarding self blood glucose monitoring, injection site, and food choices
preschool developmental issues with diabetes management
reassure child who views diabetes tasks as punishment for behavior
encourage child to participate in simple diabetes tasks
teach child to report lows to an adult
teach child what to eat when low
school age developmental issues with diabetes management
educate school personnel about diabetes
encourage age-appropriate independence
all activities must be supervised
encourage extracurricular activities and participation in social groups
11-12 year olds able to perform an occasional injection
adolescence developmental issues with diabetes management
more capable of performing self care activities
know which foods fit into meal plan and how to adjust
more willing to perform multiple injections
risk takers - may not be checking
needs continues parental involvement and support
glucose will drop when drinking alcohol, make sure they keep snack with them if planning on drinking
sick day management
give insulin as scheduled
check blood sugar more frequently
monitor urine for ketones
complications of blood glucose alterations
hypoglycemia
hyperglycemia
ketosis
acidosis
DKA (hyperglycemia + ketosis + acidosis)
hypoglycemia
low blood glucose; treated when less than 60 mg/dl
develops because body doesn’t have enough glucose to burn energy
can happen suddenly
causes of hypoglycemia
too little food
too much insulin
vomiting
exercise
change in schedule
signs and symptoms of hypoglycemia
low blood glucose
hunger
headache
confusion
shakiness
dizziness
sweating
treatment of hypolgycemia
check blood sugar - if less than 60-65 mg/dl, treat
treat with 15 g of fast acting cho
½ cup of juice or regular soft drink
1 cup of milk (not chocolate)
glucose tablets
cake icing
follow rule of 15’s - 15 grams of cho and recheck blood sugar every 15 minutes until normal
follow with meal or snack
once above 60, give protein to keep above 60
severe hypoglycemia
if unable to swallow, use glucagon emergency kit - dose 1mg
inject into subq or muscle - once given place patient in recovery position to prevent aspiration
after awake, must feed
check glucagon expiration date
hyperglycemia
develops when body has too much glucose in blood
serious problem if not treated
major cause of complications in children with diabetes
causes of hyperglycemia
too much food (carbs)
too little activity
too little insulin
illness/infection
signs and symptoms of hyperglycemia
high blood glucose
high levels of glucose in urine
frequent urination
treatment of hyperglycemia
check urine ketones
if ketones are moderate to large, call HCP ASAP
increase fluids (caffeine free)
do not increase activity
ketones
acidic substance that are made when body breaks down fat for energy
ketosis
presence of excess ketones in body
blood ketone concentration between 0.3-7.0 mmol/L
ketoacidosis
when ketones build up in the blood, they make it more acidic
severe form of ketosis
levels of 7.0 mmol/L or higher
lowers pH to 7.3 or lower
pathophysiology of ketosis
cells don’t get glucose for energy bc of lack of insulin
body begins to burn fat for energy
ketones are produced when fat breaks down
ketones accumulate in body
acidosis
when ketones build up in blood, making it more acidic
acidemia is a pH below 7.35
signs and symptoms of acidosis
deep, rapid breathing (kussmaul’s respirations)
confusion or lethargy
abdominal pain
blood tests to diagnose acidosis
arterial or venous blood gas
electrolytes - sodium, potassium, chloride, and bicarb
anion gap (Na+K) - (Cl+HCO3); high anion gap indicates metabolic acidosis
diabetic ketoacidosis (DKA)
complex metabolic state of hyperglycemia, ketosis, and acidosis
hyperglycemia (>300 mg/dl)
evidence of significant ketosis
acidosis
life threatening and needs immediate treatment
signs and symptoms of DKA
deep, rapid breathing
very dry mouth
lethargy/drowsiness
fruity breath odor
nausea and vomiting
respiratory distress
causes of mortality with DKA
failure to make diagnosis
cerebral edema
hypokalemia/hyperkalemia
hypoglycemia
hypovolemia
electrolyte disturbances during DKA
potassium loss caused by shift of potassium from intracellular to extracellular space in exchange with hydrogen ions that accumulate extracellularly during acidosis
potassium then lost in urine because of osmotic diuresis
high serum osmality also drives water from intracellular to extracellular space causing hyponatremia
DKA therapy
fluid replacement (PRIORITY)
electrolyte replacement
insulin therapy
careful monitoring
goals for DKA
correct dehydration
correct acidosis and reverse ketosis
restore normal blood glucose levels
avoid complications of therapy
goal of first hour of treatment of DKA (IVF)
fluid resuscitation
confirmation of DKA by lab studies
goals of second and succeeding hours of treatment of DKA (IVF)
slow correction of hyperglycemia, metabolic acidosis, and ketosis
start correcting electrolyte imbalances
continued volume replacement
fluids for mild to moderate dehydration in DKA
0.9% NS 10 ml/kg/hr over initial hour
fluids for hypovolemic shock in DKA
0.9% NS 20 ml/kg/hr bolus infused as fast as possible
after first hour of IVF
replace fluid deficit evenly over 48hr with 0.45-0.9% NS
insulin administration in DKA
begun after initial fluid resuscitation; at beginning of 2nd hour
insulin therapy
turns off production of ketones
decreases blood glucose
check glucose hourly
low dose insulin infusion
decreases risk of hypoglycemia or hypokalemia
goal is to decrease blood glucose by 100 mg/dL/hr
things to know for insulin administration in DKA
do not reduce or discontinue insulin infusion based solely on blood glucose
insulin infusion should be continues until ph >7.3 and/or HCO3 >15 meq/L and serum ketones have cleared
first step of insulin administration during DKA
IV insulin infusion regular insulin 0.1 units/kg/hr
second step of insulin administration during DKA
continue until acidosis clears (pH >7.30, HCO3 >15 meq/L)
third step to insulin administration during DKA
decrease to 0.05 units/kg/hr until SQ insulin initiated
key points for insulin
prior to administration, reassess vital signs, BG levels, and neuro status
insulin is administers as a continuous IV infusion of regular insulin of 0.1 units/kg/hr
insulin is high alert med, two nurses should verify insulin order, doe, and volume prior to administration
IV tubing should be primed with insulin before administration
do not give insulin as bolus
dose of 0.1 units/kg/her continues until acidosis resolves
do not decrease rate or stop insulin administration based solely on glucose values
once blood glucose reaches 250-300 mg/dl, maintain insulin and begin dextrose infusion to keep BG from dropping too fast
at time of insulin infusion, make sure any indwelling insulin pump has been disconnected and/or stopped
guidelines for potassium administration
consult with pharmacist before administering
make sure they have urinated first
start replacing potassium after initial fluid resuscitation and concurrent with starting insulin therapy
monitor closely
in general, with DKA< there is a significant potassium deficit to replace
potassium replacement should continue throughout IVF therapy
max recommended rate of IV K+ replacement is institution specific
dextrose administration
check glucose hourly until stable
check electrolytes every 2-4 hours until stable
first step to dextrose administration in DKA
add to IVF when blood glucose reaches 250-300 mg/dl
second step to dextrose administration in DKA
change to 5% dextrose with 0.45 NaCl at rate to complete rehydration in 48 hours
third step to dextrose administration in DKA
check glucose hourly and electrolytes every 2-4 hours until stable
fourth step to dextrose administration in DKA
after resolution of DKA, initiate SQ insulin 0.5-1.0 units/kg/day (or stated otherwise)
bicarbonate therapy
bicarbonate therapy is generally contraindicated in pediatric DKA due to increased risk of cerebral edema
consult pediatric endocrinologist before initiating bicarbonate
should only be considered with
severe acidemia
life threatening hyperkalemia
monitoring DKA
hourly assessments
VS
neuro status
accurate fluid intake/output
point of care testing BG level
potassium level
every 2 hours
urine ketones
serum bicarbonate
labs
serum glucose
electrolytes
BUN
calcium
magnesium
phosphorus
hematocrit
blood gases
continuous cardiac monitoring
amount of administered insulin
administer oxygen
insert additional peripheral IV catheter
repetitive blood sampling
if insulin drip is initiated
high risk patients that have DKA
ICU admission for closer monitoring if:
severe DKA (<7.1 or <7.2 in young child)
altered level of consciousness
under age of 5 years
increased risk for cerebral edema
be prepared for intubation
caution with meds that may alter mental status
when DKA has resolved
discontinue IVF after patient tolerates oral fluids
give SQ insulin; discontinue IV insulin
at the time of SQ rapid acting insulin or after 30 mins after SQ regular insulin
transition off of IV insulin
pH >7.30 and HCO3 > 15-18
anion gap typically less than 12
patient able to eat
SQ insulin
give SQ injection, D/C IV insulin and IV dextrose, feed child
known diabetes
previous dosing
may need additional rapid actnig insulin to overcome insulin resistance after DKA
new patient 0.7-1 units/kg/day is general guideline