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DKA and HHS
what are the acute complications of insulin metabolism
DKA
profound deficiency of insulin that is characterized by hyperglycemia, ketosis, acidosis, and dehydration that is most likely to occur in those with type 1 DM, but can occur in those with type 2
illness
infection
inadequate insulin dosage
undiagnosed type 1 DM
poor self management
neglect
severe illness, infection, stress
what are RF/triggers for DKA
glucose can’t be used for energy so the body breaks down fat forming ketones as a byproduct
acidosis (low pH)
ketonuria
insulin deficiency…
impairs protein synthesis and causes excessive protein degradation and nitrogen losses from the tissues
stimulates production of glucose from proteins in the liver and leads to future hyperglycemia
additionally glucose cannot be used so BG rises more adding to the osmotic diuresis
depletion of sodium, potassium, chloride, magnesium, and phosphate
hypovolemia, shock, comatose, renal failure
dehydration: poor skin turgor, dry mucous membranes, tachycardia, orthostatic hypotension
lethargy and weakness
skin is dry and loose and eyes become soft and sunken
abdominal pain, anorexia, N/V
Kussmaul respirations, acetone on breath
BG > 250
ph < 7.30
HCO3 < 16
moderate/high ketones in urine
what are the s/s of DKA
ensure patent airway, administer O2 via NC or nonrebreather
establish IV access and begin fluid and electrolyte replacement
0.45 or 0.9% NS at a rate to restore urine output to 30-60 mL/hr and raise BP
When BG levels approach 250 mg/dL, add 5-10% dextrose to the fluid to prevent hypoglycemia nd a sudden drop, which can be associated with cerebral edema
monitor those with renal/cardiac issues for fluid overload
measure potassium before starting insulin
if hypokalemic, insulin will make it worse and can cause life threatening dysrhythmias
insulin via continuous IV at 0.1 u/kg/hr
monitor fluid balance and potassium levels
must be on continuous ECG monitoring
what does treatment for DKA include
HHS
a life threatening syndrome that can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and EC fluid depletion; most often occurs in patients older than 60 with type 2 DM and is often related to impaired thirst sensation and/or a functional inability to replace fluid
impaired thirst sensation
functional inability to replace fluids
inadequate fluid intake
mental depression
polyuria
UTIs
pneumonia
sepsis
acute illness
newly diagnosed T2 DM
what are causes/RF/triggers for HHS
fluid volume deficiency causes low sodium, potassium and phosphorus
electrolyte imbalances causes profound dehydration, hyperosmolality, and hypovolemia
hypovolemia causes…
decreased renal perfusion, oliguria, anuria
hypotension, tissue anoxia, increased lactic acid
hemoconcentration, hyperviscosity, thrombosis
does have ENOUGH circulating insulin that ketoacidosis does not occur
produces fewer S/S in the earlier stages so BG levels climb quite high before the problem is recognized
higher BG levels increase serum osmolality and cause more severe neuro effects
somnolence, coma, seizures, hemiparesis, aphasia
BG > 600
increase in serum osmolality
Ketones absent/minimal in blood and urine
what are the S/S of HHS
immediate IV admin of insulin 0.45 or 0.9% NS
usually needs more volumes of fluid replacement slowly and carefully
hemodynamic monitoring to avoid fluid overload
dextrose is added to IV fluids when BG levels fall to 250
monitor electrolytes
once stable detect and correct the underlying cause
what are the treatments for HHS
IV fluids
insulin therapy
replace and monitor electrolytes
monitor BG
assess renal status, cardiopulmonary status, and LOC
assess for signs of potassium imbalance
cardiac monitoring to detect hyper/hypokalemia
assess VS to determine the presence of fever, hypovolemic shock, tachycardia, and Kussmaul respirations
what are the similarities for treatment of both DKA and HHS