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Main Causes of DKA
•Illness or infection (insulin resistance)
•Undiagnosed/untreated diabetes
•decreased or missed dose of insulin
•Patient error
•Intentional skipping of insulin doses
•Equipment problems
•Stress
if a patient has AMS with a sugar of 40 what do you do
-give glucagon: helps it not get worse
-IV push 50% dextrose
-recheck glucose 15-30 mins later
DKA: Pathophysiology
•Insulin deficiency→ decreased amount of glucose entering the cell
•Gluconeogenesis (release of glucose by the liver) increases→ leads to hyperglycemia
•Kidneys excrete glucose along with water and electrolytes (sodium, potassium)→ osmotic diuresis (may lose up to 6.5 L of water/day)
•Insulin deficiency or deficit causes lipolysis breakdown of fat) into free fatty acids
•Free fatty acids converted into ketone bodies→ leads to metabolic acidosis
when pt is on a insulin drip you must monitor
potassium
how often do you do accucheck for DKA
-q30 for the first hour
-once stable qhr
DKA: Prevention
-teach them to
-follow up
-go to ER when they feel sick
-teach them to do accucheck
-teach them to be compliant to meds
DKA: Clinical Manifestations
•Polyuria
•Polydipsia
•Fatigue
•Blurred vision
•Weakness
•Headache
•Orthostatic hypotension
•Volume depletion→ frank hypotension
-sunken eyes
•Ketosis leads to
•Anorexia
•Nausea/vomiting
•Abdominal pain
•Acetone breath
•Hyperventilation (Kussmaul's respirations)
•Mental status changes
DKA p symptoms
polyuria and polydipsia
DKA overall vague symptoms
•Fatigue
•Blurred vision
•Weakness
•Headache
DKA volume sx
Orthostatic hypotension
•Volume depletion→ frank hypotension
-sunken eyes
DKA ketosis sx
•Anorexia
•Nausea/vomiting
•Abdominal pain
•Acetone breath
•Hyperventilation (Kussmaul's respirations)
DKA neuro changes
•Mental status changes
DKA blood glucose reading will be
vary from 300-800 mg/dL
DKA serum bicarb will be
•low serum bicarbonate (0-15 mEq/L)
DKA PH is
low pH (pH 6.8-7.3)
DKA has ____ CO2 related to _______
•low PCO2 reflects respiratory compensation (10-30 mm Hg)
DKA leads to renal _____
insufficiency which leads to increased BUN/CRT
patients with DKA will have _____ in their blood and urine which leads to _________
-ketones
-increased HCT
severity of DKA is not related to
blood glucose
how do you manage DKA?
-REHYDRATE
-CORRECT ACIDOSIS
-CORRECT ELECTROLYTE IMBALANCE
DKA management: rehydration
•Initially with 0.9% NS (may need 6-10L of IV fluid)
•Followed by 0.45% NS
•D5W after blood glucose is < 300 mg/dL (if patients anion gap is not closing we change it from D5 to D10 IF GLUC drops too low)
•rehydration leads to increased plasma volume and decreased K+, insulin enhances the movement of K+ from extracellular fluid into the cells (patient must be on the EKG)
rehydration leads to increased plasma volume and decreased
-K
-insulin enhances the movement of K+ from extracellular fluid into the cells (patient must be on the EKG)
during rehydration potassium moves back into the cells so the patient must be on the
EKG monitor
before starting insulin drip what must you do
-check potassium and correct it because insulin drives potassium into cells
how do you give potassium for DKA
-IV pump (never override the pump)
-GIVEN with fluids
DKA: Management reversing Acidosis
•Ketone bodies accumulate as a result of fat breakdown
•Reversed with insulin
•Regular Insulin infused IV (5 units/hr) at the same time AS the rehydration fluids are going
•Do not stop the Insulin! we need to make sure the gap is closing
•Blood glucose levels are usually corrected before the acidosis is corrected
what labs do we need with DKA
-k
-BUN/ crt
-ABGs (will tell us acidosis)
-will be elevated with DKA
BUN and CRT DKA levels
BUN- > 30
CRT- > 1.5
for DKA sodium will be
-above, below, within the expected range
Bicarb and sodium bicarb levels for DKA
-Sodium Bicarb- 0-15
-bicarb-1-15
For PH for DKA it will be
less than 7.35
DKA patients are _____
-acute
-everything you do is acute
when patient comes off of insulin drip we have to switch to
-sliding scale SUB Q
Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
•Secondary to lack of effective insulin (insulin resistance)
•Persistent hyperglycemia causes osmotic diuresis→ water and electrolyte losses
•Water shift from the intracellular fluid space to the extracellular fluid space
Predominating features of HHS
•Hyperosmolarity
•Hyperglycemia
•Minimal or absent ketosis
how do we fix HHS
FLUIDS
-dilutes the hyperosmotic blood
-stops the kidneys from osmotic diuresing
-lowers blood sugar
-replenishes electrolytes
HHS happens mostly with who
DM2
We check sugar and it says HI what do you do
-order a BMP
-ABG
-start fluids
HHNS: Etiology
•Occurs in older people; no known history of DM or type 2 DM.
•Can be traced to a precipitating even (acute illness; pneumonia, CVA, dialysis)
HHNS clinical manifestations
•Signs of profound dehydration
•Neurologic manifestations (cerebral dehydration)
Mortality rates: 10-40%
HHNS Assessment/Diagnostics
•Blood glucose = 600-1200 mg/dL
•Electrolytes
•BUN
•CBC
•Serum osmolality= > 350 mOsm/kg
•ABG- rule out DKA
HHS blood glucose level will be
•600-1200 mg/dL
HHS Serum osmolality
•> 350 mOsm/kg
can HHNS get insulin
-yes but it doesnt have to be AGRESSIVE
HHNS: Management
•Rehydration
•CVP monitoring
•Monitor fluid volume and electrolyte status
•Insulin administration
•Prevention
•BGSM
•Diagnosis and management of diabetes
Assess and promote self-care management skills
Insulin administartion is less important for HHS because
-it is not needed to reverse ketoacidosis
-may still be given after changing IVF to D5W once sugar drops
nursing diagnosis for DKA/HHS
•Risk for fluid deficit r/t polyuria and dehydration
•F & E imbalance r/t fluid loss or shifts
•Deficient knowledge about diabetes self-care skills
Collaborative problems for DKA/HHNS
•Fluid overload, pulmonary edema, heart failure
•Hyperglycemia/ketoacidosis
•Cerebral edema
•Hypoglycemia
•Hypokalemia
what are some things you need to monitor for during HHS/DKA and especially after a patient receives tx
•Hypoglycemia
•Hypokalemia
Nursing Interventions for DKA/HHNS
•Maintain fluid and electrolyte balance
•Increase knowledge about DM
•Monitoring & Managing potential complications
OUTCOMES OF TEACHING PATIENT SELF CARE
•Achieves fluid and electrolyte balance
•Absence of complications
•Demonstrates adequate knowledge
ph FOR HHNS
greater than 7.45
Bicarb for HHS
greater than 20
DKA main points
•Ketosis
•Acidosis
•No insulin present
•Breakdown of glucose, protein and fat→ leads to ketosis
HHNS main points
•Minimal to no ketosis
•Minimal to no acidosis
•Insulin level is too low to prevent hyperglycemia, but high enough to prevent fat breakdown
•No ketosis-related GI symptoms (do not seek care)
•Delays in therapy
•More severe: hyperglycemia, dehydration, hyperosmolarity