Diabetic Ketoacidosis (DKA) & Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

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55 Terms

1
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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

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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

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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

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when pt is on a insulin drip you must monitor

potassium

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how often do you do accucheck for DKA

-q30 for the first hour

-once stable qhr

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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

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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

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DKA p symptoms

polyuria and polydipsia

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DKA overall vague symptoms

•Fatigue

•Blurred vision

•Weakness

•Headache

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DKA volume sx

Orthostatic hypotension

•Volume depletion→ frank hypotension

-sunken eyes

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DKA ketosis sx

•Anorexia

•Nausea/vomiting

•Abdominal pain

•Acetone breath

•Hyperventilation (Kussmaul's respirations)

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DKA neuro changes

•Mental status changes

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DKA blood glucose reading will be

vary from 300-800 mg/dL

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DKA serum bicarb will be

•low serum bicarbonate (0-15 mEq/L)

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DKA PH is

low pH (pH 6.8-7.3)

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DKA has ____ CO2 related to _______

•low PCO2 reflects respiratory compensation (10-30 mm Hg)

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DKA leads to renal _____

insufficiency which leads to increased BUN/CRT

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patients with DKA will have _____ in their blood and urine which leads to _________

-ketones

-increased HCT

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severity of DKA is not related to

blood glucose

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how do you manage DKA?

-REHYDRATE

-CORRECT ACIDOSIS

-CORRECT ELECTROLYTE IMBALANCE

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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)

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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)

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during rehydration potassium moves back into the cells so the patient must be on the

EKG monitor

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before starting insulin drip what must you do

-check potassium and correct it because insulin drives potassium into cells

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how do you give potassium for DKA

-IV pump (never override the pump)

-GIVEN with fluids

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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

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what labs do we need with DKA

-k

-BUN/ crt

-ABGs (will tell us acidosis)

-will be elevated with DKA

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BUN and CRT DKA levels

BUN- > 30

CRT- > 1.5

29
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for DKA sodium will be

-above, below, within the expected range

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Bicarb and sodium bicarb levels for DKA

-Sodium Bicarb- 0-15

-bicarb-1-15

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For PH for DKA it will be

less than 7.35

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DKA patients are _____

-acute

-everything you do is acute

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when patient comes off of insulin drip we have to switch to

-sliding scale SUB Q

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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

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Predominating features of HHS

•Hyperosmolarity

•Hyperglycemia

•Minimal or absent ketosis

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how do we fix HHS

FLUIDS

-dilutes the hyperosmotic blood

-stops the kidneys from osmotic diuresing

-lowers blood sugar

-replenishes electrolytes

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HHS happens mostly with who

DM2

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We check sugar and it says HI what do you do

-order a BMP

-ABG

-start fluids

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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)

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HHNS clinical manifestations

•Signs of profound dehydration

•Neurologic manifestations (cerebral dehydration)

Mortality rates: 10-40%

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HHNS Assessment/Diagnostics

•Blood glucose = 600-1200 mg/dL

•Electrolytes

•BUN

•CBC

•Serum osmolality= > 350 mOsm/kg

•ABG- rule out DKA

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HHS blood glucose level will be

•600-1200 mg/dL

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HHS Serum osmolality

•> 350 mOsm/kg

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can HHNS get insulin

-yes but it doesnt have to be AGRESSIVE

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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

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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

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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

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Collaborative problems for DKA/HHNS

•Fluid overload, pulmonary edema, heart failure

•Hyperglycemia/ketoacidosis

•Cerebral edema

•Hypoglycemia

•Hypokalemia

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what are some things you need to monitor for during HHS/DKA and especially after a patient receives tx

•Hypoglycemia

•Hypokalemia

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Nursing Interventions for DKA/HHNS

•Maintain fluid and electrolyte balance

•Increase knowledge about DM

•Monitoring & Managing potential complications

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OUTCOMES OF TEACHING PATIENT SELF CARE

•Achieves fluid and electrolyte balance

•Absence of complications

•Demonstrates adequate knowledge

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ph FOR HHNS

greater than 7.45

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Bicarb for HHS

greater than 20

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DKA main points

•Ketosis

•Acidosis

•No insulin present

•Breakdown of glucose, protein and fat→ leads to ketosis

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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