SLOs for DKA and HHS

pathophysiology of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS)

DKA:

1. absolute lack of insulin → glucose is unable to enter cells → starving cells, lacking energy

2. body releases cortisol and glucagon to stimulate liver to convert glycogen → glucose (as a stress response) as it is trying to give the liver sugar

3. breakdown of fat releases ketones → metabolic acidosis

4. kidneys leak glucose into urine → water follows glucose (causing polyuria)

5. electrolyte imbalance occurs (hyperkalemia and hyponatremia due to fluid shift out of the cells)

HHS:

1. lack of insulin yet enough is produced that prevents ketoacidosis however body still has elevated blood glucose levels

2. body becomes resistent to glucose causing hyperglycemia

3. cells are resistent to insulin

4. kidneys leak glucose → excrete to compensate

5. more significant fluid loss due to gradual onset

   1. electrolyte imbalances occur with hyponatremia and hyperkalemia

signs and symptoms of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS)

DKA:

• hyperglycemia (>250)

  • polyuria (trying to excrete excess glucose)

  • polydipsia (increased water intake to compensate for fluid loss w/ shifting out of cells)

• hypovolemia

• hypotension

• tachcardia

• decreased skin turgor (due to dehydration)

• weight loss (cells are starved)

• fruity breath (ketone breakdown causing ketones to float around)

• kussmal respirations (increased RR and blow off CO2 levels to lower acid level)

  • metabolic acidosis

• fatigue/lethargy → not enough sugar in cells to function

• nausea/vomiting and abdominal pain

• headaches with blurry vision

HHS:

• extremely high blood sugar level

  • polyuria (excess volumes of urine excretes, >3L)

  • polydipsia (excessive thirst) → trying to replace fluid loss w/ water shifting out of cells

• dehydration (→ seizures/coma from cerebral dehydration)

  • dry mucous membranes

  • poor skin turgor

• hypovolemia

• extreme fluid shift → arrythmias

• confusion, fatigue

treatment and nursing interventions for patients w/ DKA and HHS

DKA:

• provide NS fluid to improve hypovolemia → switch to IV fluids and electrolyte replacement

  • DO NOT bolus back-to-back as it can cause fluid overload and cerebral edema → neuro changes or seizures

• give insulin gtt to improve glucose levels

  • Q15mins BS check, 1:1 w/ patient

  • monitor potassium level → starting insulin will make potassium go back into the cell so potassium levels should NOT be low when starting

    • provide insulin drip and potassium replacement levels as it is not indicated to not give insulin due to glucose levels

• strict I and Os → DO NOT WANT PATIENT EATING, will need to be NPO then on clear liquids as they will spike glucose levels and impacts insulin drip rate

• monitoring potassium levels (for both hyper and hypo)

• provide patient education on checking blood glucose levels

  • Q4hrs when sick

  • if fasting or NPO, check w/ MD on insulin dosing

HHS:

• provide IV fluid replacement (replace first 12hrs with specific amount then 24hrs later do different amount due to electrolyte levels and kg)

• frequent blood pressure checks due to hypovolemia

• insulin gtt

  • monitoring potassium levels during → monitor arrythmias

• strict intake and output

• discharge education on managing blood sugar at home

compare and contrast DKA and HHS

DKA:

• absolute lack of insulin → release of ketones → acidosis

• seen typically w/ type I

• sudden onset

• risk factor: 13-25

• kussmal respirations

• fruity breath

HHS:

• still producing an amount of insulin preventing ketoacidosis

• seen typically w/ type II

• gradual onset

• risk factor: older age

when providing insulin drips..

1. insulin used: regular insulin

2. requires 2 RN check due to high acuity tx

3. bolus is given to start then rate is based on weight and BS level

   1. need to do Q15min BS check

4. use normal saline to start → use dextrose once BS stabilizes as you will eventually need to reintroduce new sugar due to NPO status

5. frequent monitoring of potassium levels while using insulin gtt

   1. insulin pushes potassium into the cells (becoming hypokalemic)

   2. potentially need to piggyback w/ potassium

      1. can be painful at PIV site, typically try to mix w/ fluids