HHS & DKA Flashcards

Question

What is the peak of determir?

Answer 1

to provide basal insulin, overnight

Answer 2

- new onset T1D - In those with type 1 DM → who stop taking insulin for whatever reason, insulin is not effective, outdated, not stored properly; Purposeful omission of insulin for fear of weight gain, gaining control of chronic illness - Drugs that affect carbohydrate metabolism, including glucocorticosteroids, higher-dose thiazide diuretics, sympathomimetic agents, and newer “atypical” antipsychotic agents - Physical/ emotional stress. Infection or inflammatory response

Answer 3

- Sodium-glucose co-transporter 2 (SGLT2) inhibitors, mostly used in type 2 diabetes but also off-label in type 1 diabetes → There is a complex physiology that has results in reports of DKA in both types of diabetes - Cocaine use, which has been associated with recurrent DKA

Answer 4

- the cells cannot use the glucose for energy - the liver will then convert glycogen to glucose - causes hyperglycemia

Answer 5

** causes osmotic diuresis** - The hyperosmolality of the ECF stimulates thirst, resulting in polydipsia - Causes a fluid shift from the intracellular to the extracellular space - This fluid shifting causes low or normal serum sodium levels despite water losses with polyuria → Called pseudohyponatremia - The lack of insulin causes breakdown of fat (lipolysis) into free fatty acids and glycerol - The free fatty acids are converted into ketone bodies by the liver - In DKA, the excessive production of ketone bodies leads to the development of metabolic acidosis

Answer 6

Respiratory center to blow off respiratory acid, leading to rapid deep respirations known as Kussmaul respirations

Answer 7

- Blood glucose levels greater than 250 mg/dL → not as hyperglycemic as HHS - Low serum pH (6.8 to 7.3) - Low serum bicarbonate (0 to 15 mEq/L) - Accumulation of serum and urine ketones (high) - Presence of glucose in the urine - Abnormal levels of serum electrolytes (sodium, potassium, and chloride)

Answer 8

- Polyuria & polydipsia - Weakness & malaise - Blurry vision due to edema on the lens related to hyperglycemia →This comes from the edema in the macula

Answer 9

- Orthostatic hypotension - Warm, dry skin - Decreased skin turgor - Dry mucous membranes - Volume depletion causes a severe drop BP - Anorexia, N/V & abdominal pain - The acetone breath (fruity odor) - Kussmaul respirations (compensation) - Mental status changes (Na+)

Answer 10

- fluid resuscitation/rehydration → This is always the priority Tx; because it deals with ABC’s; b/c the patient’s BP will be compromised - insulin - potassium - correcting the acidosis

Answer 11

- Rehydration is important for maintaining tissue perfusion - Fluid replacement increases the excretion of excessive glucose by the kidneys - May need as much as 6-9 L of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, & vomiting

Answer 12

- Two bag protocol → start with 0.9%; as blood sugars begin to reduce more than 50/50 with 0.9% and 0.45%; blood sugar less than 300– all 0.45% - I.e. 1 to 2 L x first 1 to 2 hours and then 1 L/hr for 3-4 hrs, depending on response - Once volume restore change the fluid to 0.45% NSS - Treat the patient… assess for signs of fluid balance - Watch for cerebral edema - When blood sugar reaches 250 mg/dL should add dextrose to the IV

Answer 13

- The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown - Regular insulin is added to a saline solution & infused IV at a slow, continuous rate (0.1 U/kg/hr) - Often, a bolus is given at first - Potassium MUST be above 3.3 mEq/L before starting - f the BS does not drop by at least 50-70 mg/dL →The infusion should be doubled - The nurse must convert hourly rates of insulin infusion (frequently prescribed as “units per hour”) to IV drip rates →IV insulin 100 units/ 100 mL NSS = 1 u/ 1 mL

Answer 14

- Infuse insulin solution separately from rehydration solutions to allow for the frequent changes in the rate of the IV - Insulin is infused continuously until SQ administration of insulin can be resumed - Even if blood glucose levels are decreasing and returning to normal, the insulin drip must not be stopped until SQ insulin therapy has been started

Answer 15

**rehydration leads to increased plasma volume & subsequent decreases the serum potassium as well as increased urinary excretion of potassium** Potassium is the major electrolyte of concern during Tx of DKA - K+ can be low, normal or high - Potassium levels → may be low because of renal loss due to osmotic diuresis - It could be normal or high because of the shifting of K+ out of the cell to accompany the movement of hydrogen into the cells because of acidemia - If the K+ level is elevated, potassium replacement is withheld until serum levels fall to normal; this prevents the possibility of cardiac arrest from hyperkalemia - The serum level of potassium decreases with insulin admin as insulin facilitates movement of potassium back into the cell

Answer 16

- If K+ is low → the level must be assessed prior to starting insulin therapy because insulin will cause K+ to move into the cell– causes hyperglycemia - Potassium level must be greater than 3.3 mEq/L prior to starting insulin - Every 10 mEq of parenteral K+ should increase the serum level by ~ 0.1 mEq/L - To prevent hyperkalemia, urine output is monitored to ensure adequate kidney function - If the K+ is higher than 5.3 or the patient is anuric, potassium replacement is withheld

Answer 17

- If > than 5.0, NO Tx and assessment should be done frequently as BS comes down Serum K+ < 3.5 mEq/L: - Insulin should NOT be administered until the potassium is greater than this - IV KCl; 10-20 mEq/hour, which usually requires 10-20 mEq/L added to each liter of IV fluid, should be given Serum K+ 3.5 to 5.0 mEq/L: - If the initial serum potassium is 3.5 to 5.0 mEq/L, IV KCl (10 to 20 mEq) is added to each liter of IV fluid - Maintain level 4.0-5.0 mEq/L

Answer 18

- generalized muscle weakness - fatigue - diminished to absent reflexes - decreased GI motility - vomiting - hypotension - dysrhythmias - prolonged QT intervals - flattened, depressed T waves

Answer 19

- imapired muscle activity - muscle pain/cramps - increased GI motility - oliguria - dizziness - bradycardia - asystole - large, peaked T wave - broad, slurred QRS complex

Answer 20

- Blood glucose levels are corrected before acidosis is corrected → Therefore, IV insulin must be continued until the serum bicarb level improves to at least 15 mEq/L and the anion gap is 12 or less - Hourly blood glucose values must be measured to be sure the levels are dropping at a safe decrease - The goal is to decrease the serum glucose level by 50 to 100 mg/dL/hr to prevent complications like cerebral edema → If the BS is decreased too quickly fluid can shift to the brain - To avoid a rapid drop in the level of blood glucose during Tx, normal saline (NS) solutions with higher concentrations of glucose (D5NS, D5.45NS) are administered when blood glucose levels reach 250 mg/dL

Answer 21

Serum anion gap = serum sodium - (serum chloride + bicarbonate) In DKA can be higher than 20 mEq/L Normal = 3-10 - An elevated anion gap can indicate metabolic acidosis caused by DKA, lactic acidosis, or kidney failure - A low anion gap can suggest multiple myeloma, alkalosis, hypoalbuminemia, & specific electrolyte imbalances - Can have a normal anion gap and be acidotic

Answer 22

To prevent DKA r/t illness, patients must be taught “sick day” rules for managing their diabetes when ill - Do NOT eliminate insulin doses when N/V occur - Take regular/ rapid insulin ONLY if able to tolerate PO - The patient should take the usual insulin dose, or previously prescribed “sick day” doses, & then - Attempt to consume frequent small portions of carbs - Drinking fluids every hour is important to prevent dehydration - Blood glucose & urine ketones must be assessed every 2-3 hours if not using CBM - If the patient cannot take fluids w/o vomiting, or if elevated glucose or ketone levels persist, the patient must contact the HCP

Answer 23

HHS occurs most often in older people between 50-70 yrs old with type 2 DM

Answer 24

- Precipitating event, such as infection - Acute or chronic illness (i.e. pneumonia, stroke, UTI) - Medications or procedures that exacerbate hyperglycemia

Answer 25

Hx may include days to weeks of polyuria and polydipsia

Answer 26

Ketosis & acidosis do NOT occur in HHS → but dehydration is worse than DKA

Answer 27

- Insulin level too low/ resistant to prevent hyperglycemia & osmotic diuresis, but it is high enough to prevent fat breakdown - Osmotic diuresis comes from the insulin resistance → the more resistant the insulin the more at risk the patient is for HHS

Answer 28

- Hypotension/ orthostasis - Profound dehydration (dry mucous membranes, poor skin turgor) - Tachycardia - Neuro signs (i.e. alteration of sensorium, seizures, hemiparesis) - Mental status changes & neuro deficits are common secondary to cerebral dehydration that results from extreme hyperosmolarity → Often greater than DKA - Glucose levels are higher in HHS than in DKA - The elderly have coexisting cardiac and renal disease, the mortality rate ranges from 10-40%, usually related to the underlying illness

Answer 29

- High blood glucose, usually 600 to 1,200 mg/dL - High serum osmolality, often exceeding 350 mOsm/ kg - Electrolytes & blood urea nitrogen (BUN) are consistent with profound dehydration

Answer 30

- Replacement of fluids - Administration of insulin - Correction of electrolyte imbalances

Answer 31

- Must watch for heart failure Sx especially in those at risk Fluid Tx is started with 0.9% or 0.45% NS, depending on the patient’s sodium level & level of volume depletion - Fluid replacement is guided by central venous or hemodynamic pressure monitoring - Potassium is added to IV fluids when urinary output is adequate & is guided by continuous ECG monitoring & frequent lab potassium determination - The rehydration will affect the BG level & insulin is not as important in HHS compared to DKA → There is NO need to reverse acidosis

Answer 32

- Use dextrose IV solution when glucose falls to 250-300 mg/dL - Other therapeutic modalities are determined by the underlying illness & the results of continuing clinical & lab eval - It may take 3-5 days for neuro Sx to resolve - After resolution of Sx, most can go back to diet & oral med management - Frequent self BG monitoring (SBGM) is important in preventing recurrence of HHS when high risk events occur

HHS & DKA Flashcards

(60 cards)