DKA and HHS Flashcards
What do we generate fuel-wise in a prolonged fasting state?
- Ketones made for energy to CONSERVE protein
2. Ketonemia can lead to METABOLIC ACIDOSIS!!
Pathophys of DKA and HHS:
- Absolute or relative insulin deficiency
- Increase in counter-reg hormones: stress, infection, meds
- Volume depletion (5-12 L)
Insulin deficiency:
- Think type 1 diabetes or ketosis-prone type 2 diabetes
- Noncompliance with insulin
- Expired insulin
- Insulin pump failure
Four counter-reg hormones:
- Glucagon
- Cortisol
- Growth hormone
- Epinephrine;
think gycogenolysis and gluconeogenesis
Precipitating factors of DKA and HHS:
- Think INFECTION
- Insulin (new-onset diabetes)
- Infarct!!
How can one become volume depleted in DKA or HHS?
- Hyperglycemia (low insulin and elevated counter-reg hormone levels)
- Exceed glucose reabsorption (160-190) and you have osmotic diuresis from glucosuria and electrolyte losses (Na and K)
- Severe water loss (polyuria, dehydration, increased thirst, polydipsia, and then tissue hypoperfusion leading to lactic acidosis)
Path of DKA:
- Decreased effective insulin concentration and increase in counter-reg hormones (ketosis and hyperglycemia; have lipolysis of adipose tissue and increased FFA’s; also unrestrained hepatic FA oxidation to ketone bodies)
- Hyperglycemia: increased gluconeogensis, increased glycogenolysis, impaired glucose utilization by peripheral tissues
- Transient insulin resistance: hormone imbalance (counter-reg hormones) and elevated FFA concentrations
Path of HHS:
- Relative insulin deficiency leads to hyperglycemia leading to osmotic diuresis and then dehydration;
however enough insulin to prevent lipolysis and ketogenesis, and not enough insulin to allow for glucose utilization
Clinical presentation of DKA vs. HHS:
- DKA: type 1 DM, generally young, abdo discomfort, vomiting and Kussmaul respirations; vascular shock and mental status changes;
- HHS: type 2 DM, generally elderly, debilitating disease, volume contraction; generally WITHOUT ketoacidosis, mental status changes
DKA diagnostic criteria vs. HHS criteria:
- Hyperglycemia
- Metabolic acidosis
- Ketone production;
- Hyperglycemia
- Hyperosmolality
- Dehydration
Sick Day rules:
- Take insulin even when NOT eating
- Increase freq of testing and titrate insulin appropriately
- Drink fluids
- Monitor urine KETONES
- Worry about high glucose or vomiting
Fluids doled out as:
- IV NS 1-2 L or until patient not orthostatic
- IV NS or .5 NS depending on corrected serum Na, hemodynamics, and urine output (DON’T correct hyperosmolality too quickly, and calculate the body water deficit)
- Give IV .5 NS with D5W once glucose levels are 200 mg/dL
For insulin, when is this indicated?
Continuous regular insulin infusion preferred;
- Have glucose fall 50-75 mg/dL/hr (adjust insulin infusion)
- As glucose gets to 200-300, add fluids to maintain glucose concentrations until DKA resolves
- Hyperglycemia corrects faster than ketoacidosis
- MUST overlap insulin infusion with subq insulin by 1-2 hrs to prevent hyperglycemia/ketoacidosis recurrence
For K, what should we do?
- It enters cells with treatment of insulinopenia and acidemia
- Monitor: height of T wave directly proportional with K level
- AVOID HYPOKALEMIA (risk of ventricular arrhythmias)
What are we worried about with bicarb?
- Exacerbates hypokalemia, decreases tissue O2 uptake, cerebral edema, paradoxical CNS acidosis;
- Give ONLY in severe acidosis (pH less than 6.9) or severe hyperkalemia (K greater than 6.5 or EKG changes)
Labs to look out for in DKA or HHS:
- Na (use corrected Na to calculate water deficit)
- Leukocytosis: can be as high as 25000 b/c of stress but infection also
- Serum osmolality 281-297
Facts about ketones:
- Present under normal circumstances (starvation, alcohol, pregnancy)
- Acetoacetic acid:beta-HBA usually 1:1 up to 1:3
- In DKA, can go up to 1:10 as redox state changes (beta-HBA predominate ketone in DKA)
Ames Acid test measures _____ in blood and urine; does not test _____; what is the normal ketone range and what is it in DKA? What is the problem following ketones here?
acetoacetic acid; beta-HBA;
less than .15 mmol/L, and 3-30 mmol/L in DKA;
ketones decrease more slowly than glucose, and worried about paradoxical ketonuria with redox potential changes as more beta-HBA converted into acetoacetate
Cutoff for DKA is; we should follow
2 (beta-HBA usually .02-.27 mmol/L);
anion gap and glucose
Resolving DKA and HHS, and possible complications:
- DKA with glucose less than 200, and two of bicarb over 15, venous pH over 7.3, and calculated anion gap less than 12;
- HHS with normal osmolality and mental status;
Complications: - hypoglycemia (start dextrose with glucose less than 200)
- Hypokalemia (monitor)
- Hyperchloremic non-anion gap metabolic acidosis (recovery phase of DKA, but it’s self-limiting)
- Cerebral edema (rapid fluid correction, excessive bicarb, hyponatremia, glucose falls below 200): treat with 1-2 g mannitol, dexamethasone, and intubation with hyperventilation but not effective, so avoid onset and DKA
Acid base:
- What is the osis? Over 7.45 or less than 7.35
- Look at bicarb (metabolic or respiratory)
- Is there compensation?
- If metabolic acidosis: determine anion gap (if elevated, check Winter’s formula and delta-delta, then check ketones, and with ketones negative check other stuff)
- For delta-delta, if delta bicarb greater than delta AG then you have concomitant non-AG acidosis, and if vice versa, you have concomitant metabolic alkalosis alongside AG acidosis
What could precipitate DKA?
Infection, other physical stress, discontinued insulin, ineffective insulin, etc.
If treating DKA, best lab value to follow? What electrolytes need to be followed?
Follow AG!! Can’t follow glucose since it will resolve prior to ketone resolution, and don’t follow ketones unless beta-HBA measured directly;
Na, K, bicarb, Cl;
also follow AG!!!
In HHS, what can cause altered mental status?
- Hyperosmolar state (hyperglycemia and dehydration)
- Acute renal failure
- Hypercalcemia
For HHS, what can cause decompensation?
- Infection
- Counterreg hormone increase
- Insulin resistance
- Hyperglycemia
- Dehydration
