DKA & HHS Flashcards
Complication of Type 1 Diabetes; usually due to missed/inadequate doses of Insulin, infection, or other stressor –> insufficient insulin –> high BG and acid formation; unchecked glycogenolysis, gluconeogenesis and ketogenesis; production of ketones resulting in metabolic acidosis and hyperventilation; mortality is highest in YOUNG
Diabetic Ketoacidosis
Diabetic Ketoacidosis is usually seen in type (1/2) diabetics
Type 1
Diabetic Ketoacidosis has a high mortality in the (young/elderly)
Young
What medication requires increased insulin requirement, leading to DKA?
steroids
What drug requires increased insulin requirement, leading to DKA?
Cocaine
What counterregulatory hormones require increased insulin requirement, leading to DKA?
glucagon
cortisol
catecholamines
Symptoms of Diabetic Ketoacidosis
Thirst Polyuria Weakness SOB Abdominal pain Nausea/vomiting
Physical exam findings of Diabetic Ketoacidosis
Tachycardia Hypotension Orthostasis Dry membranes/poor skin turgor Hypothermia ** Kussmaul respirations (fruity breath)
Lab findings of Diabetic Ketoacidosis
- Elevated BG
- Positive serum and urine ketones
- Decreased HCO3, Increased AG
- pCO2 <40
Kussmaul respirations are characterized as (shallow/deep) and (rapid/slow) breaths
Deep and Rapid
*early on, can be shallow
Pathogenesis of Diabetic Ketoacidosis
- Insulin deficiency
- Glycogenolysis and gluconeogenesis–> HYPERGLYCEMIA–> osmotic diuresis–> dehydration
- Lipolysis –> Ketogenesis–> anion gap metabolic acidosis
3 MOA of the body against acidosis
- Kidney
- Excretion of ketone bodies
- Buffer ketone bodies - Blood
- Serum bicarbonate, bone, and intracellular proteins buffer hydrogen ions - Lung
- acidosis stimulates hyperventilation, and this blows off CO2
Because of the body’s defenses against acidosis –> ketone bodies are present initially in ____ without high blood levels, then later in higher concentrations in _____ without actual fall of arterial pH (due to serum bicarbonate)
- urine
- blood
When the body’s defenses against acidosis eventually fail, what characteristic picture occurs?
- Low bicarbonate
- Low pCO2
- Low arterial pH
- High anion gap
The sum of measured cations minus measured anions
anion gap
In normal anion gap, what represents unmeasured anions in the blood?
negatively charged phosphates and sulfates
In DKA, anion gap represents what unmeasured anions in the blood?
ketone bodies
The best indicator of SEVERITY of the DKA
Anion gap
Closing or normalization of ______ is the best indicator of successful treatment for DKA
Anion gap
Equation for Anion Gap
Na - (Cl + HCO3)
*should be less than or equal to 12
The Anion Gap should be less than or equal to
12
severity of (acidosis/hyperglycemia) is the best indicator of of the severity or the successful treatment of DKA
acidosis (pH, AG)
pH, HCO3, and Anion gap for MILD DKA
pH: 7.25-7.3
HCO3: 15-18
Anion Gap: >10
pH, HCO3, and Anion gap for MODERATE DKA
pH: 7.0-7.24
HCO3: 10-14
Anion Gap: >12
pH, HCO3, and Anion gap for SEVERE DKA
pH: <7.0
HCO3: <10
Anion Gap: >12
Examples of ketones
Acetone
Acetoacetate
B-hydroxybutyrate
Lab test that can be used to measure ketones
Nitroprusside Reaction
- Detects ONLY acetone and acetoacetate
Which ketone is NOT measured by the Nitroprusside reaction
B-hydroxybutyrate
the one that predominates in DKA
Which ketone predominates in DKA but doesn’t get measured by Nitroprusside Reaction?
B-hydroxybutyrate
What ketone is not an acid but can cause fruity smell?
Acetone
Why is severity of DKA measured by AG and not by amount of ketones?
- Nitroprusside reaction detects only acetone and acetoacetate but NOT B-hydroxybutyrate
- Acetoacetate can be dominant in recovery and therefore be misleading
Complication of Type 2 Diabetes; usually due to missed/inadequate doses of Insulin, infection, or other stressor –> insufficient insulin –> VERY high BG and Osmolality + DEHYDRATION; can result in confusion and dizziness; mortality is highest in ELDERLY
Hyperglycemic Hyperosmolar State (HHS)
What medications can cause HHS?
** corticosteroids
thiazides
Phenytoin (anticonvulsant)
** most common
What precipitating factors/comorbidities can cause HHS?
- Infection
- Thromboses
- Hemorrhage
- Burn
- Pancreatitis
- Renal failure
Signs/Symptoms of HHS
Thirst/Dehydration Dementia/AMS High BG High serum Osm Hypotension
Hyperglycemic Hyperosmolar States are more common in type (1/2) diabetics
Type 2
Hyperglycemic Hyperosmolar State has a high mortality in the (young/elderly)
Elderly
Pathogenesis of HHS
- Insulin deficiency
- Glycogenolysis and gluconeogenesis–> HYPERGLYCEMIA –> osmotic diuresis–> dehydration –> decreased fluid intake –> HYPEROSMOLARITY
DKA/HHS has greater severity of dehydration, hyperglycemia, hypernatremia, and hyperosmolality
HHS
(T/F) Ketogenesis in HHS is sufficient to produce a medically significant metaboilc acidosis
False
Measure of the number of dissolved particles (solute) per unit of water (solvent) in serum; the concentration of an osmotic solution
Serum osmolality
Equation for Serum Osmolality
2 x Na + glucose/18 + BUN/3
- Normal is 285-295 mosm/L
Normal Serum Osmolality
285-295 mOsm/L
What is the best indicator of severity of HHS?
degree of hyperosmolality
BG, pH, HCO3, and serum Osm for HHS
BG: Very High (>600)
pH: >7.3
HCO3: >18
Osm: >320 mOsm/kg
The mortality of (DKA/HHS) is higher
HHS because of the coexistence of a serious underlying precipitating illness (seizures, thromboses, embolism, etc.)
Treatment for DKA and HHS
**fix dehydration FIRST!
- Volume replacement (isotonic-0.9% NaCl –> hypotonic-0.45 –> 5% dextrose w/ 0.45% NaCl + insulin)
- Insulin
- POTASSIUM (arrhythmias)
What diabetes therapy can cause elevated anion gap with normal blood glucose, urinary frequency, and abdominal pain?
SGLT-2 inhibitor therapy
Why is potassium so fickle during DKA
Acidosis causes potassium to shift OUT of cells, showing hyperkalemia (masking the overall deficit)
Insulin then causes potassium to reenter cell, possibly causing life-threatening hypokalemia
What are causes of Morbidity/Mortality in DKA and HHS
Iatragenic: (due to fluid resuscitation)
- Cerebral edema
- Hypoglycemia
- Hypokalemia
- Hypophosphatemia
End-Organ Problems:
- Acute Renal failure
- ARDS
- Vascular Thrombosis
- Sepsis
When do you switch to 5% dextrose w/ 0.45% NaCl in DKA patients?
When serum glucose reaches 200 mg/dL
When do you switch to 5% dextrose w/ 0.45% NaCl in HHS patients?
When serum glucose reaches 300 mg/dL
When do you give 20-30 mEq of K+ in each liter of IV fluid to keep serum K b/w 4-5 mEq/L?
when serum K+ is 3.3 to 5.3 mEq/L
When do you hold insulin and give 20-40 mEq of K+ per hour until K+ > 3.3 mEq/L?
when serum K+ is < 3.3 mEq/L
When is K+ not needed but serum K+ must be checked every 2 hours?
when serum K+ is > 5.3 mEq/L
How much insulin should be given for DKA and HHS patients?
Regular insulin 0.1 units/kg as IV bolus
When do you reduce regular insulin infusion to 0.02-0.05 units/kg for DKA patients?
when serum glucose reaches 200 mg/dL
When do you reduce regular insulin infusion to 0.02-0.05 units/kg for HHs patients?
when serum glucose reaches 300 mg/dL
When do you give bicarbonate for DKA patients?
when pH is <6.9
Triglycerides are utilized to produce what forms of energy? (2 total)
Free fatty acids
Ketones
What are other triggers of Ketosis, besides Diabetic Ketoacidosis
Alcohol
Starvation
Isopropyl alcohol
What are other triggers of acidosis, besides Diabetic Ketoacidosis
Lactic acid
Alcohol (ETOH, methanol, ethylene glycol)
Salicylates