DKA/HHS Flashcards
DKA involves…
Ketoacidosis + Hyperglycemia
HHS involves…
More severe hyperglycemia without ketoacidosis
DKA
- More common <65
- Type 1 DM
- Can occur in type 2 under extreme conditions
HHS
Mostly Type 2
-More common >65
Extracellular concentration of glucose is regulated by?
- Insulin
2. Glucagon
Insulin restores normal glycemic levels by:
- Diminishing hepatic glucose production
- Decreases glycogenolysis + gluconeogenesis - Inc glucose uptake by skeletal muscle and adipose tissue
When serum glucose rises….
Glucose enters pancreas initiating insulin release by Beta cells
Hyperglycemia Causes
- Insulin deficiency and/or resistance
- More severe in DKA than HHS - Glucagon excess
- increased catecholamines
- Increased cortisol
DKA
Decreased Insulin secretion
-lipolysis + ketogenesis
HHS
Ineffective action of insulin
-osmotic duiresis
Serum glucose in HHS
Exceed 1000 mg/dL
Serum glucose in DKA
Below 800, often 350-450
- often present with symptoms of ketoacidosis rather than hyperosmolality
- Tend to be younger and have higher GFR
Ketone Production (DKA)
- Insulin def and resistance - can’t get glucose into the cells so body uses fat for energy (enhanced lipolysis in DKA)
- Lipolysis of peripheral fat stores releases FFA’s and glycerol
- FFAs are transported to liver and become “activated”
- Activated FFAs are converted to acetyl-CoA and enter ketogenic metabolic pathway forming “ketone bodies”
- Accumulation of ketone bodies causes a drop in pH (metabolic acidosis)
- Not seen in HHS due to having a bit more insulin available
Anion Gap Metabolic Acidosis
DKA presents with an elevated anion gap metabolic acidosis
Caused by production and accumulation of KETONES
Severity of acidosis and increase of anion gap factors
- Rate and duration of ketoacid production
- Rate of metabolism and ketoacids
- Rate of loss of ketoacid anions in urine
Anion Gap Definition
The difference between negative and positively charged electrolytes
-You want to close the gap (balance)
Plasma osmolality and sodium
Plasma osmolality is always elevated
-Higher the glucose, the higher the plasma osmolality
Hyperglycemia pulls water out of cells, expands ECF, reducing plasma sodium (dilutional hyponatremia)
Glucosuria causes osmotic diuresis leadings to excretion of NA+, K, water
Potassium
DKA + HHS have decreased K+
- increased urinary loss (with normal kidney function) GLYCOSURIA
- GI losses
* don’t treat K+ until pt. is symptomatic
Serum K+ is normal to high due to hyperosmolality and insulin deficiency
- Increased osmolality causes water + K+ to move out of cells
- Insulin normally promotes K+ uptake by the cells, lack of insulin contributes to increased K+ levels (Serum/ECF)
DKA: cellular compensation
Increase in [H+] seen in acidosis
- H+ move into cell
- More positively charged ions in the cell - K+ moves out of cell
- Electrical neutrality is restored inside of cell
- a temporary correction in pH
Process will reverse as the pH returns to normal
However, if the kidneys are working, they will excrete the excess K+ (from ECF)
Body can have depletion of K+ (dysrhythmias)
Precipitating Factors of HHS + DKA
HHS + DKA
1. Infection (PNA or UTI) without insulin adjustment
- Acute major illness or inflammatory process (MI, CVA, Sepsis, Pancreatitis)
- Drugs that affect CHO metabolism (steroids, thiazide diuretics’)
- Poorly compliance with insulin regimen or faulty sub-q insulin infusion device
DKA
- Use of SLGT2 inhibitors (treatment for type 1 or 2 DM)
- Cocaine use
- New onset of type 1 DM, DKA is often what triggers diagnosis
DKA S/S
- Rapid onset (over 24hrs)
- Polyuria, polydipsia
- GI effects (N/V/ abd pain)
- Neurologic effects
- combative
- drunk
- coma
- Volume depletion
- Dec skin turgor
- Dry mucosa
- Tachycardia
- Hypotension
- Fruity odor of breath (acetone)
- Kussmaul respirations
HHS S/S
Insidious (several days)
- polyuria
- polydipsia
- weight loss
As glucose continues to increase
- Lethargy
- Obtunded
- Coma
Signs of volume depletion similar to DKA
- Dec skin turgor
- Dry mucosa
- Tachycardia
- Hypotension
Treatments for DKA + HHS
- Fluid replacement
- Electrolyte imbalances (K+)
- Infusion of Insulin
- Sodium Bicarb
- DKA with Metabolic acidosis <7.2 - Dextrose added to saline when serum glucose fall below 200 mg/dL (DKA) if pt. still has anion gap (while still on continuous insulin infusion)
How do we know when DKA or HHS has resolved?
DKA: ketoacidosis has resolved (the anion gap has closed)
HHS: Patient is mentally alert and plasma osmolality has dropped to 315 mOsmol/kg
-Patent is able to eat and can transition back to SQ insulin (DKA + HHS)
DKA wrap up:
DKA is a condition of ketones in the blood, metabolic acidosis leading to anion gap, and usually hyperglycemia associated with insulin deficiency
Mostly affects type 1
Lack of adherence to insulin doses and or physiologic stressors (infection, MI) are common causes of DKA
Treat volume depletion rapidly with 0.9% NS, supplement K+ as needed, IV infusion of insulin
Monitor glucose, electrolytes, anion gap
HHS wrap up:
Marked hyperglycemia, dehydration, electrolyte imbalance, and hyperosmolality
Mostly affects type 2
Higher mortality rate
Symptoms of illnesses such as PNA + UTIs, insulin deficiency, inflammatory conditions (MI, Stroke, severe dehydration or use of some drugs can lead to HHS)
Treat volume depletion rapidly with NS, IV insulin, correct electrolyte imbalances
