Unit 2: Diabetic Ketoacidosis (DKA) Flashcards
Diabetic Ketoacidosis (DKA)
inadequate insulin for cells to obtain adequate glucose for normal metabolism
-seen in type 1 DM
How DKA Develops
- the body attempts to obtain energy by the rapid breakdown of fat stores, releasing fatty acids from adipose tissue
- the liver converts fatty acids into ketone bodies, which can serve as an energy source in the absence of glucose
- the ketone bodies, have a low pH = metabolic acidosis
- absence of insulin results in an increased release of hormones, such as glucagon and glycogenolysis, resulting in severe hyperglycemia; leading to hyperosmolality and osmotic diuresis
Causes of DKA
- Intentional or unintentional missed or reduced doses of insulin
- Inadequate insulin d/t increased insulin needs secondary to stress or infection
- new onset of type 1 DM
Initial Presentations of DKA
- polyuria (increased urinary output)
- polydipsia (increased thirst)
- polyphagia (increased hunger)
What Happens to the pt without treatment for DKA?
- patient becomes hypotensive and tachycardic b/c of the volume lost
- Kussmaul’s respirations
- fruity, acetone smell to breath b/c of ketone bodies
- complain of N/V
- lethargy and coma
Diagnosis of DKA
- Blood glucose greater than 250 mg/dL
- Ketonuria (ketones in urine)
- Arterial pH less than 7.3
- Serum bicarbonate level less than or equal to 18 mEq/L
Treatment for DKA
- Fluid replacement with isotonic normal saline
- Correction of electrolyte imbalances, focusing on monitoring and correction of decreased potassium level if necessary, prior to insulin administration
- Insulin administration, usually intravenously
Treatment: Fluid Replacement with isotonic normal saline
to reverse the dehydration that has resulted from the osmotic diuresis (polyuria)
Treatment: Monitoring and correcting electrolyte imbalances
to avoid dysrhythmias or neurological complications that can occur with potassium and sodium imbalances
Treatment: Administration of Insulin
to correct the hyperglycemia
Safety Alert: Correcting Potassium
- initially, hyperkalemia b/c of the movement of positively charged potassium ions out of the cell in an effort to maintain homeostasis as positively charged hydrogen ions move into the cell as they accumulate in the extracellular fluid
- hypokalemia then ensues as a result of the loss of extracellular potassium in the urine b/c of osmotic diuresis
- this results in severe total body loss of potassium, making patients susceptible to lethal arrhythmias
- care must be take to monitor potassium levels prior to treating hyperglycemia w/ insulin
- as insulin is administered to decrease hyperglycemia, potassium will also move back into the cell, worsening hypokalemia; potassium replacement is priority
Clinical Manifestation of DKA
- Polydipsia (increased thirst)
- Polyuria
- Polyphagia
- Lethargy
- Stupor
- Blurred Vision
- Fruity, acetone breath
- Kussmaul’s breathing (hyperventilation)
- N/V
- abdominal pain
- glycosuria (glucose in urine)
Kussmaul’s Respirations
rapid, deep respirations that occur as a compensatory mechanism for the acidosis
DKA Components
> No Insulin
- glucose cant enter into cells
- increased blood glucose >250
> Cells Need Fuel
- liver thinks hypoglycemic
- glucagon is released–> glycogen–>glucose
> Cells still need fuel
- body breaks down fats
- releases ketones
- acidotic (pH <7.3)
- fruity breath
> Kidneys can’t reabsorb glucose
- glucose is spilled into urine (glycosuria)
- osmotic diuresis
- Na+, K+, Cl+ are excreted
Hyperosmolar Hyperglycemia State
occurs when there is sufficient insulin to prevent rapid fat breakdown and ketone release; but there is not enough insulin to prevent severe hyperglycemia
- gradual onset
- usually for type 2 DM
- glucose level >600
- profound dehydration
- serum osmolality of 320 mOsm/kg or greater
- pH greater than 7.4
- alteration in LOC
- low/absence of ketones
