Diabetic Ketoacidosis (DKA) Flashcards
Diabetic Ketoacidosis (DKA)
Life-threatening condition
- Uncontrolled hyperglycemia,
- dehydration
- metabolic acidosis
- *PLUS production of KETONES
- Occurs with severe insulin deficiency
— Commonly in type 1 (insulin dependent)
HYPERGLYCEMIA
-Insulin is not available to put sugar into cell; Sugar levels rise
Increased blood sugar:
- Glucose can not enter cell so liver compensates via gluconeogenesis (production & release of glucose by liver)
- In response to physical & emotional stressors, there is an increase in stress hormones- these hormones promote more glucose production by liver
- If insulin levels are not increased during stress, hyperglycemia may progress to DKA
Absence of insulin= Fat is used for fuel
- glucose cannot be used by body cells for energy *AND fat is mobilized from adipose tissue to be used as a fuel source
Fat is converted by the liver into ketones
- The mobilized fat circulates in the blood- stream, from which it is extracted by the liver and broken down into glycerol and fatty acids. Fatty acids turn in to ketones.
- Ketones enter blood stream= Circulate to cells for conversion into: energy, CO2, H2O
Normally, ketones are used as fuel when glucose isn’t available
But, in DKA, ketones are produced more rapidly than body cells can use them and their accumulation produces acidemia
- Body compensates in order to buffer acidic hydrogen ions: in urine, lungs, kidneys
- Body’s compensation to buffer acidic hydrogen ions: by exchanging them for intracellular K+
— H+ions enter cells and kicks out potassium. K+ leaves the cells to be excreted in URINE - Another attempt to remove excess acid is in the LUNGS
— Kussmaul’s deep rapid respirations
— Eliminate more carbon dioxide and prevent formation of carbonic acid - KIDNEYS excrete some of the ketones thereby producing acetone in the urine
DKA=Uncontrolled hyperglycemia, metabolic acidosis and increased production of ketones
Causes of DKA
- Omission of insulin
— From decreased insulin or missed insulin dose (commonly associated with DM type 1) - Severe stress/Illness
— INFECTION, trauma, surgery, MI or stroke - Untreated or undiagnosed DM
— DKA worsens as compensatory mechanism fail.
S/S of DKA
- Hyperglycemia (serum glucose 250-800mg/dL)
— Excess glucose spills into urine
— Polyuria (increased urine)
— polydipsia (thirst)
— polyphasia (hunger) - Dehydration and electrolyte loss
— wt loss, dry skin, weakness, ha - Acidosis (Accumulation of ketone bodies)
— increased potassium
— fruity breath (acetone breath)
— kussmaul respirations - N/V, abd pain, tachycardia, orthostatic hypotension
- Glucose spills into the urine to be excreted (along with electrolyte loss; potassium)
- Blurred vision
- Drowsiness
DKA Labs:
- Serum glucose: 250-800mg/dL
- Serum pH: <7.35
- BUN >30 mg/dL (dehydrated)
- creatinine >1.5mg/dL (dehydrated)
- Serum & urine ketones: Present
- initial Na level: low or normal
- Initial K+ level: depends on length of DKA
— After therapy started (insulin drip), serum K quickly drops
DKA Nursing management
- Obtain IV access
— Blood chemistries
— CBC to check for infection (common precipitating factor)
— *IV Fluids (for hydration)
— *Insulin - Potassium monitoring & replacement
— Given with insulin drip
- Potassium monitoring & replacement
- ABG monitoring
- EKG monitoring for dysrhythmias
- Blood glucose checks
*Sick day rules
- Test your blood glucose and urine for ketones at least every 3-4hrs
- Prevent dehydration
- Call doctor for persistent nausea/vomiting
- Continue to take insulin or oral agents
- Test urine for ketones when BG > 240mg/dL
- Get plenty of rest
- If you are unable to retain fluids, you may require hospitalization to avoid DKA or even coma
A nurse assesses a client who is experiencing diabetic ketoacidosis (DKA). Which manifestations should the nurse monitor the client for? SELECT ALL THAT APPLY
- a. Deep and fast respirations
- b. Tachycardia
- c. orthostatic hypotension
- d. peripheral edema
- e. Crackles
A, B, C
