Diabetic Ketoacidosis
Pathophysiology
NO insulin → can’t get glucose into cell→ breaks down fatty acids for energy → Ketones (acids) → metabolic
acidosis
Osmotic diuresis → dehydration
No insulin → ↑ liver glucose production → hyperglycemia (higher)
Risk Factors o Type 1 diabetes not taking insulin
Signs and Symptoms Fruity breath,
(We treat signs and Rapid, deep respirations (Kussmaul)
symptoms) Weakness
Abdominal pain
Cardinal signs: Blurred vision
Fruity breath Headache
Rapid, deep respirations Polyuria
(Kussmaul) Polydipsia
Weakness Dehydration
Abdominal pain Poor skin turgor
Dry mucuous membranes
Orthostatic hypotension
Weakness
lethargy
VITALS:
RR > 30
HR > 100
BP – low
Temp – 99 – 99.5
Electrolytes
High Potassium
Low sodium
Low magnesium
Low phosphorous
Low chloride
Treatment ▫ Rehydrate NS, ½ NS (hours in to avoid FVO), D5NS (250-300, bring down slowly
to prevent hypoglycemia and rebound DKA)
Serum sodium high but ▫ K+ replacement once voiding reestablished
TRUE HYPOKALEMIA – ▫ Must be supplemented even if serum K+ normal.
not in cells where ▫ IV Regular insulin 5u/hr until serum bicarb = 15-18 mEq/mL AND pt can eat
needed ▫ Monitor orthostatic hypotension
▫ Initiate fall risk/safety precautions
▫
Labs and Diagnostic Tests
Name of Test Expected Finding Normal Finding
pH <7.35 7.35 – 7.45
HCO3 < 22 22 - 26
UA ketones No ketones
UA High range
K+ >5 3.5 - 5
Glucose 300 - 800 mg/dL 70 - 100
BUN > 20 10 – 20
creatinine > 1.2 0.6 – 1.2
Nursing Goals
Nursing Management/Interventions
Assessments First nursing action: Begin fluid replacement/ check electrolytes
Place on ECG—careful cardiac monitoring necessary
Frequent VS, lung assessment
Monitor I&O to prevent FVO
Correct acidosis
Insulin therapy → helps stop fatty acid breakdown
Insulin therapy continues until anion gap acidosis has fully resolved.
Interventions
Complications to Avoid