Nursing care
Diabetic Ketoacidosis nursing care: what to assess and what to do first
Written and reviewed by Dana Whitfield, RN, MSN · 5 min read · Updated September 2026
Short answer
Diabetic ketoacidosis is managed with IV fluids first, insulin second, and potassium replaced early because it falls once insulin drives glucose and potassium into cells together. Assess airway, breathing, and circulation, then check glucose, ketones, and electrolytes. Untreated, it progresses from Kussmaul respirations and fruity breath to cerebral oedema and cardiac arrhythmia.
The clinical picture
DKA develops over hours, usually in a patient with type 1 diabetes, though it occurs in type 2 diabetes under severe stress such as infection or missed insulin doses. The triad is hyperglycaemia, ketosis, and metabolic acidosis. Expect a glucose above 250 mg/dL, though DKA can occur with near-normal glucose in patients on SGLT2 inhibitors, pregnant patients, or those who have been fasting.
The patient compensates for the acidosis with Kussmaul respirations, deep and rapid breathing that blows off CO2. Breath often carries a fruity, acetone odour from exhaled ketones. Polyuria and polydipsia precede the acute presentation, then reverse into dehydration as the patient becomes too unwell to keep drinking. Abdominal pain, nausea, and vomiting are common and can mimic a surgical abdomen, which delays recognition in patients who do not have a known diabetes diagnosis.
Assessment: what to look for and in what order
Start with airway, breathing, and circulation. A patient who is obtunded or vomiting needs airway protection before anything else. Check level of consciousness: DKA causes drowsiness through acidosis and dehydration, and a sudden change, especially in a paediatric patient, raises concern for cerebral oedema.
Move to vital signs. Expect tachycardia and hypotension from volume depletion, and Kussmaul respirations with a respiratory rate that looks laboured but is actually compensatory, not primary respiratory distress. Assess skin turgor, mucous membranes, and capillary refill for dehydration severity. Order point-of-care glucose, venous or arterial blood gas, serum ketones or beta-hydroxybutyrate, and a basic metabolic panel including potassium, before any treatment starts. The anion gap and bicarbonate track how deep the acidosis runs and how treatment is progressing.
Immediate interventions
Fluids come before insulin. The first hour typically calls for isotonic saline, often 15 to 20 mL/kg or roughly a litre in an adult, to restore intravascular volume and improve perfusion before insulin is started. Giving insulin into an underfilled circulation risks a precipitous drop in blood pressure and does little to correct the underlying acidosis if tissues are not being perfused.
Once fluids are running, start a continuous IV insulin infusion, typically 0.1 units/kg/hour, to switch off ketogenesis and lower glucose gradually. The potassium level often looks normal or even high at presentation because acidosis shifts potassium out of cells into the serum. Insulin reverses that shift, driving potassium back into cells, so the measured level falls fast once treatment starts. Potassium replacement is started proactively, before the number on the chart looks low, and insulin is held if potassium is already under 3.3 mEq/L to avoid a dangerous further drop.
Ongoing nursing management
Monitor glucose hourly and electrolytes, particularly potassium, every two to four hours while the insulin infusion runs. Glucose should fall by no more than 50 to 100 mg/dL per hour; a faster drop risks cerebral oedema, especially in children. Once glucose reaches around 200 mg/dL, dextrose is added to the fluids so the insulin infusion can continue correcting the acidosis without causing hypoglycaemia.
Track strict intake and output, and watch for signs of fluid overload in patients with renal or cardiac impairment. Do not stop the insulin infusion once glucose normalises; the acidosis, not the glucose, is what the infusion is treating, and it closes only once the anion gap normalises and bicarbonate recovers. Overlap subcutaneous insulin with the IV infusion by one to two hours before discontinuing it, since stopping the infusion abruptly risks rebound ketosis.
Patient and family education
Sick-day rules are the single most useful thing a patient leaves with. Insulin is never stopped during illness, even when appetite drops, because counter-regulatory hormones raise glucose regardless of intake. Teach the patient to check glucose and ketones every four hours when unwell, and to seek care if ketones are moderate to large or if vomiting prevents fluid intake.
Review the events that led to this admission with the patient: a missed dose, a pump failure, an infection, or a first presentation of undiagnosed diabetes. Confirm they know how to recognise early symptoms, polyuria, polydipsia, fatigue, and abdominal discomfort, and who to call before those symptoms progress to Kussmaul breathing. Involve family or caregivers in insulin administration and glucose monitoring where the patient's ability to self-manage during illness is in doubt.
How this appears on the NCLEX
NCLEX items on DKA frequently test the fluids-before-insulin sequence, and a distractor answer that starts insulin first is the classic wrong choice. Expect questions that give a potassium level within normal range and ask what to do before starting the insulin infusion; the correct answer holds or adds potassium proactively, because the exam is testing whether you understand the shift insulin is about to cause.
Priority questions often present Kussmaul respirations alongside fruity breath and ask what they indicate; select respiratory compensation for metabolic acidosis, not primary respiratory failure. Select-all-that-apply items test the full assessment picture: polyuria, polydipsia, fruity breath, abdominal pain, and altered mental status. Watch for questions distinguishing DKA from HHS by the presence of ketones and a lower glucose threshold.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our endocrine practice questions are the closest set to what this page covers.
Common questions
Why is insulin held even though the potassium level looks normal in DKA?
Acidosis pushes potassium out of cells, so the serum level often reads normal or high despite total-body potassium being depleted. Once insulin starts, it drives potassium back into cells and the serum level drops quickly. Insulin is withheld or given cautiously if potassium is below 3.3 mEq/L until replacement is underway.
How fast should glucose come down in DKA treatment?
No more than 50 to 100 mg/dL per hour. A faster correction, especially in children and adolescents, is linked to cerebral oedema. Dextrose is added to the IV fluids once glucose reaches around 200 mg/dL so the insulin infusion can keep correcting the acidosis without overshooting the glucose drop.
Can DKA happen with a near-normal blood glucose?
Yes. This is called euglycaemic DKA and is seen with SGLT2 inhibitor use, pregnancy, or prolonged fasting. The ketosis and acidosis are still present, so diagnosis relies on the anion gap and ketone levels rather than glucose alone.
When is the IV insulin infusion stopped?
Once the anion gap has normalised and bicarbonate has recovered, not simply when glucose falls into range. Subcutaneous insulin is overlapped with the IV infusion for one to two hours before the infusion is discontinued, to prevent a gap in insulin coverage that can trigger rebound ketosis.
What distinguishes DKA from HHS on assessment?
DKA presents with ketosis, a significant anion gap, and Kussmaul respirations, usually at a lower glucose than HHS. HHS involves markedly higher glucose with little or no ketosis, because residual insulin is enough to prevent ketogenesis but not enough to control glucose.