Free interactive case study · NGN style
The six steps of an NCLEX case study on a live patient: recognize, analyze, prioritize, act, evaluate. Every value on the panel answers the way a real patient’s would, and a wrong move runs and shows its harm before you rewind.
Tap the finding that tells you what is wrong with her.
Anything with a dashed outline is tappable — labs, vitals, the strip, the tank.
Handoff · 24-year-old, type 1 diabetes, insulin pump failed two days ago
Breathing deeply and fast, breath smells fruity, abdominal pain and vomiting since yesterday. Alert but exhausted, mucous membranes dry, heart rate 112. Glucose reads HIGH on the meter. The potassium came back at 5.4 and the new graduate wants to hold potassium replacement.
Arterial blood gas
Chemistry
Bedside monitor · pattern
Less circulating volume means less venous return, so the heart rate rises to defend the pressure before the pressure falls.
A compensatory sinus tachycardia — usually volume, pain, fever or hypoxia until proven otherwise.
Tachycardic, hypotensive, oliguric, dry axilla, tenting skin. Isotonic fluid and hourly urine output.
Explore the physiology
Starts on her arrival numbers, with the lungs free to compensate. Every readout comes from the same model as the case.
An osmole outside the cell: it dilutes the sodium, drags water into the urine, and — without insulin — leaks potassium out of cells.
The ketoacid burden. As it falls the pH falls, potassium trades out of cells, and the lungs answer with Kussmaul breathing (Winter’s formula).
What the serum shows. Compare it with the shift the model calculates — the difference is the potassium she has actually lost.
pH
7.22
PaCO₂
20
Winter’s 18–22
RR
29
Kussmaul when deep + fast
Anion gap
24
high — acid added
Na⁺ measured
128
Na⁺ corrected
136
+1.6 per 100 of glucose
K⁺ that is shift
2.9
acidosis 1.6 · no insulin 1.3
Volume
76%
Severe deficit
Urine
117 mL/h
polyuric AND dry
HR / BP
112 · 86/53
Why values move together
DKA is not a sugar problem with an acid attached. It is a volume problem, then a potassium problem, then an insulin problem — and the classic fatal shortcut is insulin first.
Fluids first — isotonic saline restores perfusion and starts lowering the glucose before any insulin is given.
Potassium next — replace once it is under 5.2 with urine output present. Hold insulin entirely below 3.3.
Insulin third — a continuous infusion, never a bolus, and never before you know the potassium.
The acidosis corrects itself as insulin stops ketone production. Bicarbonate is reserved for a pH below about 6.9.
Add dextrose when glucose reaches roughly 200 so the insulin can keep running until the gap closes.
The exam does not ask what a value is. It asks what the value means for this patient — and in DKA three of them mean the opposite of what they say.
Acidosis pushes potassium out of cells and insulin deficiency keeps it there, so the serum level reads high — while the osmotic diuresis has been dumping total-body potassium into the toilet for two days. This patient is potassium DEPLETED at a level of 5.4. The moment insulin starts, potassium crashes.
Corrected for a glucose of 620, that sodium of 128 is really about 136. Nothing is wrong with the sodium. Treat the glucose and it comes back on its own — in fact it will RISE as the glucose falls, which is expected, not a complication.
A CO₂ of 22 is the lungs defending the pH against a gap acidosis of 24. Do not sedate it and do not be reassured when it slows down — a falling respiratory rate here means the patient is tiring, and the pH is about to fall off a cliff.
Fluids first, potassium second, insulin third. Isotonic saline restores perfusion and starts lowering the glucose by itself. Potassium is checked and replaced once it is below about 5.2 with urine output present, because insulin will drive it into cells. Insulin runs as a continuous infusion only after the potassium is known, and dextrose is added when the glucose reaches roughly 200 so the insulin can keep running until the anion gap closes.
Acidosis moves hydrogen ions into cells and potassium out, and without insulin nothing moves potassium back in. The serum level reads high or normal while two days of osmotic diuresis have been losing potassium in the urine. Once insulin starts, the shifted potassium returns to the cells within hours and the serum level falls fast — which is why potassium is replaced while insulin runs, not after the level drops.
Glucose is an osmole that stays outside the cell, so it pulls water out of cells and dilutes the sodium reading. Corrected sodium adds about 1.6 mEq/L for every 100 mg/dL of glucose above 100. A sodium of 128 with a glucose of 620 corrects to about 136, which is normal. The sodium rises as the glucose falls, and that rise is expected rather than a complication.
No. Deep, fast breathing blows off carbon dioxide to defend the pH against the metabolic acidosis. It is compensation, and Winter’s formula (expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2) shows whether the lungs are on target. A respiratory rate that slows before the acidosis clears is a sign of fatigue and an emergency, not an improvement.
The acidosis corrects itself once insulin stops ketone production. Bicarbonate drives potassium into cells and worsens the hypokalemia that follows, shifts the oxygen curve the wrong way, and can cause paradoxical acidosis in the brain. It is reserved for a pH below about 6.9.
When the glucose reaches about 200–250 mg/dL, dextrose is added to the fluids so the glucose holds while the insulin keeps running. The insulin is there to shut off ketone production, not to lower the glucose. DKA is resolved when the anion gap has closed and the bicarbonate has recovered, whatever the glucose reads.
With an overlap. Once the gap is closed and the patient is eating, the basal subcutaneous insulin is given first and the drip continues for one to two hours afterwards, so there is never a moment without insulin on board. Stopping the drip and giving the injection later reopens the gap in the hours between.
No. It is a nursing education model. The couplings reproduce the direction and rough size of the relationships students are tested on, the compensation band uses Winter’s formula, and the intervention effects are authored to match the textbook response. Real patients move on their own schedule and depend on the cause, the timing and the whole clinical picture.
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