Endocrine · Topic 12 of 17
A blood glucose of 350 mg/dL with a pH of 7.2 and fruity breath tells you the body is burning fat for fuel — and the acid it produces can kill before the sugar does.
This topic's case study · live
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.
Start here
Absolute or relative insulin deficiency forces the body to burn fat for fuel. Lipolysis and ketogenesis flood the blood with ketoacids (beta-hydroxybutyrate, acetoacetate, acetone), overwhelming buffers and producing an anion-gap metabolic acidosis. Hyperglycemia drives osmotic diuresis, causing profound dehydration and total-body electrolyte loss. Often triggered by missed insulin doses or an acute illness.
Pathophysiology of DKA
mg/dL
Clinical Pearl
Fluids first, potassium second, insulin third: if K+ is below 3.3, insulin will crash the heart before the acidosis does.
DKA occurs when absolute or relative insulin deficiency forces the body to break down fat for energy, producing ketone bodies (beta-hydroxybutyrate, acetoacetate, acetone) that overwhelm buffering capacity and cause metabolic acidosis. Classic lab findings: blood glucose typically 250–600 mg/dL, arterial pH below 7.30, serum bicarbonate below 18 mEq/L, positive serum ketones, and an elevated anion gap. Clinical presentation includes Kussmaul respirations (deep, rapid breathing — the lungs compensating for acidosis), fruity acetone breath, polyuria, polydipsia, nausea/vomiting, abdominal pain, and altered mental status. Treatment priorities follow a specific sequence: aggressive IV fluid resuscitation first (0.9% NS initially to correct dehydration), then continuous IV regular insulin infusion (not subcutaneous, not rapid-acting analogs), and potassium replacement guided by serum levels — potassium must be at least 3.3 mEq/L before starting insulin, because insulin drives potassium intracellularly and can cause fatal hypokalemia. Monitor glucose hourly; when it drops to 250 mg/dL, switch IV fluids to D5 with half-normal saline to prevent hypoglycemia and cerebral edema while continuing the insulin drip until the anion gap closes.
Don't confuse DKA with HHS — DKA has significant acidosis and ketones with moderately elevated glucose; HHS has extreme hyperglycemia (often >600 mg/dL) with minimal ketosis and no significant acidosis. Students assume you correct glucose first, but fluids come first and potassium status determines when insulin can safely start. Kussmaul respirations are compensatory for metabolic acidosis, not a respiratory problem — do not treat with oxygen or bronchodilators.
Fluids first, potassium second, insulin third. If K+ is below 3.3, giving insulin without replacing potassium can stop the heart before the acidosis does.
3 quick questions on the must-knows for this topic.
What is given first in DKA treatment?
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