{"operator":"Indus Intellect LLC","notice":"Every case is a Draft - not clinically validated, pending Dr. Carlo Raj clinical sign-off. Educational simulation content only; not medical advice. No doses are published. No CME.","access":"teaser","case":{"id":"ER_DKA_001","title":"Diabetic ketoacidosis — ER resus bay (vertical slice)","draft_flag":"Draft - pending Dr. Carlo Raj clinical sign-off","validated":false,"objectives":["Insulin deficiency -> increased fat catabolism -> ketone bodies (beta-hydroxybutyrate, acetoacetate, small amounts of acetone).","Calculate the anion gap, Na - (Cl + HCO3), normal 8-12, and place DKA in the high-AG (MUDPILES) differential.","Kussmaul respirations are respiratory compensation for metabolic acidosis (decrease in pCO2 = 1.25 x change in HCO3).","Potassium shifts: acidemia and insulin deficiency move K out of cells; insulin moves K into cells; DKA causes renal K loss.","Management: IV fluids; insulin infusion until the AG acidosis resolves; dextrose once glucose < 200 mg/dL; monitor and replete K, Mg, phosphate; SC insulin overlap before stopping the infusion; find the precipitant."],"foundation_concept":null,"presentation":{"symptoms":"fatigue, blurred vision, polydipsia, polyuria, weight loss, nausea, vomiting, abdominal pain","signs_breathing":"Kussmaul (rapid, deep) respirations, fruity breath","signs_habitus":"drowsy and thin"},"vitals":{},"history_items":["Asks about missed insulin","Asks about polyuria/polydipsia","Asks about weight loss","Asks about nausea, vomiting, abdominal pain"],"exam_items":[],"orders":["Orders electrolytes incl. K","Look for the precipitant (new-onset DM, missed insulin, infection)"],"results":{"pattern":"hyperglycemia, anion gap acidosis, ketonemia","pH_arterial":"7","glucose":"575 mg/dL","BUN":"74 mg/dL","creatinine":"2 mg/dL","formula_AG":"AG = Na - (Cl + HCO3), normal 8-12","formula_osm":"Calculated osmolarity = 2[Na] + BUN/2.8 + Glucose/18"},"interventions":["IV fluid resuscitation","Insulin infusion until AG acidosis resolves","Stops the insulin infusion","Add dextrose to IVF when glucose < 200 mg/dL","Monitor and replete K, Mg, phosphate","SC insulin before discontinuing the infusion"],"differential":[],"critical_actions":["Fluids started early","Anion gap calculated","K checked before/with insulin and repleted","Insulin infusion started","Dextrose added at glucose < 200 while insulin continues","Insulin continued until the gap closes","SC overlap before stopping the drip","Precipitant searched for"],"harmful_actions":["Stopping insulin because glucose normalised while the gap is still open","Starting insulin with no K monitoring (insulin shifts K into cells)"],"mechanism":{"prompt":"Why is this patient acidotic and breathing like this?","steps":["Insulin deficiency -> fat catabolism -> beta-hydroxybutyrate, acetoacetate, acetone","Protein catabolism to glucose (muscle wasting)","Unmeasured ketoacid anions -> high-AG metabolic acidosis","Kussmaul breathing raises alveolar ventilation to compensate","K shifts with acidemia and insulin"],"question":{"text":"R1 Question 1 (IndusIntellect-owned; cleared 2026-09-25)","options":[{"id":"beta_hydroxybutyrate","text":"Correct. Without insulin, fat breakdown accelerates and the liver turns it into ketone bodies: beta-hydroxybutyrate, acetoacetate and a little acetone. That ketoacid load explains the very low pH, the fruity breath and the rapid, deep (Kussmaul) breathing."},{"id":"ammonia","text":"Ammonia rises when nitrogen can't be cleared through the urea cycle (e.g. OTC deficiency, where BUN is low) or in fatty-acid oxidation defects such as MCAD. This patient's BUN is high, and his acid is ketoacid from fat breakdown, not ammonia."},{"id":"carnitine","text":"Fatty acyl-carnitines build up when fat can't be broken down (MCAD deficiency), which presents with low glucose and no ketones. This patient is the opposite: glucose 575 with ketoacidosis."},{"id":"isovaleric_acid","text":"Not one of the ketone bodies produced in DKA (beta-hydroxybutyrate, acetoacetate, acetone)."},{"id":"sodium","text":"Not increased. High glucose causes an osmotic diuresis, a renal loss that tends toward low (hypovolemic) sodium, not high."}],"answer":"beta_hydroxybutyrate"}},"disposition":null,"notes":["HHS: mainly T2DM; osmolarity > 320, glucose > 600, pH > 7.3"]}}