Pathophysiology - Sugar High, Acid Low
- Absolute or relative insulin deficiency coupled with ↑ counter-regulatory hormones (glucagon, cortisol, catecholamines) is the central defect.
⭐ The accumulation of ketone bodies (anions) consumes bicarbonate (buffer), creating a high anion gap metabolic acidosis. Calculate it: $Anion~Gap = Na^+ - (Cl^- + HCO_3^-)$.
Presentation & Diagnosis - The Fruity Breath Clue
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Classic Triad (3 P's): Polyuria, Polydipsia, Polyphagia.
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Dehydration Signs: Tachycardia, hypotension, ↓ skin turgor, dry mucous membranes.
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Pathognomonic Signs:
- Kussmaul Respirations: Deep, rapid breaths to compensate for acidosis.
- Fruity Breath: Acetone odor.
- Abdominal pain, nausea/vomiting (can mimic acute abdomen).
- Altered mental status (lethargy, coma).
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Diagnostic Criteria (The "D-K-A"):
- Diabetes: Blood Glucose > 250 mg/dL.
- Ketosis: Positive serum or urine ketones.
- Acidosis: Arterial pH < 7.3 AND Serum Bicarbonate < 18 mEq/L.
- Anion Gap: Elevated, $AG = Na^+ - (Cl^- + HCO_3^-)$.
⭐ Despite normal or even high initial serum K+, patients have a profound total body potassium deficit due to transcellular shifts. Insulin therapy will unmask severe hypokalemia if not corrected.
Management & Complications - The Fluid-Insulin Fix
Core goals: Restore volume, correct acidosis/hyperglycemia, replete electrolytes, and treat the precipitate.
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IV Fluids (First!):
- Start with 1-2L of 0.9% NaCl (isotonic saline) over the first 1-2 hours.
- When serum glucose reaches ~200-250 mg/dL, switch to D5 1/2 NS to prevent hypoglycemia.
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Insulin Therapy:
- Start after initial fluid resuscitation and checking potassium.
- Regular insulin IV infusion at 0.1 U/kg/hr.
- Goal: ↓ glucose by 50-75 mg/dL/hr.
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Potassium (K+):
- ⚠️ Total body K+ is depleted, even if serum levels are normal/high.
- Insulin drives K+ into cells, causing rapid ↓ in serum K+. See flowchart for specific management.
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Resolution Criteria:
- Glucose < 200 mg/dL
- Anion Gap < 12 mEq/L (Formula: $Na^+ - (Cl^- + HCO_3^-)$)
- Serum HCO3 ≥ 15 mEq/L
⭐ The most common iatrogenic complication and cause of mortality in pediatric DKA is cerebral edema, often due to overaggressive fluid resuscitation and rapid reduction in plasma osmolality.
- DKA is a triad of hyperglycemia, ketosis, and anion gap metabolic acidosis.
- Primarily in Type 1 Diabetes, often precipitated by infection or insulin non-compliance.
- Presents with Kussmaul respirations and a characteristic fruity breath odor.
- First step in management is always aggressive IV fluid resuscitation, followed by IV insulin.
- Total body potassium is depleted, although serum levels may be normal or high initially.
- Monitor and correct hypokalemia as insulin will shift potassium into cells.
- The primary therapeutic goal is to close the anion gap.
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