Outpatient management of diabetic ketoacidosis is inherently limited to early intervention during impending ketosis, as overt DKA with metabolic acidosis and volume depletion mandates emergency evaluation and inpatient intravenous resuscitation. In ambulatory patients with elevated capillary beta-hydroxybutyrate and hyperglycemia, home triage focuses on aggressive subcutaneous rapid-acting insulin administration, oral carbohydrate-electrolyte rehydration, and frequent ketone monitoring. However, persistent hyperketonemia exceeding 3.0 mmol/L, refractory nausea, vomiting, mental status alteration, or hemodynamic instability represent unequivocal failure of outpatient management requiring immediate transfer for intravenous insulin infusion, potassium repletion, and systemic acid-base correction.

Familial hyperaldosteronism type 2 is an autosomal dominant form of primary aldosteronism caused predominantly by gain-of-function mutations in the CLCN2 gene, which encodes the ClC-2 voltage-gated chloride channel. These mutations lead to increased channel opening, resulting in membrane depolarization of adrenal zona glomerulosa cells, activation of calcium signaling, and autonomous overproduction of aldosterone. Unlike type 1, this condition is non-suppressible with glucocorticoids and exhibits significant phenotypic overlap with sporadic primary aldosteronism, frequently presenting with early-onset hypertension, variable hypokalemia, and a high prevalence of aldosterone-producing adenomas. Diagnostic evaluation relies on demonstrating primary aldosteronism in multiple family members after excluding glucocorticoid-remediable aldosteronism, and clinical management centers on mineralocorticoid receptor antagonists or surgical adrenalectomy when unilateral adenomas are identified.