Euglycemic DKA and Following the PATH

Euglycemic DKA and Following the PATH

Euglycemic DKA is ketoacidosis without marked hyperglycemia, and a normal fingerstick can delay diagnosis in patients with an anion gap metabolic acidosis. Uninsured diabetes care also fails when clinicians treat insulin access alone and miss transportation, food insecurity, health literacy, and behavioral health needs. Recognizing Euglycemic DKA Normal glucose trap: Euglycemic DKA can present with serum glucose around 90 to 120 mg/dL, so a reassuring point-of-care glucose should not exclude ketoacidosis when the acid-base picture fits. SGLT2 inhibitor risk: SGLT2 inhibitors are the standout medication trigger, and patients may be taking a “-liflozin” for heart failure or CKD without an obvious diabetes label in the chart. Compatible bedside picture: Nausea, vomiting, abdominal pain, tachypnea, and even Kussmaul respirations still define the syndrome; polyuria may be less impressive when glucose is not markedly elevated. Beta-hydroxybutyrate value: Beta-hydroxybutyrate is the key confirmatory test in unexplained anion gap acidosis, with levels above about 3 mmol/L supporting clinically meaningful ketoacidosis. Overlap ketoacidosis syndromes: Starvation ketosis and alcoholic ketoacidosis can closely resemble euglycemic DKA, and the distinction matters less than recognizing when both processes may need treatment. We get into that overlap in the episode. Managing Euglycemic DKA Insulin still closes the gap: The core pathophysiology is ongoing ketogenesis, so insulin remains essential even when glucose is normal because it is the treatment that reverses the metabolic process. Early dextrose strategy: Dextrose-containing fluids usually need to start early rather than waiting for glucose to fall, because dextrose protects against hypoglycemia while insulin keeps running. Two separate treatment dials: Think of insulin and dextrose as independent dials: insulin suppresses ketone production and closes the anion gap, while dextrose maintains a safe serum glucose. Potassium before insulin: Potassium assessment comes first, because insulin rapidly shifts potassium intracellularly and can worsen dangerous hypokalemia before the acidosis has time to improve. Resolution markers that matter: Serum glucose is not the endpoint; resolution is tracked by closing the anion gap, improving bicarbonate and pH, and following ketosis markers. We walk through those priorities in the chapter. PATH Clinic for Uninsured Diabetes Care Whole-person diabetes barriers: Uninsured diabetes care breaks down from food insecurity, housing instability, transportation limits, and low health literacy as often as from lack of insulin itself. Multidisciplinary wraparound model: PATH pairs diabetes management with social work, behavioral health, nutrition, optometry, and wound care, reflecting that glucose control alone does not prevent complications. Prescription access infrastructure: Prescription Assistance Programs can secure insulin, GLP-1 agents, SGLT2 inhibitors, inhalers, and DOACs, but the real intervention is staff who know how to navigate the paperwork. Care coordinator impact: Care coordinators are the operational backbone, actively rebooking missed visits and reconnecting patients to specialty and primary care instead of waiting for them to return. Transitional clinic design: PATH is built as a bridge rather than permanent primary care, with handoffs that include current regimens, assistance renewals, and follow-up after transfer. That transition piece is worth hearing in the podcast. Building a similar program: A practical starting point is one high-utilization population and one achievable intervention, then tracking ED use, admissions, and cost avoidance to make the case for institutional support.