Euglycemic Ketoacidosis Entered Through the Asthma Doorway
A 19-year-old man arrived in the emergency department with nausea, mild dyspnea, restlessness, and drowsiness. He also had a prior label of mild intermittent asthma, and the first bedside impression fit that history: wheezing, mild hypoxia, and no dramatic hyperglycemia. Oxygen was started, the saturation improved, and the early working diagnosis was an acute asthma exacerbation.
The physiology was pointing elsewhere.
Within two hours, the clinical picture shifted. He developed abdominal pain, vomited twice, became more drowsy, and his breathing grew shallow. A repeat glucose value rose only modestly, first to 212 mg/dL and then to 198 mg/dL when euglycemic diabetic ketoacidosis was formally recognized. That limited rise in glucose is exactly what makes euDKA dangerous in practice: the patient can look too well for diabetic ketoacidosis, and the absence of extreme hyperglycemia can distract clinicians from the acid-base disorder unfolding beneath the surface.
Acid-Base Collapse Without Marked Hyperglycemia
Arterial blood gas analysis revealed severe acidemia with a pH of 7.01, bicarbonate of 14 mEq/L, and an anion gap of 19 mEq/L. Urine ketones were positive. Lactate remained normal at 1.34 mmol/L, which helped separate the disorder from lactic acidosis, while creatinine and blood urea nitrogen stayed within reference range, arguing against renal failure as the primary driver. The chemistry profile also showed sodium of 133 mEq/L, potassium of 3.9 mEq/L, and chloride of 100 mEq/L.
A single result captured the clinical weight of the episode: the glucose was only 198 mg/dL, yet the patient was already in severe ketoacidosis.
The diagnosis of euDKA rests on that mismatch. Ketone-driven acidosis can develop when insulin deficiency pushes the body toward lipolysis and hepatic ketogenesis, while carbohydrate restriction blunts the hyperglycemic signal that usually pushes clinicians toward classic DKA. In this case, the precipitating context was unusually clear only after the emergency presentation had already evolved. The patient had been following a strict carbohydrate-restricted diet, estimated at less than 20 to 30 g per day, for one week in preparation for a football tournament.
Diet-Triggered Ketosis Met the Biology of Insulin Deficiency
The case is clinically important because it combined two elements that can work in the same direction: carbohydrate restriction and previously unrecognized diabetes with low endogenous insulin production. HbA1c was 8.9%, indicating sustained hyperglycemia over the prior two to three months, while serum insulin measured 2.6 mU/L and fasting C-peptide was 0.39 ng/mL, both pointing to reduced insulin secretion. His mother had type 1 diabetes, which adds biologic plausibility to an insulin-deficient state presenting in a young adult.
Low carbohydrate intake alone can drive ketosis. When insulin reserve is limited, the same dietary pattern can move from benign nutritional ketosis into life-threatening ketoacidosis. The liver responds to carbohydrate deprivation by increasing ketone production, but without sufficient insulin, peripheral utilization cannot keep pace and acid accumulates. In a patient already carrying occult diabetes, a short period of aggressive carbohydrate restriction can therefore become the final trigger that pushes the metabolic system past its compensatory limit.
Wheezing and Hypoxia Can Mislead the First Pass
The initial bedside trap in this case was respiratory. Mild hypoxia and wheezing fit the established asthma history, and there was no overt hyperglycemic crisis to challenge that impression. Yet euDKA can present with tachypnea, dyspnea, and an appearance of respiratory distress that mimics airway disease. As acidemia worsens, respiratory compensation can become deeper and more labored, and a clinician focused only on bronchospasm can miss the underlying metabolic reason for the abnormal breathing pattern.
That diagnostic overlap has a practical consequence in emergency care: failure to obtain an arterial blood gas and ketone testing early can delay treatment precisely when the patient is starting to decompensate. In this case, the shift toward abdominal pain, vomiting, worsening drowsiness, and shallow respirations prompted the correct tests. The urine ketone result was particularly valuable because serum β-hydroxybutyrate was unavailable at the facility, leaving urine ketone testing as the only accessible marker of ketosis.
Bedside Workup Must Reach Beyond Glucose
The differential diagnosis was appropriately broadened once the acid-base problem became visible. Thyroid dysfunction was excluded through normal thyroid function testing. There was no convincing evidence for infection, and routine inflammatory assessment did not support an infectious source. Toxic ingestion such as alcohol or salicylates was considered clinically unlikely from the history, although confirmatory serum levels were not obtained. Renal function remained preserved, which helped keep the focus on ketoacidosis rather than uremic acidosis.
The case also shows the limits of glucose-based screening. Random glucose of 164 mg/dL at presentation did not fit the usual mental image of diabetic ketoacidosis, and that number could easily have reassured the team too early. Yet the pathophysiology of euDKA does not require striking hyperglycemia; it requires insulin deficiency, ketone production, and a patient who is acidotic enough to become unstable. The blood glucose may be only mildly elevated, but the metabolic injury is already severe.
Why This Case Matters for Emergency Diagnosis
The report’s value lies in the sequence of events, not just the final label. A young man with no prior diabetes diagnosis, a family history of type 1 diabetes, and a week of strict carbohydrate restriction arrived with respiratory symptoms that seemed compatible with asthma. He then deteriorated into severe high-anion-gap metabolic acidosis with ketonuria and only modest hyperglycemia. The clinical lesson is not subtle: respiratory complaints in a patient with vomiting, drowsiness, and abdominal pain should trigger an acid-base evaluation even when glucose is not dramatically elevated.
For emergency clinicians, the case supports a low threshold for arterial blood gas and urine ketone testing when the story and the bedside findings do not align. For patients and families, especially those with a background risk of autoimmune diabetes, it is a reminder that very low-carbohydrate diets can carry real danger when insulin deficiency is present or developing. The report does not offer a broad population estimate or comparative outcome data; it instead delivers a narrow but clinically sharp warning from a single patient: euDKA can hide behind an asthma-like presentation and a near-normal glucose reading, and the delay in recognition can be dangerous.