Therefore, based on the clinical and laboratory findings, the diagnosis of eu-DKA due to the use of the SGLT-2 inhibitor was made. The patient also had no history of methanol, ethanol, and paraldehyde ingestion. A euglycemic state was indicated in basal metabolic tests with an elevated anion gap and ketosis. Analysis of arterial blood gas (ABG) and serum electrolytes revealed a decrease in pH, with hypobicarbonatemia, hypokalemia, and hypocarbia. Her laboratory results revealed increased white blood cell (WBC) count and raised glycosylated hemoglobin (HbA1c) levels (Table 1).
The rest of the systemic examination was unremarkable. Neurological examination showed normal tone, power, and reflexes, but she had bilaterally impaired vibration sense in her lower limbs. Her pulse rate was 106 beats per minute (BPM) and regular, blood pressure (BP) was 110/70 mmHg with no postural drop, respiratory rate was 22 breaths per minute (BPM), peripheral capillary oxygen saturation (SpO 2) was 88% at room air, and she was afebrile. She had pallor and was slightly drowsy, but easily arousable dehydrated but without jaundice and lymphadenopathy. On examination, she had no hyperthyroid or hypothyroid features.
She had recently recovered from a COVID-19 infection two weeks ago. She was married, a non-smoker, and a non-alcoholic. She denied any history of chronic abdominal pain, weight loss, hypertension, ischemic heart disease, thyroid disease, stroke, substance abuse, or recent travel. She had no fever, cough, sore throat, chest pain, syncope, headache, vomiting, diarrhea, or urinary problems.
There were no preceding respiratory, gastrointestinal, or cardiovascular symptoms. She presented with complaints of increasing lethargy and weakness for the last two days. She saw her primary care physician, who added empagliflozin to the prescription five days prior to her presentation at the emergency department. We present here the case of a 45-year-old woman, a known case of type 2 diabetes mellitus (T2DM) for the last five years, poorly controlled with oral hypoglycemic medications including glimepiride, vildagliptin, and metformin. Serum ketones should be obtained in diabetic patients with symptoms of nausea, vomiting, or malaise while taking SGLT-2 inhibitors, and SGLT-2 inhibitors should be discontinued if ketoacidosis is confirmed. Given the absence of significant hyperglycemia, recognition of this entity by clinicians may be delayed. In this report, our aim is to discuss the relationship between SGLT-2 inhibitors with eu-DKA. She was successfully treated according to the DKA protocol and discharged in good condition. Therefore, the diagnosis of euglycemic diabetic ketoacidosis (eu-DKA) was made. However, her lab results showed significant metabolic acidosis and ketonemia with no clinical or laboratory features of sepsis. Based on the clinical examination and lab findings, DKA was suspected, but her glucose level was below the cutoff value for DKA diagnosis. Before her presentation, her physician had recently added empagliflozin, a sodium-glucose cotransporter-2 (SGLT-2) inhibitor, to her anti-diabetic drug regimen along with glimepiride and a combination drug of vildagliptin and metformin. We discuss a case of a 45-year-old woman with T2DM who presented to the emergency room with worsening lethargy and weakness. Diabetic ketoacidosis (DKA) is considered a medical emergency, most commonly associated with type 1 diabetes mellitus, and is relatively rare in type 2 diabetes mellitus (T2DM).
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