Clinical Case Report Details
A woman in her thirties experienced severe euglycemic ketoacidosis following her initial dose of tirzepatide for weight loss. She arrived at the emergency department at Tawam Hospital in the United Arab Emirates reporting six days of persistent vomiting. The patient, who had no history of diabetes, could not tolerate solid foods and had only consumed small amounts of liquid. This case highlights a potentially dangerous reaction to dual incretin receptor agonists, even in individuals without underlying metabolic disorders.
Physician Humaid Sadiq and his team documented the event, noting that the patient ingested 5 mg of the medication shortly before the onset of her symptoms. She reported burning epigastric pain that radiated to her chest, accompanied by significant fatigue and abdominal discomfort. Her physical examination confirmed epigastric tenderness. She had not had a bowel movement in four days. Crucially, the patient was not taking SGLT2 inhibitors or other medications known to trigger ketoacidosis, nor did she consume alcohol.
Examination and Diagnostic Findings
Upon admission, clinical staff recorded her blood pressure at 116/77 mm Hg with a heart rate of 98 beats per minute. Her respiratory rate was 20 breaths per minute. Venous blood gas analysis provided the primary indicators for her condition. The results showed a pH of 7.16, a bicarbonate level of 11 mmol/L, and an anion gap of 19. Her glucose level sat at 2.5 mmol/L, which confirmed a euglycemic state. Testing further revealed hyponatremia at 133 mmol/L and elevated beta-hydroxybutyrate levels at 6.4 mmol/L.
Medical teams performed imaging studies, including chest and abdominal X-rays along with an ultrasound, to rule out acute intra-abdominal pathology. These tests returned negative results for organ damage or blockages. Laboratory tests on her renal, hepatic, and pancreatic functions also appeared normal. The medical team prioritized stabilization by administering one liter of normal saline, acetaminophen, metoclopramide, and pantoprazole, yet the metabolic acidosis remained unresponsive to these initial treatments.
ICU Management and Long-Term Implications
Admission to the Intensive Care Unit became necessary once the acidosis failed to improve. The staff initiated a rigorous treatment plan involving intravenous fluids, electrolyte replacement, dextrose, insulin, and potassium. This intervention led to a gradual reversal of her condition. She spent three days under specialized care before her release in stable condition. A follow-up examination confirmed that she remained symptom-free.
This specific incident demonstrates that clinicians must watch for ketoacidosis in patients starting incretin-based therapies, particularly when GI side effects like vomiting occur. While tirzepatide remains effective for many, the risk of metabolic derangement increases when oral intake drops significantly. Authors of the report suggest that more data is necessary to refine prescribing guidelines and patient safety protocols. Moving forward, providers should educate patients on identifying early signs of dehydration and metabolic distress to prevent similar acute events.