A 30-Year-Old Woman's Severe Abdominal Pain Led to a Surprising Diagnosis: Type 1 Diabetes and Diabetic Ketoacidosis

Disclaimer: This article is intended for educational and informational purposes only. To protect patient privacy, all personal and identifying information has been anonymized and modified.

Summary: From Acute Abdominal Symptoms to a Life-Changing Diagnosis

A seemingly straightforward case of abdominal pain, nausea, and vomiting in a young woman turned out to be far more complex than initially suspected. While early tests pointed toward acute pancreatitis, further investigation revealed a much more serious underlying condition—type 1 diabetes mellitus complicated by diabetic ketoacidosis (DKA). Despite normal imaging findings in some areas, persistent hyperglycemia, undetectable C-peptide levels, and metabolic acidosis led clinicians to uncover the true culprit. With aggressive fluid resuscitation, insulin therapy, and close monitoring, the patient responded well to treatment. After three weeks of hospitalization and two months of outpatient follow-up, her condition stabilized, highlighting the importance of comprehensive metabolic evaluation in acute presentations.

Patient Profile at a Glance

Age & Gender: 30-year-old femaleDiagnosis: Type 1 Diabetes Mellitus with Diabetic KetoacidosisHospital: Beijing Hospital (treatment facility)Date of Admission: September 2019Treatment Approach: Multimodal medical management including insulin therapy, electrolyte correction, and supportive careTreatment Duration: 3 weeks inpatient, followed by 2 months of outpatient monitoringOutcome: Successful stabilization of blood glucose, resolution of ketoacidosis, and ongoing improvement in metabolic markers

Initial Presentation: When Abdominal Pain Hides a Bigger Problem

The patient arrived at the emergency department complaining of severe lower to mid-abdominal pain that had persisted for three days. She also reported nausea, recurrent vomiting, and a low-grade fever (measured at 37.5°C). Notably, she had no significant prior medical history and was previously considered healthy.

On physical examination, she appeared acutely ill with signs of dehydration—poor skin turgor and visible distress. Her abdomen was soft but tender in the lower quadrants, with mild rebound tenderness, though no palpable masses were detected. Cardiopulmonary auscultation showed no abnormalities other than sinus tachycardia on ECG.

Critical Lab Findings Raise Red Flags

Emergency lab work revealed alarming results:

• White blood cell count: 16.13 × 10⁹/L (elevated, indicating inflammation or infection)

• Neutrophil percentage: 87.9% (suggesting an acute inflammatory response)

• Urinalysis: Glucose (++++) and Ketones (+++)

• Blood glucose: 27.3 mmol/L (extremely high)

• Arterial blood gas: pH 7.09 (severe acidosis), HCO₃⁻: 5.7 mmol/L, base excess: -22.3 mmol/L

• Serum lipase: 995 U/L (markedly elevated)

• Amylase: 129 U/L (mildly elevated)

Imaging studies—including abdominal ultrasound, gynecological scan, and CT—showed changes consistent with acute edematous pancreatitis and a small calcified spot in the liver. Based on these findings, the initial diagnosis was acute pancreatitis with suspected secondary metabolic complications.

Uncovering the Root Cause: Beyond Pancreatitis

Once admitted, additional testing was conducted to explore potential triggers. Results included:

• Procalcitonin: 2.05 ng/mL (elevated, but not indicative of bacterial sepsis)

• Liver, kidney, cardiac enzymes, calcium, thyroid function, and tumor markers—all within normal limits

• Fasting insulin: 0.5 μU/mL (very low)

• Fasting C-peptide: 0.03 ng/mL (critically low, suggesting minimal endogenous insulin production)

• Autoantibodies (IAA, ICA, GAD): Negative—which is unusual but not impossible in early type 1 diabetes

Why Pancreatitis Was a Symptom, Not the Cause

Although elevated pancreatic enzymes and imaging supported pancreatitis, the profound metabolic derangement told another story. The presence of severe hyperglycemia, ketonuria, and life-threatening acidosis strongly suggested diabetic ketoacidosis (DKA) as the primary driver. In fact, DKA can cause transient elevations in lipase and amylase—a phenomenon sometimes referred to as "pseudo-pancreatitis."

This insight shifted the treatment focus from managing isolated pancreatitis to addressing systemic metabolic failure due to absolute insulin deficiency.

Treatment Strategy: Correcting Metabolic Chaos

The medical team initiated a dual approach targeting both symptom control and root cause:

Supportive Care for Pancreatic Rest

The patient was placed on strict NPO (nothing by mouth) status. She received:

• Lansoprazole enteric-coated capsules to reduce gastric acid secretion

• Intravenous somatostatin to suppress pancreatic enzyme output

• Reduced glutathione injection for hepatic protection

• Electrolyte replacement with calcium gluconate, potassium chloride, and sodium chloride infusions

Aggressive Management of Diabetic Ketoacidosis

To reverse DKA, the protocol included:

• Large-volume intravenous fluid resuscitation to correct dehydration and improve circulation

• Continuous IV infusion of low-dose recombinant human insulin to gradually lower blood glucose and halt ketone production

By day 2, arterial blood gas improved significantly—pH normalized to 7.35, bicarbonate rose to 18 mmol/L—and insulin therapy was transitioned to subcutaneous injections using a basal-bolus regimen: insulin aspart (rapid-acting) before meals and insulin detemir (long-acting) once daily for baseline coverage.

Disease Confirmation: The Role of C-Peptide Testing

Repeated measurements of fasting C-peptide over the next week showed levels dropping below 0.01 ng/mL—an unmistakable sign of near-total loss of beta-cell function. By day 15, while blood glucose had improved (fasting: 7.01 mmol/L, postprandial: 13.29 mmol/L), insulin and C-peptide remained extremely low, confirming permanent insulin dependence.

An enhanced upper abdominal CT on day 12 showed regression of pancreatic swelling and absorption of peripancreatic fluid collections—further evidence that the initial "pancreatitis" was likely a consequence, not the cause, of metabolic crisis.

Recovery and Long-Term Outlook

After 21 days of intensive care, the patient was discharged with stable glucose control and a clear diagnosis of type 1 diabetes. Outpatient follow-up two months later confirmed ongoing progress:

• Fasting blood glucose ranged between 4.9–10.6 mmol/L
• Postprandial (2-hour) glucose: 4.6–12.3 mmol/L
• C-peptide remained undetectable (0.01 ng/mL)
• Insulin antibody levels slightly elevated at 22.71 IU/mL (possibly due to exogenous insulin use)

These results confirmed successful adaptation to insulin therapy and ruled out alternative forms of diabetes such as type 2 or latent autoimmune diabetes in adults (LADA).

Key Takeaways for Patients and Clinicians

This case underscores several crucial points:

Monitor Blood Sugar Early and Often in Unexplained Abdominal Illness

In patients presenting with nausea, vomiting, and abdominal pain—even without a known history of diabetes—checking blood and urine glucose and ketones should be routine. Delayed diagnosis of DKA can lead to organ failure or death.

Don't Overlook Metabolic Causes Behind Elevated Pancreatic Enzymes

Elevated lipase does not always mean acute pancreatitis. Conditions like DKA, starvation ketosis, or even renal failure can mimic it. Always correlate labs with clinical context.

Early Insulin Therapy Saves Lives and Preserves Function

In type 1 diabetes, prompt insulin initiation prevents further beta-cell destruction and reduces the risk of complications. Even with negative autoantibodies, clinical judgment based on C-peptide and glucose trends remains essential.

Lifestyle Guidance for Ongoing Management

For long-term success, the patient was advised to:

• Maintain regular meal timing and avoid skipping meals
• Limit intake of refined sugars and processed carbohydrates
• Adjust insulin doses according to carbohydrate consumption and activity level
• Engage in moderate aerobic exercise—such as brisk walking or light jogging—for 20–30 minutes after meals, provided blood glucose is above 5.6 mmol/L and no ketones are present
• Avoid intense physical activity during episodes of hypoglycemia or uncontrolled hyperglycemia

Final Reflections: A Call for Clinical Vigilance

Type 1 diabetes is often thought of as a childhood disease, but it can emerge at any age—even in adulthood, as seen here. This case reminds healthcare providers to remain vigilant when evaluating acute abdominal syndromes. Symptoms like abdominal pain may mask dangerous metabolic disturbances.

Relying solely on imaging or isolated lab values can lead to misdiagnosis. Instead, integrating clinical signs, serial glucose monitoring, insulin/C-peptide assessment, and acid-base balance offers a more complete picture. Early recognition of type 1 diabetes—not just its complications—is key to preventing morbidity and saving lives.