ST-segment elevation is a concerning feature on electrocardiogram (ECG), and ST-elevation myocardial infarction (STEMI) is an urgent diagnosis to exclude. However, 11–36% of such patients have no significant coronary artery disease on coronary angiography [1,2], and abdominal pathologies are rare causes. We present a case of severe pancreatitis complicated by diabetic ketoacidosis, masquerading as STEMI.
A 78-year-old male with a history of well-controlled hypertension presented to the emergency department with a sudden onset of shortness of breath associated with a 1-day history of fever and vomiting, but no chest pain. On examination, he was confused, heart sounds were normal, and chest was clear on auscultation. Abdomen was soft and nontender. Observations showed blood pressure of 117/58 mmHg, pulse of 93 beats per minute, respiratory rate of 28 breaths per minute, oxygen saturation of 99% on room air, and temperature of 36.8°C.
An ECG in the emergency department showed ST elevation in inferior leads and right ventricular infarct pattern on right-sided leads (Fig. 1a). High sensitivity troponin I was elevated (44.8 ng/L, normal: <17.4 ng/L). The patient was urgently sent for coronary catheterization under suspicion of an inferior STEMI, which revealed normal coronary arteries. Arterial blood gas demonstrated pH of 6.99 (normal: 7.35–7.45), pCO2 of 8.5 mmHg (normal: 35.0–45.0 mmHg), pO2 of 115.0 mmHg on room air (normal: 75.0–100.0 mmHg), bicarbonate of 2.0 mmol/L (normal: 23.0–33.0 mmol/L) and base excess of −29.0 mmol/L (normal: −2.0 to 2.0 mmol/L). Blood glucose levels were elevated at 54.6 mmol/L (normal: 3.0–6.0 mmol/L), with raised β-hydroxybutyrate (6.7 mmol/L, normal: <0.6 mmol/L), lactate (5.6 mmol/L, normal: 0.7–2.1 mmol/L), urea (27.6 mmol/L, normal: 2.5–7.1 mmol/L) and potassium (6.5 mmol/L, normal: 3.5–5.0 mmol/L). The anion gap was elevated (39.0 mEq/L, normal: 8–16 mEq/L) and the delta ratio was 1.05. The eGFR deteriorated to 24 ml/min (normal: >60 ml/min) from 69 ml/min 1 month prior. Diabetic ketoacidosis (DKA) complicated by severe metabolic acidosis, acute kidney injury (AKI) and hyperkalaemia was diagnosed. DKA was managed with intravenous fluids, insulin infusion and close serological monitoring after initial intravenous sodium bicarbonate. Four hours post-presentation, the patient deteriorated into shock with Glasgow Coma Scale of E1VTM1.
Collateral history revealed a habit of heavy alcohol use, and lipase and amylase were elevated at 493 U/L (normal: 5–50 U/L) and 998 U/L (normal: 0–110 U/L) respectively. Based on admission blood tests, the modified Glasgow Imrie severity criteria for acute pancreatitis  was six (age 78, WBC 19.6 × 109/L, ionized Ca 1.15 mmol/L, urea 27.6 mmol/L, albumin 30 g/L, glucose 54.6 mmol/L), classifying him at a high risk of severe pancreatitis. Intravenous imipenem and fluid resuscitation were additionally given, and the patient stabilized after 2 days. An ultrasound of the hepatobiliary system performed 3 days after admission, avoiding contrast-enhanced CT in the first 72 h due to significant AKI, was consistent with resolving acute pancreatitis (Fig. 1b and c).
DKA with ECG changes are often mistaken as myocardial infarction, and can cause elevated troponin levels . ST-elevation, most commonly anteroseptal , is thought to be due to hyperkalemia secondary to deficiency of insulin action and extracellular accumulation of potassium. Notably, this patient had no history of DM, and HbA1c 7 months prior to presentation was 5.3% (normal: 4.5–7.0%). Young patients with T1DM can present initially with DKA. This is caused by immune-mediated beta cell destruction. In type 2 DM, DKA typically occurs after a protracted history of DM and beta-cell function loss. It is thus uncommon for DKA to develop in an elderly patient with no previous history of DM . Destruction of pancreatic beta cells in acute pancreatitis is associated with hyperglycemia, but reports of secondary DKA are rare .
Although DKA can be associated with elevated amylase and lipase in 16–25% of cases, acute pancreatitis may co-exist with DKA in at least 10–15% of DKA patients . Acute pancreatitis is more likely in severe DKA with significant acidosis and hyperglycemia , as observed in this case, and imaging was also consistent with a diagnosis of acute pancreatitis. Acute pancreatitis is an uncommon cause of ST elevation, most commonly in inferior leads with or without concomitant changes in cardiac markers [10,11]. The pathophysiology behind this is unclear, but proposed mechanisms include coronary artery spasm, vagal stimulation and myonecrosis due to pancreatic enzyme release. It is important to differentiate acute pancreatitis from acute myocardial infarction as misdiagnosis can lead to morbidity and mortality.
This case illustrated a patient presenting with DKA due to severe acute pancreatitis, mimicking acute inferior STEMI. Acute pancreatitis may present with DKA, raised cardiac enzymes and ST elevation on ECG. However, the investigations for alternative diagnoses for ST-elevation on ECG must be balanced with the time delay in managing myocardial ischemia.
Written informed consent has been obtained from the patient for the writing of this report.
Conflicts of interest
There are no conflicts of interest.
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