Case Report

Acute inferior pseudoinfarction pattern in a patient with normokalemia and diabetic ketoacidosis^?

Abstract

Diabetic ketoacidosis is an important medical emergency and may cause electrocardiogram changes mimicking myocardial infarction. In the literature, hyperkalemia-associated ST-segment elevations have been defined in DKA; it has been demonstrated that these changes resolve completely after the treatment of hyperka- lemia. We aimed to present a case with DKA in whom ST- segment elevation in inferior derivations was observed, but serum potassium level (4.4 mEq/L) was normal. The patient was admitted to the emergency department with complaints of nausea, bloody vomiting, and Epigastric pain. Intravenous 0.9% saline, soluble insulin, and proton pump inhibitor were begun. Because of bloody vomiting, antiaggregant and anticoagulant therapy was not adminis- tered and coronary angiography was not considered at the beginning. Two hours after the beginning of the treatment, the blood glucose level dramatically decreased (from 712 to 263 mg/dL), and the metabolic acidosis view in arterial blood gas sample was improved. The repeated ECG depicted complete ST segment resolution. transthoracic echocardiogram determined normal ventricular wall mo- tion. Cardiac biomarkers remained in normal limits in the follow-up period. Coronary angiography performed 3 days after hospital admission was evaluated as normal. The patient recovered uneventfully, and gastrointestinal tract bleeding did not repeat. The ECG was repeated, and ST segments in izoelectric line were observed.

Diabetic ketoacidosis (DKA) remains one of the most serious acute metabolic complication of diabetes mellitus . The estimated mortality rate for DKA is between 2% and 10% [1,2]. Myocardial infarction (MI) is a well recognized precipitating cause and the leading coexisting cause of death in this entity [3,4]. However, DKA may imitate electrocardiogram (ECG) findings of MI. ST-segment elevations in anterior and inferior derivations have been

^? No financial support from any organization was used in the preparation of this paper.

demonstrated in such patients without any evidence of myocardial injury [3,5]. The ECG changes have been connected to hyperkalemia and disappeared with the treatment of hyperkalemia [3,5]. We present a case with DKA in whom ST-segment elevation in inferior derivations was observed without hyperkalemia and completely resolved after the treatment of ketoacidosis.

A 58-year-old man with DM was admitted to the emergency department with complaints of nausea, bloody vomiting, and epigastric pain. He stated that he had been thirsty, polyuric, and tired for 2 to 3 days. It has been learned that he had not attended his diet and had neglected his oral antidiabetic drugs for 1 week. In addition, he stated that bloody vomiting had also occurred 1 week ago. The history of chest pain was not present. He had had type 2 DM for 10 years and used oral antidiabetic drug. He was smoking and had no familial history of ischemic heart disease.

In physical examination, he was drowsy, tired, and dehydrated. His blood pressure was 110/80 mm Hg, heart rate was 112 beat/min, and respiration rate was 32 breaths/ min. The oxygen saturation was 96%. Melena was not observed in rectal examination.

Serum glucose level was measured with a glucometer and was found to be 712 mg/dL. A Urine dipstick test showed three positive (+++) ketones. In arterial blood gas sample, metabolic acidosis was present (pH 7.15; pCO2, 21 mm Hg; bicarbonate, 11 mmol/L). Diabetic ketoacidosis was diag- nosed, and he was administered intravenous 0.9% saline solution and intravenous soluble insulin at 6 units/h. His laboratory data were the following: sodium, 133 mEq/L; potassium, 4.4 mEq/L; blood urea nitrogen, 58 mg/dL; kreatinine, 1.1 mg/dL; chloride, 83 mEq/L; calcium, 9.7 mg/ dL; phosphate, 2.7 mg/dL; and magnesium, 2.2 mg/dL. White blood cell count was 11.8 x 10⁹/L. The ECG demonstrated ST-segment elevation in inferior derivations (Fig. 1). Because of bloody vomiting, proton pump inhibitor was started. The patient was consulted to the general surgery department. It was suggested that antiaggregant and/or anticoagulant therapies should not be started. In this respect, coronary angiography was not planned at the beginning. The fecal occult blood test was one positive. Consecutive Hemoglobin levels were determined and found as 15.4, 14.1, and 12.7 g/dL. Thus, any significant gastrointestinal tract bleeding was not thought by a gastroenterologist. Transthoracic echocardiogram was performed to the patient

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251.e4 Case Report

Fig. 1 The ECG depicted ST-segment elevation in inferior derivations.

and revealed normal ventricular wall motion. Two hours after the starting of the treatment of ketoacidosis, the following results were obtained: serum glucose, 263 mg/dL; pH 7.34; pCO2, 32 mm Hg; bicarbonate, 21 mmol/L. The ECG was repeated, and it was observed that ST segments were in izoelectric line (Fig. 2). Serum Troponin-I level was normal at admission, 6 and 24 hours after admission (b0.01 ug/L). He

was referred to our coronary angiography department 3 days after hospital admission, and his coronary arteries were evaluated as normal.

The patient did not define any cardiac complaint, and gastrointestinal tract bleeding did not repeat in the follow-up period. ST segment in control ECGs was in izoelectric line. He recovered completely and was discharged.

Fig. 2 The control ECG showing ST segments are in isoelectric line.

Case Report 251.e5

Myocardial infarct may accompany DKA and contributes in mortality in this clinical condition. In this respect, correct and immediate diagnosis of MI is very important in such patients. However, ECG findings mimicking MI may be observed in DKA without myocardial damage, and this condition is named as ‘pseudoinfarction’ [3,5].

It has been demonstrated that pseudoinfarction pattern has been related to hyperkalemia and fully resolved after the treatment of hyperkalemia in patients with DKA [3,5]. In our opinion, such an interesting case is the first one in the literature, the association between pseudoinfarction and DKA without hyperkalemia, and we also displayed the disappearance of ST-segment elevations after the treatment of ketoacidosis. In our case, ST-segment elevations may arise from metabolic acidosis or other metabolic abnormalities specific to DKA. Coronary vasospasm might also have contributed to this ECG change.

This case shows that MI diagnosis has to be made very carefully in DKA cases. Arterial blood gas sample examina- tion and detailed biochemical evaluation should also be performed. The first effort should be focused on the correction of metabolic acidosis and other metabolic abnormalities. The diagnosis of MI should be made after repeating ECG, transthoracic echocardiogram, and cardiac biomarkers. Thus, it can be avoided from unnecessary drug treatment, coronary angiography, and the related risks.

Enbiya Aksakal MD Hakan Duman MD

Department of Cardiology School of Medicine Ataturk University Erzurum, Turkey

Taner Ulus MD Ednan Bayram MD Department of Cardiology Erzurum Numune Hospital 25200 Erzurum, Turkey

E-mail address: [email protected]

doi:10.1016/j.ajem.2008.06.024

References

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3. Moulik PK, Nethaji C, Khaleeli AA. Misleading electrocardiographic results in patient with hyperkalaemia and diabetic ketoacidosis. BMJ 2002;325:1346-7.
4. Basu A, Close CF, Jenkins D, et al. Persisting mortality in diabetic ketoacidosis. Diabetic Med 1993;10:282-4.
5. Wang K. Images in clinical medicine. “Pseudoinfarction” pattern due to hyperkalemia. N Engl J Med 2004;351:593.