American Journal of Emergency Medicine 33 (2015) 741.e3–741.e5

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Case Report

Internal hernia presenting as pseudomyocardial infarction Abstract We report the case of a 54-year-old man with an internal hernia presenting as myocardial infarction. The patient presented at the emergency department with acute epigastric pain. In the electrocardiography at admission, there were ST elevations in the leads V2 and V3. The patient had a medical history of an anterior wall infarction 18 years earlier. Because of the previous myocardial infarction, the diagnosis of another STelevated myocardial infarction was initially made. However, emergency coronary angiography ruled out myocardial infarction. As the abdominal pain persisted, a computed tomography were performed, which showed a bowel obstruction. In a subsequent operation, an incarcerated internal hernia has been found. Very few cases of pseudomyocardial infarction with abdominal pathologies have been reported. A pseudomyocardial infarction in association with an internal hernia has not yet been reported. Acute abdominal symptoms may, in rare cases, be accompanied by electrocardiographic (ECG) changes, although no myocardial infarction occurred. Very few cases of such ECG changes have been reported in association with pancreatitis [1,2], cholecystitis [3], biliary colic [4], perforated duodenal ulcer [5], appendicitis [6,7], rectus sheath hematoma [8], traumatic rupture of the diaphragm [9], and hiatus hernia [10]. A pseudomyocardial infarction in association with an internal hernia has not yet been reported. An internal hernia is defined as a protrusion of viscera through a normal or abnormal peritoneal or mesenteric aperture within the abdominal cavity [11,12]. This aperture may be congenital, or it may develop as a result from surgery, trauma, or infection. Internal hernias are the cause of 0.5% to 5.8% of all bowel obstructions [11-13]. The most suitable diagnostic procedure for an internal hernia is computed tomography (CT) [11]. A 54-year-old male patient presented at the emergency department with acute epigastric pain. There was no previous surgery in the medical history, but the patient had suffered an anterior wall myocardial infarction 18 years earlier. Ever since, he took 100 mg acetylic acid per day as long-term medication. Clinical examination revealed a slight tenderness of the upper abdomen and decreased peristalsis but not as an acute abdomen with abdominal guarding. There was no nausea, vomiting, or constipation. Treatment was initiated with intravenous analgesia and fluid administration. In the ECG, there were ST elevations in the leads V2 and V3 (Fig. 1). Because of the previous myocardial infarction, the diagnosis of another ST-elevated myocardial infarction was initially made. Blood was drawn for cardiac enzyme measurement, and these were within reference range but coronary angiography was performed before the results. Emergency coronary angiography ruled out myocardial infarction. Blood tests at admission for C-reactive protein, white blood cells, and lactate were normal.

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As the abdominal pain persisted, sonography was performed and showed a small amount of free fluid in the lesser pelvis, dilated bowel segments in the right hemiabdomen, and nonpropulsive peristalsis in the bowel segment. An abdominal CT was performed because the sonography had identified evidence of a bowel obstruction with a small amount of free fluid in the lower abdomen. The CT showed a bowel obstruction with suspicion of a volvulus (Fig. 2). In the meantime, the patient's clinical condition had deteriorated dramatically, and he had developed an acute abdomen. We decided to perform a laparotomy. Intraoperatively, there was an incarcerated internal hernia with small bowel gangrene of 1.5-m length. There was an adhesion of a section of the omentum majus near the mesenteric root with an aperture above the proximal jejunum (Fig. 3). In addition, there was a protrusion of a 1.5-m small bowel loop from the right side. We dissected the adhesion, resected the gangrenous small bowel section, and reconstructed with an end-to-end anastomosis (Fig. 4). The postoperative course was uneventful. In the postoperative ECG, there were no ST elevations visible. The patient was discharged on the ninth postoperative day in good general condition. We interviewed the patient postoperatively with respect to the cause of the adhesions. There was no previous trauma in the area. Indigestion occurred once to twice per year, mostly after alcohol consumption or fatty meals, and no medical attention was sought for this. The patient had no recollection of an infection with abdominal pain. Numerous internal hernias from adhesions have been reported, but these had developed mainly after previous surgery. Electrocardiographic changes have not yet been reported. It is probably a very rare clinical presentation of internal hernias. In our case, the precise cause, which has led to the gap, was unclear. It is most probable that the adhesion on the omentum to the mesenterium was caused by a spontaneous hemorrhage after a minor trauma in the context of platelet inhibition with acetylic acid medication since 1996. However, numerous other pathologies may have caused this adhesion. In our case, the internal hernia presented initially with the clinical signs of upper abdominal pain and ECG changes, which may have been manifestations of a myocardial infarction. Because myocardial infarctions may be accompanied by a bowel paralysis, the decreased peristalsis was plausible. The bowel obstruction was confirmed by an abdominal CT, but the correct diagnosis was not possible with the CT alone. Ultimately, only the operation did conclusively confirm the diagnosis of an incarcerated internal hernia. Our case was a diagnostic dilemma. Diagnosing an internal hernia from clinical symptoms only is impossible. Only the resulting ileus can be verified clinically. Computed tomography also does not always yield the correct diagnosis. In addition, the prolonged diagnostic procedures and the delay of surgery because of the coronary angiography in our case have most certainly resulted in irreversible damage of the bowel. Still, the cardiology intervention was indicated because of the ST elevations in the ECG.

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M. Ardelt et al. / American Journal of Emergency Medicine 33 (2015) 741.e3–741.e5

Fig. 1. The ST elevations in V2 and V3 in the ECG at admission.

Fig. 2. Left: The distortion of the mesenteric vessels. Right: A volvulus suspicious formation of the small bowel.

M. Ardelt et al. / American Journal of Emergency Medicine 33 (2015) 741.e3–741.e5

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Michael Ardelt, MD⁎ Johanna Taut Yves Dittmar, MD Falk Rauchfuss, MD Rene Fahrner, MD Hubert Scheuerlein, MD Utz Settmacher, MD Department of General, Visceral and Vascular Surgery University Hospital Jena, 07747 Jena, Germany ⁎Corresponding author. Tel.: +49 3641 9322675 fax: +49 3641 9322602 E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2014.11.031 References Fig. 3. Omentum-mesenterial adhesion with jejunum underneath after reposition of a 1.5m-long incarcerated small bowel loop (view toward the left).

Fig. 4. Incarcerated small bowel after reposition with distal constriction.

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Internal hernia presenting as pseudomyocardial infarction.

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