To quickly and effectively identify high-risk chest pain individuals is of great clinical importance and essential in emergency medical practice. From the results of a large multi-center study, chest pain patients accounted for about 5% of all emergency visits (1), and acute myocardial infarction (AMI) only accounted for a quarter of them.

Acute pericarditis is an important cause of non-ischemic related chest pain with ST segment changes, which makes it challenging to be distinguished from AMI. There are various causes associated with it, both infectious (viral, bacterial) and non-infectious (auto-immune disease, cancerous, traumatic) (2). The definitive diagnosis often requires auscultation (pericardial rub), ECG, echocardiography, blood analysis and chest X-ray (2). Most acute pericarditis is self-limited with favorable prognosis, while a small portion of them—the purulent pericarditis—can be devastating. Here we present a case of purulent pericarditis caused by esophageal perforation.

A 52 year-old male with continuous chest pain and dyspnea for 16 h was admitted to our hospital. Physical examination was unremarkable, and vital signs were normal. His initial troponin-T level was 20.9 ng/L (limit of reference, 0–14), and the NT-proBNP level was 2,774 ng/L (0–227). Twelve-lead electrocardiogram (ECG) findings included ST-segment elevation at the inferior and lateral leads (I, II, III, AVF, and V2 to V6) (Figure 1).

Due to the typical presentation of chest pain, positive biomarkers and ECG findings, the initial diagnosis was ST-Elevation myocardial infarction (STEMI). The patient was immediately transferred for emergency coronary angiography (CAG), which demonstrated normal patent left and right coronary arteries (Figure 2). Next, a bedside transthoracic echocardiography (TTE) was performed and revealed a massive pericardial effusion (Figure 3). Furthermore, his blood routine examination showed leukocytosis (32.42 × 10⁹/L) and elevated neutrophil count (88.2%). Considering the possibilities of an acute pericarditis, a pericardiocentesis was performed. And about 250 ml of yellowish-green pus-like fluid was extracted, with biochemical examination revealed elevated lactic dehydrogenase (TLDH) (5,443 IU/L) and positive pus cells (Other biochemical results included 3,400 × 10⁶/L of nucleated cells, 1,000 × 10⁶/L of red cells, 52.5 g/L of total protein, 30.3 g/L of albumin, 146.0 IU/L of adenosine deaminase, <0.11 mmol/L of glucose, 133 mmol/L of sodium, 3.4 mmol/L of potassium and 93 mmol/L of chlorine). Therefore, purulent pericarditis was suspected. Consequently, a furthered detailed history exam was conducted, which then, the patient further revealed a week history of sore throat with prior fever as well as dysphagia for 4 days that self-resolved. Furthermore, the patient complained that a “fishbone got stuck in his throat more than a week ago.” Due to the combined presentation of chest pain, dyspnea, history of esophageal injury, and purulent pericardiocentesis fluid, we suspected a pathogenesis of esophageal perforation resulting in mediastinal infection leading to purulent pericarditis.

Moreover, computed tomography (CT) further demonstrated the presence of pneumopericardium, effusions in mediastinum and pericardium (Figure 4). The heart team highly recommended immediate gastroscopy and surgery. However, the patient and his family refused further treatment considering the associated surgical risk and poor prognosis of this disease. We did not get to perform the cultivate of the puncture fluid either due to the requested discharge. The patient passed away shortly the next day after hospital discharge. We posted the detailed timeline of this patient from the symptoms onset to discharge and death (Figure 5).

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All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.