American Journal of Emergency Medicine 33 (2015) 126.e3-126.e5

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American Journal of Emergency Medicine

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Case Report

The spontaneous pneumopyopericardium simultaneously masquerading as acute myocardial infarction and surgical abdomen: a case report

Abstract

Pneumopyopericardium is a rare disease, presenting clinically as a spectrum of acute myocardial infarction or severe surgical abdomen, which includes various symptoms and changes in cardiac enzymes and electrocardiogram. Here, we report a case of pneumopyoper- icardium in a 61-year-old male farmer in China. An early diagnosis of pneumopyopericardium was difficult due to his acute myocardial infarction- and severe surgical abdomen-like symptoms and signs. The electrocardiogram, esophagogram, and chest computed tomo- graphic scan commonly revealed Pericardial fluid and air and excluded a gastrointestinal perforation in late stage of severe inflammation. Despite therapy with antibiotics and pericardial open surgical drainage, his severe inflammation was not well controlled, partly due to the pericardial cavity drainage obstruction induced by pericardial adhesion. The present case indicated the importance of early diagnosis and treatment of pneumopyopericardium.

The incidence of pneumopyopericardium is rare, with known causes including spontaneous pneumopyopericardium and intraper- icardial perforation of a gastric ulcer [1,2]. The clinical signs of pneumopyopericardium are usually diverse due to its pathologic variability and mainly associated with cardiac tamponade. Therefore, the mortality rate of pneumopericardium is high, if the patient does not receive an appropriate surgical intervention. In this report, we described a case of 61-year-old Chinese farmer who presented with spontaneous pneumopyopericardium simultaneously mimicking both acute myocardial infarction (AMI) and severe surgical abdomen (SSA). To our knowledge, this unique presentation of pneumoper- icardium has never been reported previously.

The present patient visited the emergency department with 30 minutes of acute Epigastric pain radiating to his back and left shoulder, which is associated with heavy sweating, chest distress, and brachypnea. His epigastric pain had been increasing and relenting during the past 30 days but had never completely subsided. He originally visited a community hospital and presented with marked convex ST-segment elevation in the anteroseptal precordial leads V1 and V2 (Fig. 1). The patient has a remarkable history of Duodenal ulcer, which had been in remission for at least 6 months because of oral omeprazole. No other relevant history was reported. He had a negative history for alcohol, tobacco, or drug use. There was no family history of any cardiac problems or early death. Physical examination revealed a thin, healthy-appearing Chinese man with a pained expression. His body temperature was 36.7?C, heart rate was 76 beats per minute, and blood pressure was 120/70 mm Hg. Discrete rales were found in the lower lung fields. Meanwhile, abdominal

rigidity and epigastric or subxiphoid tenderness were noticed, with no rebound tenderness. Initial laboratory data revealed that his blood glucose was elevated to 6.63 mg/dL (3.6-6.1). Complete blood count tests showed an abnormal lymphocyte percentage of 15.5 (20-40) and an increased neutrophile granulocytes percentage of 76.1 (50-70). His initial set of cardiac enzymes displayed elevated levels of both creatine kinase of 211 (24-195) and myoglobin of 171 (0-90). His Lipid panel was within normal limits. Subsequently, an echocardiogram documented small pericardial effusions, and a chest computed tomographic (CT) scan demonstrated a band-like lower density shadow in pericardial space, inflammatory response in inferior lobe of left lung, and small pleural effusion (Fig. 2). An esophagogram also documented small amount of pneumoprecardium and hydropericar- dium as well as small pleural effusion and inflammation in left lung. However 24 hours later, the patient began experiencing severe epigastric pain with compulsive position, widely abdominal tender- ness, and board-like rigidity, which remained constant for several hours, without responding to serum and urine amylase, nitroglycerin, and ST-segment changes. On clinical examination, the patient was taken directly to Exploratory laparotomy, with, however, no positive findings. Repeat echocardiograms subsequently documented moder- ate pericardial effusion, suggesting that the diagnosis of pneumopre- cardium could not be excluded. After Pericardial aspiration was performed and 200 mL of turbidly yellow fluid was drained, the patient’s symptoms of breathlessness resolved. Cytology of the fluid revealed abundant polymorphonuclear cells, but no malignant cells were found. Biochemical results of the aspirate also were consistent with inflammatory exudates. Pericardial fluid culture demonstrated Staphylococcus caprae. Over the next 3 days, 100 mL turbidly yellow fluid and 300 mL locoregional gas were drained again from the pericardial cavity because of repeat echocardiogram documenting of significantly larger amounts of pericardial effusions and pneumo- precardium accumulation and pericardial cavity conglutination on left posterior ventricular wall. Shortly afterward, subxiphoid pericardial window open cleaning and drainage were performed because of the pericardiac adhesion-induced pericardial cavity drainage obstruction. No communications were noted between the pericardium and adjacent organs. Although a strong antibiotic therapy and supportive care were always used, the patient always experienced sharp symptom of deterioration and reoccurrences of pericardial effusion and pneumoprecardium. Moreover, the per- centage of neutrophil granulocytes always ranged from 70% to 90% during the hospitalization period (Fig. 3). A diagnosis of acute infectious pneumopyopericardium was finally established as the cause of his death.

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Fig. 3. The changes of neutrophil granulocytes during the hospitalization period.

Fig. 1. Preadmission electrocardiogram (limb and chest leads).

This is the first reported case of pneumopyopericardium simulta- neously masquerading as an acute ST-elevation myocardial ischemia and an acute surgical abdomen. In all nonTraumatic cases of gas accumulation, 2 most possible origins of gas in pneumopyopericar- dium are as follows: gas deriving from an intrinsic source (ie, caused

by rupture of a gas-filled organ) and gas originating in loco (ie, by the action of gas-producing organisms) [3]. Therefore, the clinical manifestations of pneumopyopericardium vary too. The present case illustrated several clinical presentations of pneumopyopericar- dium and its ability to mimic AMI. Meanwhile, acute epigastric pain and signs of an acute surgical abdomen led to a perforation of a gastrointestinal ulcer than to an AMI. The clinical presentation of both AMI and SSA made early Diagnosis difficult. We excluded the possibility of ectopic gas accumulation deriving from rupture of a gas-filled organ by exploratory laparotomy, although clinical reports

Fig. 2. A chest CT. There are inflammatory response in inferior lobe of left lung and small pleural effusion. The band-like lower density shadow was noted in pericardial space (double arrows).

W. Zhang et al. / American Journal of Emergency Medicine 33 (2015) 126.e3-126.e5

of intestinal sources of pneumopericardium or pneumopyopericar- dium concerned esophageal perforation and perforation of a gastric or duodenal ulcer [4,5]. The fact that the patient had no dynamic change in creatine kinase-MB levels during 24 hours after the onset of

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Weiping Zhang, MD Xiaojun Bai, MD Xiaolin Xue, MD?

Department of cardiovascular medicine

epigastric pain ruled out the possibility of AMI. Although the electrocardiogram low voltage complexes or nonspecific T-wave and ST-segment changes can be seen sometimes in pericarditis or pneumopericardium [6,7], echocardiogram and radiologic imaging via an esophagogram or CT scan commonly identify the presence of air and fluid in the pericardial cavity. Therefore, the action of gas- producing organisms was the primary cause of pneumopyopericardium in this case. But hematogeneous infection with gas-producing organ- isms in pericardial sac is rather uncommon. acute treatment of pneumopyopericardium involves pericardial decompression by either insertion of a pericardial drain or direct aspiration and subsequent management directed at the strong antibiotics to eliminate the precipitating cause. In fact, the death of the 61-year-old patient in this report was probably connected to the fact that his inflammation was not well controlled, partly due to the pericardial adhesion-induced pericardial cavity drainage obstruction, although pericardiectomy was left open to attenuate the cardiac tamponade. In conclusion, pneumo- pyopericardium simultaneously masquerading as AMI and SSA is difficult to diagnose before clear radiographic evidences. A correct early diagnosis of pneumopyopericardium has important Therapeutic implications for individual patients. Therefore, pneumopyopericardium should be considered in the differential diagnosis of acute coronary syndrome and SSA in patients presenting with Typical symptoms of acute coronary syndrome or SSA.

The First Affiliated Hospital of Medical School, Xi‘an Jiaotong University No. 277, Yanta West Road, Yanta District, Xi‘an, Shaanxi 710061, China

?Corresponding author. Tel.: +86 29 85323815; fax: +86 29 85323709

E-mail addresses: [email protected], [email protected]

http://dx.doi.org/10.1016/j.ajem.2014.06.012

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