Acute tension pneumopericardium due to perforated gastric ulcer without diagnostic radiographic findings 72 h before perforation

Abstract

Introduction

Acute tension pneumopericardium due to gastric perforation is a rare and often lethal condition. Only a few case reports have been described in the literature. Diagnosis based on clinical evaluation is difficult and it is usually made incidentally upon computed tomography (CT) or plain radiography of the chest. Since cardiac tamponade caused by pneumopericardium is life-threatening, immediate diagnosis and emergent therapy is vital.

Case report

We report a 75-year-old male with peptic ulcer disease associated with perforation of the pericardium and acute shock. It is the first reported case with a series of two computed tomograms performed during the 72 h preceding the acute onset of tension pneumopericardium. No radiographic evidence of ulcer perforation was present in the three days prior to the acute event.

Discussions

Gastric ulcer perforation into the pericardium is rare and could not be detected by CT scan prior the deletorious event. Pneumopericardium seems to be fateful and could not be foreseen by clinical or radiological findings.

<Learning objective: Pericardial air tamponade due to ulcer Perforation is a very rare reason for cardiogenic shock. It could not be foreseen by CT scan.>

Introduction

Penetration of a gastric ulcer into the pericardial sac or cardiac ventricle is a rare complication of peptic ulcer disease and only a few cases have been reported. Since the first historical reports by Bricketeau in 1844, approximately 225 cases of non-traumatic pneumopericardium have been reported [1], [2]. Most result from gastro-pericardial or esophago-pericardial fistulas after prior surgery.

Case report

A 75-year-old male was admitted to our hospital in September 2017 complaining of a sharp pain in the region of the thoracic spine radiating to the left shoulder. The pain was not relieved by ibuprofen. The patient had a history of metastatic colonic adenocarcinoma of the sigmoid colon diagnosed in 2013 and treated with palliative ileostomy, sigmoid resection, and several cycles of chemotherapy with good response initially. In 2016, a left lateral hemihepatectomy was performed. One month later, the patient underwent thoracotomy with laser metastasectomy and lymphadenectomy. Three weeks prior to presentation, a restaging examination showed tumor progression with new hepatic and pulmonary metastasis. Chemotherapy with leucovorin, fluorouracil, and irinotecan (FOLFIRI) and aflibercept was initiated the week before admission.

Physical examination showed a patient in poor physical condition, but afebrile. Pulmonary examination was normal and the abdomen was non-tender to palpation and showed normal bowel sounds in all four quadrants. Inspection demonstrated multiple scars consistent with multiple prior surgeries. The spine and shoulders were painful on examination.

Upon admission, laboratory results showed mild anaemia (hemoglobin 7266 mmol/l, hematocrit 34.6%), elevated liver and slightly elevated pancreatic enzymes (gamma-glutamyl transpeptidase 409 U/l, lactate dehydrogenase 330 U/l, lipase 112 U/l). Absolute leucocyte count was normal but showed a left shift (white blood cell count 5990/μl; neutrophils 75.3%). C-reactive protein (CRP) was elevated (86 mg/l). A chest and abdominal computed tomography (CT) scan was performed to exclude pulmonary embolism or aortic dissection and to identify a possible source of infection (Fig. 3). This showed progression of the hepatic metastasis and small pulmonary metastases, pulmonary dystelectasis without infiltration, multiple incisional hernias of the abdominal wall without evidence of bowel incarceration, and a hiatal hernia. No pulmonary embolism or aortic dissection was detected and there was no sign of pericardial effusion. The thoracolumbar spine showed moderate degenerative changes, but no evidence of osseous metastasis or spondylodiscitis. A myocardial infarction was excluded by electrocardiogram (ECG) and troponin-testing.

Fig. 3.

Transverse computed tomography scan showing intrathoracic stomach with cardiac adhesions 72 h prior to perforation.

Initial interventions included opioid infusion for pain control and intravenous antibiotics (piperacillin/tazobactam). While this alleviated the pain, laboratory results on the third hospital day showed increasing infection parameters (CRP 130 mg/l).

During the night of the fourth hospital day, the patient reported acute onset of severe thoracic pain. This exacerbation of presenting symptoms was associated with acute shock, so the patient was transferred to the intensive care unit (ICU). On arrival at the ICU, the patient’s blood pressure was 80/40 mmHg and the ECG showed a sinus tachycardia up to 135/bpm; on clinical findings there was a jugular venous distention with a slow capillary filling time over 2 s. Unfortunately, we have no information about the central venous pressure due to the lack of a central venous line at this stage.

Echocardiography was performed but was limited secondary to suboptimal examination conditions. To exclude pulmonary embolism, another chest CT scan was performed. This CT scan obtained approximately 72 h after admission showed pneumopericardium. Pericardial air tamponade of the right ventricle was determined to be the etiology of acute obstructive cardiogenic shock (Fig. 1, Fig. 2).

Fig. 1.

Pneumopericardium with air tamponade of the right ventricle.

Fig. 2.

Sagittal computed tomography scan after pericardial perforation shows the compression of the right ventricle causing pericardial tamponade.

Given the presence of pneumopericardium , we decided not to perform echocardiographic-guided pericardiocentesis, because the right ventricle was not visible in echocardiogram from the subxiphoid point. Instead, the patient was immediately brought to the operating theater. Despite therapy with high-dose epinephrine and bolus intravenous fluids, the patient’s hemodynamic status deteriorated rapidly. An emergent laparotomy was performed with intensive adhesiolysis of perigastric adhesions. Pericardial fenestration, with decompression of air tamponade improved the hemodynamic situation. The paraesophagheal hernia was reduced and the stomach was returned to the abdomen. Further examination showed a 15 mm gastric perforation caused by an active peptic ulcer; this was closed by suturing. Because of massive intraoperative hemorrhage, the spleen was resected. After ensuring hemostasis, the abdominal cavity was extensively irrigated and the surgical incision was closed. Post-operatively, the patient was readmitted to the ICU. On post-operative day 5, the patient died secondary to multisystem organ failure.

Discussion

Pneumopericardium is defined as the presence of air or other gas in the pericardial sac. The rare occurrence was first described by Bricketeau in 1844. Most often the result of traumatic or iatrogenic injury, exceptional cases arise from fistulous tracts from air-containing viscera such as the esophagus or stomach [3]. Some reported cases of pneumopericardium are caused by bronchopericardial fistula formation due to bronchogenic carcinoma or pulmonary metastasis [4], but most described cases resulted from gastropericardial fistulas [5]. A review of cases of pneumopericardium noted that nearly 80% of gastropericardial fistulas were secondary to prior surgery including fundoplication, esophagectomy, bariatric surgery, or partial gastrectomy [6], [7]. A minority of patients with pneumopericardium are the result of gastric peptic ulcer disease in the setting of upside-down stomach or a large hiatal hernia [8], [9].

In our case, the patient had a known hiatal hernia and was taking a non-prescribed non-steroidal anti-inflammatory drug, increasing the likelihood of gastric ulceration. More than 50% of patients with penetrating gastric ulcer into the pericardium die secondary to uncontrolled massive internal hemorrhage, septic peritonitis, or prolonged multisystem organ failure due to hypovolemic or cardiogenic shock [3].

Pneumopericardium is difficult to diagnose on clinical evaluation because of the nonspecific presenting symptoms, such as severe chest pain or dry cough. Furthermore, there are no specific clinical signs on physical examination. Thus, perforation of a peptic ulcer into the pericardium cannot be diagnosed based on clinical signs or symptoms alone. Acute cardiac (acute coronary syndrome or myocardial infarction) or vascular events (pulmonary embolism, aortic dissection, or spine-syndrome) are far more likely and are primarily considered in patients who present with acute chest pain [2], [3], [10]. Jugular venous distention, low blood pressure, and tachycardia are typical findings in obstructive cardiogenic shock. Indeed, the lack of a sufficient acoustic window above the heart could have been a sign of pneumopericardium. However, pneumopericardium was not considered at this stage of work-up when the patient arrived on the ICU.

Perhaps earlier consideration of gastroscopy would have led to the diagnosis before the catastrophic perforation of the gastric peptic ulceration into the pericardial cavity.

This case is the first to document the absence of radiographic findings indicative of incipient pneumopericardium secondary to perforation of a gastric ulcer on a CT scan performed within 72 h of the acute event. Typical radiographic signs such as pericardial thickening, tear-drop shaped gas pointing toward the heart, or an air-filled fistula tract from adjacent viscera were not observed in the initial CT scan.

Author contributions

All authors have read and approved the manuscript.

Funding

This work was not supported by funding.

Conflict of interest

This case was not reported before in any form. There is no conflict of interest to disclose for all authors.

Statement of consent

We confirm that informed consent was obtained from the patient and his relatives to publish the case report and the figures contained within.