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Volume: 17 Issue: 4 August 2019


Cardiac Tamponade Due to Pneumopericardium After Liver Transplant

Pneumopericardium is a rare cause of cardiac tamponade, and it is an extremely rare complication of liver transplant. Here, we present a patient with cryptogenic liver cirrhosis who experienced cardiac tamponade secondary to a tension pneumo­pericardium during the postoperative course after liver transplant.

Key words : Cardiogenic shock, Liver cirrhosis, Pericardial air


Pneumopericardium, an accumulation of air in the pericardium, is a rare cause of cardiac tamponade. It is also a rare disorder with varying presentation. Patients with pneumopericardium are frequently asymptomatic; however, cardiac tamponade or cardiogenic shock may occur due to quick accumulation of more air in the pericardial sac. Pneumopericardium usually presents after open chest trauma, although it can also be a manifestation of increased intrathoracic pressure, as occurs in closed chest trauma, asthma attacks, obstructive laryngitis in children, or barotrauma in patients on positive-pressure mechanical ventilation. More rarely, it can be an indication of an infectious or postoperative complication in a neighboring organ, especially the lungs and trachea.1

Case Report

A 56-year-old male patient underwent liver trans­plant for cryptogenic liver cirrhosis. The patient’s history showed no other medical complications except for hypopituitarism, which required follow-up by an endocrinology clinic. After liver transplant, the patient’s 2-day intensive care unit stay and 4 days of inpatient hospitalization were uneventful.

On postoperative day 7, the patient suddenly developed symptoms of dyspnea, cold sweating, nausea, and palpitation. On physical examination, blood pressure was 85/65 mm Hg, heart rate was 113 beats/minute, and respiratory rate was 25 breaths/minute. Routine laboratory results were normal except for high levels of D-dimer (4.49 mg/L). An immediate abdominal ultrasonography and Doppler examination were performed because of suspicion of bleeding into the abdomen. The ultrasonography revealed no evidence of bleeding in the abdomen. Duplex ultrasonography showed normal blood flow detected from the hepatic artery, hepatic vein, portal vein, and inferior vena cava.

A radiologic examination revealed that the pericardial sac was clearly separated from the heart shadow (pneumopericardium; Figure 1). The high D-dimer value necessitated the elimination of pulmonary embolism as the differential diagnosis. An image of the patient’s heart could not be obtained via transthoracic echocardiograpy due to massive air in the pericardial cavity. Massive air accumulation in the pericardium, which clearly obstructed com­pliance of the right ventricle, was noted on the thorax computed tomography scan. No thrombi were observed in the pulmonary arteries (Figure 2).

The patient’s general condition was gradually deteriorating, and presence of confusion began to develop. The patient required urgent open tube pericardiostomy. The previous incision line was observed to be reaching the xiphoid process. Under local anesthesia, a few upper sutures were removed. Superior to the diaphragm, the pericardium was explored and a 2-cm pericardial incision was made. As soon as the pericardium was opened and the air released, the blood pressure values of the patient suddenly returned to normal. After pericardial incision, a tube was placed because of suspician that pericardial air had been passing from the abdomen. The patient was taken to the intensive care unit in stable condition. The pneumopericardium decreased (verified by chest radiography; Figure 3), but chest tube-mediated air leak lasted for 10 days. Indeed, on postoperative days 3 and 5, pneumopericardium was repeated on radiographic images after the pericardial tube was clamped for 8 hours (Figure 4). This was probably as a result of continued air passage from the abdomen to the pericardium.

The pericardial tube was removed by clamping the tube on postoperative day 10 after confirmation of no air by radiographic scan. The patient’s clinical condition improved gradually, and the patient was discharged 15 days after chest tube insertion. Five days after discharge, no findings were shown in the pathologic examination.


Pneumopericardium, a rare and sometimes asymp­tomatic event, can lead to cardiogenic shock due to cardiac tamponade. Causes leading to pneumo­pericardium, especially with cardiac tamponade, are rarely due to clinical manifestations. Lung cancer, broncho-pericardial fistula, gastro-pericardial fistula, postlobectomy, pacemaker implantation, and penetrant or blunt chest trauma are some of the clinical events that can result in cardiac tamponade due to pneumopericardium.2-8 To our knowledge, this is the first case in which pneumopericardium occurred and resulted in cardiac tamponade after liver transplant.

In our patient, air had accumulated in the pericardium, causing the patient to develop cardiac tamponade. We believe that air, which normally remains in the abdomen postoperatively, may have somehow passed through and into the pericardial space. The most probable scenario that could have led to the passage of air into the pericardial opening occurred during inferior vena cava clamping. This operative complication perhaps resulted in massive accumulation of air in the pericardium.

The most sensitive method to diagnose cardiac tamponade is transthoracic echocardiography; however, if the pneumopericardium is suspected to be the reason for cardiac tamponade, a thorax computed tomography should be conducted. Pericardial intense air content makes imaging impossible with ultrasonographic examinations.


After liver transplant, another reason for a decline in a patient’s condition may be the development of cardiac tamponade due to pneumopericardium.


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Volume : 17
Issue : 4
Pages : 568 - 570
DOI : 10.6002/ect.2017.0287

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From the 1Cardiovascular Surgery Department, School of Medicine, Akdeniz University; the 2Cardiology Department, Atatürk State Hospital; and the 3General Surgery Department, School of Medicine, Akdeniz University, Antalya, Turkey
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Cemal Kemaloğlu, Akdeniz Üniversitesi Tıp fakültesi Hastanesi, 07070 Dumlupınar Bulvarı, Antalya, Turkey
Phone: +90 505 899 0739