Pericardial Tamponade: A Life Threatening Complication of Laparoscopic Gastro-oesophageal Surgery
Article Outline
Laparoscopic surgical procedures involving the gastro-oesophageal region are commonly performed for the management of morbid obesity and refractory gastro-oesophageal reflux disease (GORD). In general, laparoscopic procedures are associated with lower morbidity and mortality in comparison with open techniques. This report highlights cases of potentially life threatening, late onset pericardial tamponade, occurring in the absence of infection or trauma, complicating laparoscopic gastro-oesophageal surgery. Possible mechanisms, clinical manifestations, diagnostic investigations and management of pericardial tamponade are reviewed.
Keywords: Percardial tamponade, Sympathetic effusion, Laparoscopic surgery complications, Postoperative chest pain
Introduction
Laparoscopic surgical procedures involving the stomach and lower oesophageal junction are commonly performed for the management of morbid obesity and refractory gastro-oesophageal reflux disease (GORD). In general, the morbidity and mortality of laparoscopic surgery is significantly lower than open techniques [1]. Laparoscopically assisted gastric banding (LAGB) has a mortality of 0.05% [2] and a late complication rate of 11%, predominantly due to device related issues [2], [3]. Laparoscopic anti-reflux surgery, such as Nissen fundoplication, also has a low post-operative complication rate of 2.6% with negligible procedure-related mortality [1], [4].
There are sporadic reports of pericardial complications related to laparoscopic gastro-oesophageal surgery in the literature. Complications secondary to infection or direct trauma such as pericardiotomy-like syndrome [5] and gastro-pericardial fistula [6] have been reported. Bui et al. postulated “sympathetic” pericardial effusion secondary to an infected LAGB system in 2003 [7]. To the authors’ knowledge, there have been no reports of pericardial complications without infection or a direct fistulous communication from laparoscopic gastro-oesophageal surgery. We report two cases of life threatening cardiac tamponade, presenting as a late complication of laparoscopic surgery involving the stomach and low oesophagus without evidence of infection or trauma. Both cases required urgent surgical intervention with pericardiotomy and drainage.
Case Study 1
A 63 year-old woman with morbid obesity (140
kg) and Barrett's oesophagus underwent an elective LAGB and reduction of hiatus hernia (Bard®-composix®-E/X-mesh). Her early recovery was complicated by atrial fibrillation (AF) and acute pulmonary oedema. Trans-thoracic echocardiography (TTE) performed on day four post-operatively, demonstrated a small to moderate pericardial effusion (maximal dimension 2.6
cm) without features of tamponade. She was treated conservatively with commencement of amiodarone for AF without anticoagulation.
In the post-operative period, the patient had recurrent presentations to the emergency department with chest pain and rapid AF but displayed no clinical evidence of cardiac tamponade and was managed conservatively. Five weeks post-surgery, she represented with chest pain, hypotension (103/60
mm
Hg), distended neck veins and muffled heart sounds. Chest X-ray demonstrated globular cardiomegaly (Fig. 1). Inflammatory markers were elevated (leucocytes 12.4
×
109
L−1, neutrophils 9.0
×
109
L−1, C-reactive protein was 306
mg
L−1). A computed tomography pulmonary angiogram (CTPA) revealed a large pericardial effusion (Fig. 2). TTE confirmed a large global pericardial effusion (maximal thickness 3.8
cm) with evidence of cardiac tamponade. The patient underwent urgent drainage of the effusion via a lower third mini hemi-sternotomy. Microbiological analysis of the pericardial fluid excluded an infective or haemorrhagic aetiology. Post-drainage TTE demonstrated no recurrence of the pericardial effusion. The patient subsequently made excellent progress with weight loss of 60
kg and no further cardiac symptoms.

Figure 1.
Chest X-ray demonstrating cardiomegaly with poor visualisation of the left costophrenic sulcus.

Figure 2.
Chest computed tomography (axial view) demonstrating a pericardial effusion and the close proximity of the surgical material (white long arrow) to the pericardium (white short arrow).
Case Study 2
A 75 year-old woman with history of pulmonary embolism (PE) requiring lifelong anticoagulant therapy underwent an uncomplicated laparoscopic hiatus hernia repair with mesh (GORE® dual-mesh) and loose Nissen fundoplication for treatment of symptomatic para-oesophageal hernia with gastric volvulus.
Thirteen days post-surgery, the patient presented to the emergency department with chest pain. A ventilation-perfusion lung scan demonstrated a low probability of PE and the patient was discharged with analgesia. She re-presented on the same day with severe pleuritic chest pain. Electrocardiography (ECG) demonstrated new widespread concave ST segment elevation. An urgent TTE revealed normal cardiac function but demonstrated a small circumferential pericardial effusion without evidence of tamponade. Chest computed tomography (CT) performed to exclude surgical complications, but confirmed a small pericardial effusion (Fig. 3). The patient was diagnosed with acute pericarditis and commenced on non-steroidal anti-inflammatories and colchicine. She remained haemodynamically stable and was discharged four days later with follow-up echocardiography organised. Anticoagulation was recommenced four weeks after surgery.

Figure 3.
Chest computed tomography (coronal view) demonstrating a small pericardial effusion and the close proximity of the surgical material (three white arrows) to the pericardium.
Thirty-seven days post-surgery, the patient represented to hospital with worsening dyspnoea and reduced exercise tolerance. Physical examination revealed raised neck veins and peripheral oedema with audible heart sounds. She was haemodynamically stable and afebrile. TTE showed a moderate pericardial effusion with right atrial compression, an early sign of compromised cardiac filling. A repeat TTE three days later demonstrated increased pericardial fluid accumulation with Doppler and 2D features of cardiac tamponade. The patient underwent pericardial drainage with creation of a pericardial window from the sub-xiphoid approach. The pericardial fluid was blood stained without evidence of infection. Findings were consistent with haemorrhagic transformation of the effusion. Her preceding coagulation studies demonstrated therapeutic, but not excessive anticoagulation.
Follow-up echocardiography demonstrated no recurrence of the pericardial effusion. The patient has remained well with resolution of gastrointestinal symptoms.
Discussion
Chest discomfort following gastro-oesophageal surgery represents a difficult and diagnostic challenge. These cases highlight that pericarditis with associated pericardial effusion is an important and potentially life threatening complication of laparoscopic gastro-oesophageal surgery and should be considered alongside standard surgical complications and pulmonary thromboembolism. Significant pericardial effusions can rapidly progress to life threatening pericardial tamponade characterised by hypotension, tachycardia, pulsus paradoxus, Kussmaul's sign and distant or absent heart sounds. Early cardio-thoracic imaging with chest CT and/or TTE is essential in cases of unexplained or persistent post-procedural chest discomfort.
Pericardial effusions may complicate pericarditis in the acute or late post-operative phase. Once identified, monitoring for progressive fluid accumulation and tamponade is essential. Potential mechanisms for the development of a pericardial effusion following gastro-oesophageal surgery include: direct pericardial trauma, spread of infection from implanted prosthetic material and “sympathetic” pericarditis with effusion [5], [6], [7]. Sympathetic pericarditis may result from reactive pericardial inflammation in response to foreign material in close proximity to the pericardium and from pericardial trauma related to the surgical procedure. Therapeutic anticoagulation or other bleeding diatheses may precipitate haemorrhagic transformation of an existing pericardial effusion or cause a primary haemorrhagic effusion.
In these case studies, an infectious cause was excluded by pericardial fluid analysis and direct pericardial trauma is unlikely given the delayed presentations. Figure 2, Figure 3 demonstrate the proximity of the pericardium to the surgical field supporting the hypothesis for a reactive sympathetic process, with case two undergoing secondary haemorrhagic transformation despite the absence of documented excessive anticoagulation.
The management of a pericardial effusion is dependent upon its size and haemodynamic consequences. Pericardial drainage with minimally invasive pericardiocentesis or open pericardiotomy should be performed emergently in patients with pericardial tamponade. For diagnostic purposes, drainage of large asymptomatic effusions may also be indicated. Laboratory analysis of the pericardial fluid is essential to identify the underlying aetiology. Although a percentage of patients with reactive pericardial effusion may resorb over time, once identified, a repeat echocardiography is recommended within one to two weeks to determine if there is progression or echocardiographic evidence of tamponade even in the absence of clinical deterioration or signs of progression. This is particularly important in patients requiring anticoagulation for coexisting conditions such as AF, mechanical heart valves and pulmonary emboli.
In conclusion, late onset pericardial tamponade is a rare but important complication of laparoscopic gastro-oesophageal surgery. Early recognition and prompt management of this complication is essential to avoid associated morbidity and mortality.
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PII: S1443-9506(11)01058-4
doi:10.1016/j.hlc.2011.08.002
Crown Copyright © 2011. Published by Elsevier Inc. All rights reserved.
