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Cardiac herniation following closure of atrial septal defect through limited posterior thoracotomy
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     a Division of Pediatric Cardiac Surgery, Amrita Institute of Medical Sciences, Elamakkara P.O., Kochi 682026, Kerala, India

    b Division of Cardiac Anesthesiology, Amrita Institute of Medical Sciences, Elamakkara P.O., Kochi 682026, Kerala, India

    Abstract

    Objective: We report an unusual complication following closure of atrial septal defect through right limited posterior thoracotomy. Methods: An eight-year-old girl underwent closure of atrial septal defect through right limited posterior thoracotomy. She developed cardiac herniation in the early post-operative period following a tension pneumothorax on the left side, while recovering in the intensive care unit. Results: Cardiac herniation was promptly recognized, albeit subtle hemodynamic changes, and was reduced through re-operation. Conclusion: Liberal use of pericardium for closure of intra-cardiac defects results in a gap in the pericardial sac. Posterior thoracotomy approach for closure of atrial septal defect has a higher propensity for cardiac herniation owing to the small size and postero-lateral location of the pericardial defect. Recognition and early treatment of cardiac herniation is important since it can mimic cardiac tamponade. Cardiac herniation can be avoided either by enlarging the pericardial defect or by closing it with a prosthetic patch.

    Key Words: Congenital-acyanotic; Atrial septal defect; Pericardium; Thoracotomy

    1. Introduction

    Limited posterior thoracotomy (LPT) approach for atrial septal defects (ASD) gives an excellent cosmetic result [1]. The pericardial defect left by harvesting the patch is usually small and is located on the right lateral aspect of pericardial sac. Hence there is a preponderance for the heart to herniate into the right pleural cavity. We herewith report one such rare event and prompt successful management following closure of atrial septal defect employing LPT.

    2. Case summary

    An 8-year-old girl with 20x20 mm secundum ASD underwent elective closure through LPT. The right pleural space was entered through the 4th space. After removal of right lobe of thymus, a small pericardial patch was harvested anterior to the right phrenic nerve. Cardiopulmonary bypass (CPB) was established with aortic and bicaval cannulation. ASD was closed with the pericardial patch under moderate hypothermia and cardioplegic arrest. CPB was discontinued uneventfully after re-warming. Two chest drains were placed, one into the pericardium and the other into the right pleural cavity. The thoracotomy was closed and the patient was transferred to the ICU.

    Post-operatively, the patient maintained good hemodynamics in the ICU and she was being weaned off the ventilator. Immediate postoperative chest roentgenogram was normal (Fig. 1). A few hours later, she developed mild hypotension (systolic blood pressure from 110 to 78 mmHg) with sudden increase in CVP (13 from 5 mmHg) and decrease in urine output. Arterial blood gas analysis showed acceptable gas exchange [PaO2: 146 and PaCO2: 34.6]. However, there was an increase in serum lactate levels compared to the previous value (4.0/1.8 mmol/l). Clinical examination revealed diminished breath sounds on the left side. The peak and mean airway pressures were also normal (18:8 cm). Immediate chest roentgenogram revealed a tension pneumothorax on the left side with gross mediastinal shift (Fig. 2). A left intercostal drainage tube was inserted promptly, and the left lung expanded fully and trachea became central. However, cardiac shadow failed to return to its normal position (Fig. 3). Left lateral position failed to reposition the heart spontaneously even after 24 h. Hence the patient was taken back to the operating room, where she developed severe hypotension on induction of anesthesia. On reopening of thoracotomy, the heart was found to have herniated to the right pleural cavity. The pericardial defect was small and the edges were preventing spontaneous reduction of the heart back into the pericardial sac. The heart was manually reduced, after the blunt dissection to release the flimsy adhesions between the heart and pericardium. Following this, the hemodynamics returned to normal. The pericardial defect was left as such as the precipitating factor for cardiac herniation (the tension pneumothorax on left side) was dealt with adequately. She had an uneventful recovery since then, cardiac position in the chest X-ray normalized (Fig. 4). She was extubated after 8 h and was discharged home on the sixth day.

    3. Discussion

    Cardiac herniation is a rare event. Most of cardiac herniations are caused following blunt trauma producing rupture of the pericardium [2–4]. The use of the pericardium for the closure of various intracardiac defects leaves a gap in the pericardial sac, through which the heart can herniate. But cardiac herniation after cardiac surgery is a rare event, though there are reports of it following intra-pericardial pneumonectomy [5]. This is probably because most cardiac defects are corrected through sternotomy and the defect in the pericardium left by harvesting the patch is large and located anteriorly. Thus, we believe, eliminating the risk of cardiac herniation.

    LPT is an excellent cosmetic approach for ASD closure. In our unit, more than 300 cases of ASD closure have been performed through this approach with good results and the initial results were published earlier [6]. In this technique, the heart is approached across the right pleural space and the pericardial defect produced by harvesting the patch is small and located posteriorly on the right side. This creates a propensity for the heart to herniate into the right pleural space. However, spontaneous cardiac herniation is a rarity. In our child, left tension pneumothorax had forced the heart out of the pericardial sac through the defect created by the harvesting of the patch. The defect was small and hence the edges of the pericardium were preventing spontaneous reduction of the ventricular mass after release of the tension pneumothorax. Though cardiac instability was marginal in this child, the hemodynamic alterations were similar to cardiac tamponade (i.e. rise in CVP, in urine output and in lactate levels). Hence we believe prompt recognition and proactive management are critical in avoiding cardiac decompensation.

    To sum up, it is important to leave a large gap in the pericardial sac after harvesting a patch for intracardiac repairs. This, we believe, minimizes the risk of cardiac herniation. In addition, it is very essential to leave an adequate amount of pericardium in the region where the right dome of the diaphragm meets the anterior chest wall while harvesting the patch. This might further facilitate in preventing herniation, by retaining the ventricular mass in the pericardial sac. Alternatively, the defect can also be closed with a pericardial membrane or prolene mesh. ‘Darning’ of the defect with a 3/0 Prolene is another alternative.

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