Cardiac tamponade as a life-threatening complication in antireflux surgery

Cardiac tamponade as a life-threatening complication in antireflux surgery

The American Journal of Surgery 191 (2006) 139 –141 Brief reports Cardiac tamponade as a life-threatening complication in antireflux surgery Beat Pe...

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The American Journal of Surgery 191 (2006) 139 –141

Brief reports

Cardiac tamponade as a life-threatening complication in antireflux surgery Beat Peter Müller-Stich, M.D.a,*, Georg Linke, M.D.a, Bettina Leemann, M.D.b, Jochen Lange, M.D.a, Andreas Zerz, M.D.a b

a Department of Surgery, Kantonsspital, 9007 St. Gallen, Switzerland Department of Anesthesiology, Kantonsspital, 9007 St. Gallen, Switzerland

Manuscript received January 22, 2005; revised manuscript August 15, 2005 Presented at the 57th Annual Meeting of the Southwestern Surgical Congress, San Antonio, Texas, April 10 –12, 2005

Abstract Background: While injuries to the esophagus, stomach, spleen and pleura are well-known, cardiac lesions resulting from complications of surgery at the esophagogastric junction are rarely reported in the literature. Methods: We report on two of our own patients with cardiac tamponade after surgery at the esophagogastric junction and present a review of the literature. Results: We overview seven patients (including our own). In five cases a stitch to the diaphragm was the cause. The lesions became apparent during and up to fourteen days after the operation. In three cases the complication led to death. Conclusions: It is essential to consider the risk of cardiac lesions with surgery at the esophagogastric junction, especially if sutures or staples are placed in this region. Only with an appropriate alertness and management can this complication be prevented and its potentially fatal issue averted. © 2006 Excerpta Medica Inc. All rights reserved. Keywords: Cardiac tamponade; Hiatal hernia repair; Fundoplication; Complications; Mortality; Surgical staples

The frequency of intraoperative complications related to antireflux procedures and hiatal hernia repairs has been found to be as high as 19%. Although injuries to the esophagus, stomach, spleen, and pleura, and problems related to anatomic difficulties and bleeding are well known, they mostly can be resolved without serious consequences. Lifethreatening complications are uncommon; however, because of the close proximity of the mediastinum, injuries to the esophagus with consecutive mediastinitis are a special cause for concern [1]. In contrast, there are few reports on cardiac lesions as a result of surgery at the esophagogastric junction, even in large reviews. With the present report we aim to create awareness of a probably underestimated complication of this type of surgery. Precautionary measures that, on the one hand, prevent such complications and, on the other hand, avert their fatal course are discussed.

* Corresponding author. Tel.: 0041-71-494-13-44; fax: 0041-71-494-28-86. E-mail address: [email protected]

Within a period of 1 year we were confronted with 2 patients sustaining a cardiac tamponade after hiatal hernia repair. A 74-year-old woman presented with a request for a second antireflux surgery 7 years after the primary surgery. Despite treatment with 40 mg pantoprazol , she suffered from heartburn, chronic cough, and hoarseness, and severe liquid reflux restricted the patient’s quality of life. Preoperative esophagogastroscopy and upper-gastrointestinal barium contrast series revealed a 6-cm sliding hiatal hernia with grade II esophagitis according to Savary and Miller [2]. Additional test results comprising laboratory diagnostics, echocardiography, and spirometry were normal. The only relevant secondary diagnosis was well-treated hypertensive heart disease. Because of the previous surgical intervention we chose an upper median laparotomy as access. After repositioning of the transdiaphragmatically herniated structures and complete reopening of the partially ruptured fundoplication, mesh-reinforced hiatoplasty with anterior fundophrenicopexy was performed as an antireflux procedure.

0002-9610/06/$ – see front matter © 2006 Excerpta Medica Inc. All rights reserved. doi:10.1016/j.amjsurg.2005.08.006

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B.P. Müller-Stich et al. / The American Journal of Surgery 191 (2006) 139 –141

Fig. 1. Thoracic computed tomography revealing a cardiac tamponade after hiatal surgery. CT, cardiac tamponade; RV, right ventricle; LV, left ventricle; A, aorta; E, esophagus; D, diaphragm.

A 6 ⫻ 6-cm prolene mesh with an excentric 2-cm hole was applied from behind around the esophagus and fixated to the diaphragm with 10 helical staples (7 mm, ProTak, Autosuture; Tyco Healthcare, Wollerau, Switzerland). Instead of a fundoplication, a fundophrenicopexy was performed with 8 polyfile nonresorbable sutures, fixating the cardia and the fundus to the left dome of the diaphragm. The intraoperative course was uneventful. A few hours postoperatively, a decrease in blood pressure occurred, although the hemoglobin value remained stable and respiratory conditions were normal. A chest radiograph indicated increased cardiac volume with a dilated azygous vein, and the subsequent computed tomography scan confirmed a suspected cardiac tamponade (Fig. 1). An emergency relaparotomy with pericardial fenestration was performed. Venous bleeding from the myocardium of the right ventricle, probably caused by a fundophrenicopexy suture, was stopped by resuturing, the pericardium was left open, and the left hemithorax was drained. Immediately after surgical reintervention, laboratory diagnostics and electrocardiography indicated an inferior myocardial infarction probably as a consequence of the myocardial resuturing. Intensive care resulted in stabilization of the cardiac condition. A further complication in the clinical course occurred on account of a subglottic stenosis induced by intubation requiring a tracheostomy for 1 week. The patient could not be discharged before the 24th day. Three months postoperatively she was in good general condition. The gastroesophageal reflux had been resolved completely, a fact that could be objectified both with a Gastrointestinal Symptom Rating Scale questionnaire and 24-hour esophageal pH monitoring. However, there still was an exertional dyspnea New York Heart Association class II with an exercise stress test that had to be discontinued because of angor. T-wave inversion in leads II, aVF, and V2-V6, and R loss over the anterior wall were documented by an electrocardiogram. Coronary angiography revealed an occlusion of

a collateral of the right coronary artery with inferomedial and apical hypokinesia but preserved ejection fraction. Another 82-year-old man was admitted for surgical repair of a large symptomatic hiatal hernia after years of dysphagia, regurgitation, and chronic recurrent coughing fits. Treatment with 20 mg esomeprazol and 10 mg domperidon did not lead to major improvement in the patient’s condition. Preoperative work-up including esophagogastroscopy, thoracic computed tomography scan, and an upper-gastrointestinal barium contrast series revealed an 8-cm mixed hiatal hernia with grade IV esophagitis according to Savary and Miller [2]. The 24-hour esophageal pH monitoring did not, however, show evidence of a pathologic reflux. The manometric examination, which confirmed normal esophageal motility, and laboratory diagnostics were without pathologic findings. As a relevant secondary diagnosis, the patient suffered from arterial hypertension and was under oral anticoagulant therapy because of 2 incidents with pulmonary embolism. The first occurrence was bilateral and had occurred 2 years earlier, the second occurrence was central and had occurred 1 year earlier. Surgical treatment consisted of a laparoscopically mesh-augmented hiatoplasty with anterior fundophrenicopexy, as described earlier, after complete dissection of the hernia sac. Because of an accidental rupture of the right crus of the diaphragm, a 15 ⫻ 15-cm prolene mesh was necessary to reconstruct the hiatus. The mesh was fixed by 16 helical staples (ProTak, Autosuture), and the fundophrenicopexy was performed with 8 polyfile nonresorbable sutures. During the first 24 postoperative hours, deteriorating oxygen saturation with increasing dyspnea was most notable, although the patient’s circulatory conditions remained stable. When the radiologic evidence confirmed an acute pulmonary edema, the patient was transferred to the intensive care unit. The cause of the pulmonary edema remained unclear. Left-sided heart failure in the context of an acute coronary syndrome with slightly increased troponin level was suspected. The electrocardiogram remained unchanged. Forced diuretic treatment and intravenous anticoagulation with heparin was initiated, the latter also within the scope of the 2 earlier incidents of pulmonary embolism. After 42 hours, the first episode of a tachycardic atrial fibrillation with heart rates of up to 150 bpm but without hypotension occurred. The therapy with amiodaron led to the decrease of the heart rate to less than 100 bpm. However, a second chest radiograph revealed progredient bilateral transudation and pleural effusions. After 48 hours, the patient experienced severe retrosternal pressure with simultaneous tachyarrhythmia and consecutive circulatory failure. Within a very short time, pulseless electrical activity was diagnosed, whereupon the patient died despite resuscitation attempts. The autopsy revealed a cardiac tamponade originating from an epicardial vascular erosion caused by one of the helical staples, probably with the patient’s anticoagulant therapy as a cofactor. Antireflux procedures and hiatal hernia repairs may be associated with life-threatening complications, and a mor-

B.P. Müller-Stich et al. / The American Journal of Surgery 191 (2006) 139 –141

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Table 1 Overview of all the cases with cardiac tamponade caused by hiatal surgery found in the literature Access

Cause

Time

Course

Trastek et al [3] Thijssens et al [4] Kemppainen and Kivilvoto [5]

Open Laparoscopic Laparoscopic

Not specified Helical staple Angled staple

Death Recovery Death

Farlo et al [6] Firoozmand et al [7]

Laparoscopic Laparoscopic

Suture Liver retractor

1/2 day after surgery 14 days after surgery After surgery; point of time not specified During surgery During surgery

tality rate of up to 5% has been reported [1]. In consideration of this fact, a critical indication for these surgical procedures is essential. Although esophagogastric lesions as potentially life-threatening complications are well known, there are few reports on cardiac lesions. In the Pubmed Medline database (National Library of Medicine), we were able to find only 5 cases by combining the key words “cardiac tamponade” with “reflux,” “hernia,” or “fundoplication” (Table 1). Creating awareness for this kind of complication is important primarily because it rapidly leads to circulatory failure and, with inadequate management, to death. Thus, 3 of the 7 patients in our review (our own patients included) died. Cardiac lesions are caused mainly by stitches. The instrument used to place the stitches does not seem to be relevant. The fact that the transdiaphragmatic distance to the pericardium is in several places only a few millimeters is of far greater importance. Thus, when the first cardiac tamponade occurred at our hospital after open surgery, in which the lesion was caused by a suture, we concluded that it is advantageous to use staples for procedures at the diaphragm because the given length of the staples excludes deeper injuries. One year later we were confronted with another cardiac tamponade caused by a 7-mm helical staple. This experience is also reported in the literature, in which various types of staples and sutures are mentioned as causes for cardiac injuries (Table 1). To lower the risk induced by staplers, we since have been using angled staples (Multifier Endo Hernia stapler, Autosuture, Tyco Healthcare) for the mesh fixation, which penetrates 4 mm when open and 2.5 mm when closed. In an experimental postmortem test, none of the staples penetrated the pericardium, unless counterpressure was exerted manually from the thorax. For fundophrenicopexy we continued using sutures, which, however, are placed deliberately on the surface. The type of abdominal access does not seem to be of any significance either. Thus, in our experience, 1 of the 2 patients had open surgery and the other patient underwent

Recovery Recovery

laparoscopic surgery. Accordingly, the reports in the literature also concern both open surgery and laparoscopic procedures (Table 1). Clinical manifestation may occur at any time in the postoperative course. Cardiac tamponades were diagnosed up to the 14th postoperative day (Table 1). Furthermore, it can be masked by other more common postoperative problems, such as heart failure and tachyarrhythmia. This is why patients require thorough long-term postoperative care. In the case of cardiopulmonary insufficiency, a thoracic computed tomography scan, or at least echocardiography, definitely should be indicated. A conventional chest radiograph is not sufficient. As a matter of principle, it is essential to consider a potential cardiac tamponade after surgery to the esophageal hiatus, especially if sutures or staples were placed in this region. Only then can the signs of this life-threatening complication be recognized in time and their fatal consequences averted by means of adequate management.

References [1] Bowrey DJ, Peters JH. Laparoscopic esophageal surgery. Surg Clin North Am 2000;80:1213– 42, vii. [2] Savary M, Miller G. Der Oesopagus. Lehrbuch und Endoskopischer Atlas. Solothurn: Verlag Gassman AG; 1977;135–9. [3] Trastek VF, Deschamps C, Allen MS, et al. Uncut Collis-Nissen fundoplication: learning curve and long-term results. Ann Thorac Surg 1998;66:1739 – 44. [4] Thijssens K, Hoff C, Meyerink J. Tackers on the diaphragm. Lancet 2002;360:1586. [5] Kemppainen E, Kiviluoto T. Fatal cardiac tamponade after emergency tension-free repair of a large paraesophageal hernia. Surg Endosc 2000;14:593. [6] Farlo J, Thawgathurai D, Mikhail M, et al. Cardiac tamponade during laparoscopic Nissen fundoplication. Eur J Anaesthesiol 1998;15: 246 –7. [7] Firoozmand E, Ritter M, Cohen R, et al. Ventricular laceration and cardiac tamponade during laparoscopic Nissen fundoplication. Surg Laparosc Endosc 1996;6:394 –7.