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Ann Thorac Surg 1999;67:818-820
© 1999 The Society of Thoracic Surgeons

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Original Articles

Primary esophageal repair for Boerhaave’s syndrome

^a Department of Thoracic Surgery, Harefield Hospital, Harefield, Middlesex, United Kingdom

Accepted for publication August 18, 1998.

Address reprint requests to Mr Fountain, Department of Thoracic Surgery, Harefield Hospital, Harefield, Uxbridge, Middlesex UB9 6JH, United Kingdom
e-mail: w.fountain{at}rbh.nthames.nhs.uk

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. Boerhaave’s syndrome is the most sinister cause of esophageal perforation. The mediastinal contamination with microorganisms, gastric acid, and digestive enzymes results in a mediastinitis that is often fatal if untreated.

Methods. We present a series of 21 patients seen in our unit in the 10 years 1987 to 1996. Esophageal repair was performed in 17 (81%) of them. After the resuscitation of the patient in the intensive care unit, our strategy is primary esophageal repair with a single layer of interrupted absorbable sutures combined with mediastinal toilet, mediastinal drainage, and drainage gastrostomy. The majority of patients (12/21) were referred more than 24 hours after perforation.

Results. The mean age of the patients was 60 ± 17 years. The mean stay in the intensive care unit was 1.6 ± 1.8 days and the median hospital stay, 14 days. There were three deaths, an overall mortality rate of 14.3%.

Conclusions. When combined with mediastinal toilet, mediastinal drainage, and drainage gastrostomy, primary esophageal repair for Boerhaave’s syndrome gives an acceptable mortality and should not be reserved for patients seen within 24 hours after spontaneous rupture.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
Esophageal perforation is a serious injury associated with an overall mortality rate of 20% to 30% [1, 2]. Spontaneous esophageal rupture, or Boerhaave’s syndrome, is the most sinister cause of esophageal perforation. This is because, in addition to the resulting esophageal injury, the gastric contents are forcibly expelled into the mediastinum and the pleural cavity. The combination of gastric acid and digestive enzymes causes mediastinitis and sepsis, which is fatal in most untreated cases. Iatrogenic esophageal perforation is a less severe injury; when it is treated in specialized thoracic units, the mortality rate can be 10% [3]. Current literature on the management of esophageal perforation is confusing because this heterogeneous group of conditions results in a variable amount of mediastinal contamination in each case. When operation is deemed necessary, we use a strategy in which primary esophageal repair is combined with mediastinal and pleural drainage and drainage gastrostomy. Operation is performed after resuscitation of the patient and is not reserved for patients seen within 24 hours after perforation. We present our results with this strategy in the management of 21 patients with Boerhaave’s syndrome.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Twenty-one patients with Boerhaave’s syndrome were treated in our unit between January 1987 and December 1996. There was a clear history of forcible vomiting preceding the onset of symptoms in 18 of these patients. Although the other 3 patients did not describe forcible vomiting, there was no history of esophageal instrumentation, foreign-body ingestion, or trauma. Case notes were reviewed retrospectively. All patients were resuscitated in the intensive care unit after admission, and the site of esophageal perforation was identified by soluble contrast swallow. This was later confirmed by upper gastrointestinal endoscopy. Resuscitation involved insertion of a central venous cannula, radial artery line, and urinary catheter. All patients required infusion of a crystalloid or colloid solution and administration of intravenous antibiotics. Only 4 patients (19%) required inotropic support. All patients had a urinary output of more than 0.75 mL · kg^-1 · L^-1 and a mean arterial pressure of at least 60 mm Hg after resuscitation.

The patients were divided into three groups: group 1, localized mediastinal collection and no systemic sepsis; group 2, systemic sepsis or nonlocalized collections; and group 3, delayed presentation with empyema thoracis.

Group 1 comprised 2 patients (9.5%) with minimal extravasation of contrast medium demonstrating a localized collection in the mediastinum and no signs of systemic sepsis. They were managed conservatively. These patients were fed parenterally and had nothing by mouth for 7 days. Intravenous antibiotics were continued for 6 to 10 days. The contrast swallow was then repeated. When it was confirmed that the perforation had healed, oral fluids were begun, and then the patient was weaned to solid food over 3 to 4 days.

Patients in group 2 (n = 17; 87%) had nonlocalized collections or evidence of systemic sepsis. They underwent primary esophageal repair. Thoracotomy was performed, and the site of perforation was identified. Necrotic tissue was debrided, and the thoracic cavity was irrigated. The viable mucosal edge of the perforation was identified and approximated using interrupted 3-0 Vicryl sutures. The chest was closed with two large (32-gauge) thoracostomy tubes in situ. One drain was placed in close proximity to the repair. A laparotomy was then made, and a drainage gastrostomy was performed. Some patients had a feeding jejunostomy constructed at this time, and others were fed by total parenteral nutrition depending on the preference of the operating surgeon; no patient received anything by mouth. Intravenous antibiotics were prescribed for all patients. Contrast esophagoscopy was performed 7 to 10 days postoperatively. Oral intake was commenced if there was no evidence of leak at the site of repair or anastomosis.

Group 3 comprised 2 patients with empyema thoracis referred more than 2 weeks after spontaneous esophageal rupture. Soluble contrast swallow demonstrated healed esophageal perforations. The 2 patients were treated by thoracoscopic debridement of empyema [4]. They were returned to the main ward with two chest drains in situ. The patients were discharged on postoperative days 7 and 11.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
The mean age of the patients in this series was 60 ± 17 years. The mean stay in the intensive care unit was 1.6 ± 1.8 days, and the median hospital stay was 14 days (range, 3 to 183 days). Nine patients were referred within 24 hours after perforation; there were two deaths in this group. One of the 12 patients seen more than 24 hours after perforation died. The overall mortality rate was 14.3%, and all three deaths occurred in group 2 (Table 1).

Group 2
The 17 patients in this group underwent thoracotomy and laparotomy. Eight patients were seen within 24 hours after perforation. One patient underwent esophageal resection because of the presence of a long distal esophageal stricture; the other 16 patients had esophageal repair. There were three deaths (17.6%) in this group. Two of the patients seen within 24 hours died. Contrast study on postoperative day 7 demonstrated four leaks. These were managed conservatively and were shown to have healed at subsequent contrast swallow 7 days later. There was no associated mortality with these leaks.

Group 3
Both patients in this group underwent thoracoscopy and drainage of empyema. Contrast study revealed healed esophageal perforations. Existing empyema thoracis was treated by thoracoscopic debridement. Both patients survived.

	Comment

Top Abstract Introduction Material and methods Results Comment References

 
Boerhaave’s syndrome accounts for 30% to 40% of all cases of esophageal perforation. Esophageal perforation is associated with high morbidity and mortality because the anatomic location of the organ predisposes patients to the development of fatal mediastinitis and multisystem organ failure [5]. Esophageal perforation is also associated with a costly hospital stay. Approximately 30 cases of spontaneous esophageal rupture are reported to the United Kingdom Thoracic Registry each year.

The diagnosis of esophageal rupture is often delayed because esophageal perforations can masquerade as many other clinical disorders [6]. It is traditionally associated with the triad of vomiting, pain in the lower thorax, and subcutaneous emphysema described by Mackler [7]. However, these signs are often absent, as reflected in our series by the fact that more than 50% of patients were referred more than 24 hours after the original injury. A high index of suspicion is required if patients with this condition are to be treated within 24 hours after injury.

All patients were resuscitated on admission. For those undergoing operation, this included the insertion of a central venous line and an arterial line in the intensive care unit. All but three operative procedures were performed more than 24 hours after esophageal injury. It has been reported that patients seen late (longer than 24 hours after perforation) have a poorer prognosis [8]. Indeed, some authors [9] suggest that primary repair of the esophagus with mediastinal drainage should be reserved for patients operated on within 24 hours after injury and recommend nonoperative management for patients with perforations seen late. Our series is too small to show significant advantages for one group over another, but primary esophageal repair was performed in 9 of 12 patients seen more than 24 hours after esophageal rupture with one death.

The management of esophageal perforation is controversial. This is due to the heterogeneity of causes and management strategies reported in the literature [10]. In our experience with the management of rupture of the thoracic esophagus, surgical intervention is usually required because the intrathoracic esophagus is poorly supported and the esophageal contents spill diffusely into the mediastinum. The reestablishment of esophagogastric continuity at first operation is usually possible by primary repair after debridement of necrotic tissue and mediastinal toilet. The suture line is protected from gastroesophageal reflux by a drainage gastrostomy. This combined with mediastinal drainage is essential. Our technique of a single layer of interrupted, vertically mattressed absorbable suture serves to keep the debrided mucosal edges in apposition. Although four leaks were demonstrated at 1 week, they was not associated with an increased mortality and were shown to have healed within 14 days. We do not routinely use pleural flaps, intercostal muscle buttress, or fundic patches in repairing esophageal perforation.

Primary repair is not suitable when there is coexisting disease of the esophagus such as malignancy or undilatable stricture. A high incidence of preexisting esophageal disease in patients with esophageal perforation has previously been reported [11]. The majority of these cases, however, were iatrogenic in etiology. The use of T-tube drainage and esophageal resection for large perforations has been successful [12].

The overall mortality rate in this series was 14.3% and was not related to the interval between perforation and presentation at our unit. We have found that time spent adequately resuscitating a patient before operation is worthwhile even though it often means the patient cannot have operation within 24 hours of presentation.

In summary, esophageal perforation remains a challenging problem with a high mortality. Patients with Boerhaave’s syndrome are an especially high-risk group because of the extensive mediastinal and pleural contamination that results from this injury. We have found that when operation is necessary, primary esophageal repair combined with mediastinal drainage and drainage gastrostomy provides results comparable to those achieved with other techniques. We believe that operation should not be reserved for patients whose perforations are less than 24 hours old and suggest this option be extended to include perforations that are up to 72 hours old.

	References

Top Abstract Introduction Material and methods Results Comment References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): David R. Lawrence Edward R. Townsend Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lawrence, D. R. Articles by Fountain, S. W. Search for Related Content PubMed PubMed Citation Articles by Lawrence, D. R. Articles by Fountain, S. W.