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Ann Thorac Surg 2003;75:342-347
© 2003 The Society of Thoracic Surgeons

Original article: general thoracic

Infectious necrotizing esophagitis: outcome after medical and surgical intervention

Henning A. Gaissert, MDa*, Charles L. Roper, MDa,b, G. Alexander Patterson, MDa,b, Hermes C. Grillo, MDa,b

a Thoracic Surgical Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
b Thoracic Surgical Unit, Barnes–Jewish Hospital, Washington University, St. Louis, Missouri, USA

Accepted for publication August 21, 2002.

* Address reprint requests to Dr Gaissert, Thoracic Surgical Unit, Blake 1570, Massachusetts General Hospital, Fruit Street, Boston, MA 02114, USA
e-mail: hgaissert{at}partners.org


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
BACKGROUND: Immunodeficiency predisposes to invasive esophageal infections. The treatment of perforation, respiratory fistula, and necrosis due to transmural esophageal infection is guided by anecdote. We wish to determine treatment and outcome of local complications of necrotizing esophagitis.

METHODS: We report our experience over a 7-year period and review published reports since 1976. We treated 4 patients and found 21 reported patients with perforation (11/25), fistula (8/25), and necrosis (6/25) at a mean age of 35 years. Twenty-one patients were immunodeficient (84%) due to acquired immunodeficiency syndrome in 8, acute leukemia in 6, renal transplant in 3, diabetes mellitus, renal failure, and corticosteroids in 1 each. Pathogenic organisms were fungal in 15 cases, viral in 7, and bacterial in 7.

RESULTS: Treatment consisted of antibiotic therapy in 13 patients and surgical intervention combined with antibiotic therapy in 12: esophagectomy in 6, esophageal stenting and drainage in 2, drainage alone in 2, and salivary diversion in 2. Overall mortality was 48% (12/25). Mortality without surgical intervention was 90% (9/10) and with surgical intervention 27% (3/11). One of 6 patients undergoing esophagectomy (17%) died. The difference in mortality was due to sepsis, which was the cause of death in 8 patients treated with medical intervention and only 1 treated with surgical intervention.

CONCLUSIONS: Local complications of necrotizing esophagitis have a high mortality due to sepsis. Surgical intervention, in particular esophagectomy, controls sepsis in published case reports and should be considered in selected patients. Further study is required to determine the true prevalence of these complications and the outcome of intervention.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
The normal esophageal mucosa is remarkably resistant to infection. Invasive esophageal infections occur with few exceptions in immunodeficiency arising from hematologic malignancy, acquired immunodeficiency syndrome (AIDS), and bone marrow or solid organ transplantation. Our understanding of the natural history of these infections is evolving. Superficial mucosal infections due to fungal or viral organisms are common in high-risk populations and respond well to specific antibiotic therapy, although recurrence rates are high [1, 2]. From this larger pool of patients, some deteriorate to life-threatening illness. The incidence of necrotizing infection in transplant patients is related to immune status. For example, a decreased T-cell helper or suppressor ratio due to an increase in the number of suppressor cells in solid transplant recipients is associated with cytomegalovirus (CMV) esophagitis [3]. In recipients of liver grafts, a high intraoperative transfusion requirement and posttransplant bacterial infection are risk factors for invasive fungal infection [4].

Systemic illness in immunocompromised patients is rarely attributed to the esophagus unless complications have occurred. One autopsy study of bone marrow recipients demonstrated ulceration covering one third or more of esophageal length in 42% of necropsies [5]. Extensive destruction of the esophageal wall was present in 7 of 8 early deaths (87.5%) in this study. This association suggests a contributory or causative role of esophageal infection in death after bone marrow transplant, even in the absence of perforation. Esophageal abnormalities in these patients are not always pursued aggressively with endoscopic inspection and biopsy. Indeed, endoscopy was not performed in the above-mentioned study in "critically ill patients already receiving systemic antifungal and antiviral therapy and those with transient symptoms.'' Experience in endoscopy is needed to distinguish superficial ulcers from full-thickness necrosis. Total esophageal necrosis has been mistaken for simple ulceration, both on endoscopic and radiographic examination [6]. Tissue biopsy or culture may fail to show a typical infectious lesion. Hence, the physician investigating a deteriorating patient often lacks precise information. When the full extent of esophageal destruction is known, the therapy of life-threatening infection usually does not escalate beyond the use of antibiotics unless perforation is proven. And even if complications occur, the surgeon asked to consider resection or drainage receives little if any guidance from individual case reports.

This study reviews 4 patients with intrinsic esophageal infection, complicated by perforation, who were treated at three hospitals over a 7-year period. Surgical intervention was considered in all 4 and undertaken in 3, with survival in 2. These patients are placed in the context of case reports dating from 1976 to the present to describe the complications of invasive mucosal infection and their management. In the course of this review, we encountered reports of mycobacterial infections arising in immunodeficient patients outside the esophagus with delayed rupture into the lumen. Cases were excluded from review when mediastinal adenopathy was identified as the origin of perforation despite similarities in presentation and management. In the absence of a clearly stated extraluminal cause, we chose to include reports. The purpose of the study is to collect the reported experience, to compare conservative and surgical therapy, and to report the outcome of these infections.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
Case 1
A 24-year-old woman seropositive for human immunodeficiency virus since 1991 was followed for idiopathic esophageal ulcers during 1 year before presentation and had received empiric oral fuconazole and acyclovir. Cultures from esophageal biopsies were positive for CMV in May 1994 (Fig 1). She presented with cough in August, and contrast esophagography demonstrated an esophagobronchial fistula with barium soiling the left bronchial tree. An esophagoscopy showed a shallow ulcer between 24 and 28 cm from the incisors and adjacent healed ulcers. On bronchoscopy, the fistula was 1.5 cm central to the left lobar carina. Oral intake was discontinued and nutrition maintained via jejunostomy. Because of persistence, the fistula tract was divided and closed through the right chest in October with interposition of intercostal muscle. When the fistula recurred in December 1994, total esophagectomy and immediate esophagogastrostomy were performed via left thoracotomy with closure of the bronchial opening. The esophageal wall had a large defect with adjacent transmural fibrosis and obliteration of normal layers. CMV was suspected from cytopathic changes and confirmed by immunohistochemical stains. The patient received intravenous gancyclovir. She had an uneventful recovery and returned to a regular diet. Nine months later, she died of CMV pneumonia without recurrence of the fistula.



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  		Fig 1. Endoscopic view of mid-esophageal ulcerations due to cytomegaly virus in acquired immunodeficiency syndrome (case 1, May 1994). Note deep ulcers and pseudopolyp at 12 o’clock.

 
Case 2
A 41-year-old patient underwent human lymphocyte antigen-identical bone marrow transplant for non-Hodgkin’s lymphoma following total body irradiation, cyclophosphamide, and intrathecal methotrexate in June 1996. Veno-occlusive disease of the liver 2 weeks after engraftment was treated with tissue plasminogen activator. One month after transplant, the patient developed progressive dyspnea, chest pain, and a large pleural effusion. A chest tube drained gastric contents and a contrast swallow showed a leak from the esophagogastric junction. On exploration of the right chest, a large perforation was encountered with full-thickness esophageal necrosis. The esophagus was resected with cervical salivary diversion and closure of the cardia. Histologic examination of the esophageal wall showed branching hyphae invading blood vessels. Saccharomyces cerevisiae was isolated from pleural fluid cultures and liposomal amphotericin was administered. Gradual onset of hepatorenal failure and pancytopenia lead to the patient’s death 3 weeks after operation. Autopsy demonstrated severe veno-occlusive liver disease and splenic infarction. Neither active fungal disease nor lymphoma was found.

Case 3
Eight days after cadaveric renal transplant for hypertensive glomerulopathy in January 2000, a 31-year-old man presented with abdominal pain and hypotension. At laparotomy, a necrotic cecum required right colectomy, ileostomy, and mucus fistula. Peritoneal, blood, and urine cultures remained without growth. Pathologic examination was consistent with ischemic necrosis, and fungal stains were negative. The cause was attributed to cyclosporine [7], and immunosuppression was continued with FK 506. Sixteen days following colectomy, reexploration for abdominal pain disclosed mid-jejunal ischemia and a small bowel resection was performed. Three days later, 27 days after transplant, a right hydropneumothorax was discovered. A chest tube drained gastric contents. Abdominal reexploration demonstrated a necrotic esophagogastric junction. The cardia was oversewn and the mid-esophagus stapled in the right chest above an inflamed and perforated lower esophageal wall. Following thoracic consultation, an esophagectomy was performed with cervical esophagostomy. Histologic examination of the esophagus showed transmural necrosis and viral cytopathic changes.

Immunohistochemistry with polyclonal antibodies to Herpes simplex virus type I and II was positive. Culture of the esophageal wall grew Candida krusei, and pleural fluid grew Candida krusei, Staphylococcus aureus, and enterococcus. Viral cultures of tissue and pleural fluid remained negative. The patient was treated with intravenous amphotericin and acyclovir. Seven months later, the patient underwent a substernal gastric pull-up and cervical esophagogastrostomy. Three months later, he required readmission for abdominal pain and underwent left colectomy for an ischemic stricture. Thereafter, he slowly began to tolerate an oral diet. Nineteen months after transplant, total parenteral nutrition was reinstituted for gradual weight loss.

Case 4
A 25-year-old woman presented to an outside hospital with back pain in April 2001 and was found to have acute lymphocytic leukemia. Induction chemotherapy included cyclophosphamide, daunorubicin, vincristin, L-asparaginase, and prednisone. Neutropenic fever and hypotension on day 13 after induction progressed to septic shock and respiratory failure. Methicillin-resistant Staphylococcus aureus was isolated from an intravenous catheter and she was treated with broad-spectrum antibiotics. Four weeks after induction and while on antibiotics, sputum cultures grew Aspergillus flavus. Multiple lung abscesses and ring-enhancing brain lesions were discovered and amphotericin was started. Days later, an acute abdomen necessitated a laparotomy. Several sharply demarcated regions of full-thickness necrosis were identified at the esophagogastric junction, along the greater gastric curvature, in the antrum, and the ileum. The esophagus was stapled and divided, gastric ulcers were excised, and an ileocecal resection and ileostomy were performed. Before exploration, the patient was difficult to ventilate and gastric distension was noted. An intraoperative endoscopy demonstrated a tracheoesophageal fistula 1 cm above the carina within esophageal necrosis. The patient was transferred to Massachusetts General Hospital. An endoscopy of trachea and esophagus showed a small additional tracheoesophageal fistula 1.5 cm below the cricoid ring and a total of five separate punched-out esophageal ulcers. Aspergillus flavus was found in all histologic specimens obtained during laparotomy. Surgical closure of the fistula was inadvisable due to hemodynamic instability and advanced respiratory failure. Despite supportive therapy, the patient expired 43 days after institution of chemotherapy.


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
A review of the literature identified 21 additional patients with intrinsic invasive infections of the esophagus between 1976 and the present. Inclusion criteria were: (1) a transmural injury arising within a region of esophageal damage or associated with additional, separate mucosal lesions; (2) histologic identification of the organism or of viral cellular injury in esophageal tissue, or a positive tissue culture; (3) a positive culture of the same organism from esophageal lumen, from sputum when a fistula is present, or from pleural fluid after perforation; (4) absence of extrinsic disease such as mediastinal adenopathy; and (5) absence of vomiting before the onset of symptoms. In total, 16 male and 9 female patients with an average age of 35 years were identified. Immunologic impairment was known in 21 patients (84%) and unknown in 4, of whom 1 was a newborn. Eight patients had AIDS, 6 acute leukemia or aplastic anemia, and 3 received immunosuppression after renal transplant. One each had a bone marrow transplant, diabetes mellitus alone, and chronic renal failure. The oldest patient took corticosteroid medication for Sjögren’s syndrome. The interval from first symptoms related to swallowing or thoracic disease until diagnosis lasted from 1 day to weeks in most patients. The interval was longer than 2 months in 5 patients. Two diabetic kidney transplant recipients lingered with mediastinal abscesses for 3 and 6 months, respectively, before succumbing to complications. One patient with AIDS had esophageal ulcers for 2 years before progressing to flagrant necrosis. The two largest groups of immunodeficient patients presented at different times: all 6 patients with acute leukemia became ill during observation after induction chemotherapy, whereas in AIDS the interval ranged from 1 day to 24 months.

Patient characteristics are listed in Table 1. Every patient who underwent a surgical procedure also received specific antibiotic therapy. In the combined group, there were 11 free perforations into mediastinum or pleural space, 6 long-segment necroses, 4 tracheoesophageal fistulae, and 4 bronchoesophageal fistulae. Candida or Torulopsis were present in 11 (in 2 as a second organism), Herpes simplex virus in 6, M. tuberculosis in 3, and a variety of bacteria in 4. The report of Walsh and associates [9] argues convincingly for the presence of invasive bacterial esophagitis, and 3 of their patients proven to have transmural necrosis on autopsy were included in our review. Cytomegalovirus, Saccharomyces cerevisiae (brewer’s yeast), M. avium, Nocardia, Penicillium chrysogenum, and Aspergillus flavus were found in 1 patient each. While the perforation in case 3 could have conceivably been associated with cyclosporine [7] or with candidiasis, examination of the esophageal wall demonstrated cytopathic changes specific to herpes simplex and no hyphae.


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  		Table 1. Collected Cases of Necrotizing Esophagitis

 
There was a marked difference in mortality between patients treated with medical therapy alone and combined medical and surgical intervention. Overall mortality was 48 % (12/25) and, in immunodeficient patients, 57% (12/21). Of 13 patients treated with specific antibiotic therapy and supportive care, the outcome was reported in 10 of whom 9 died (90%). Esophageal perforation led to death in all 9: sepsis was the immediate cause in 7, hemorrhage in 1, and a combination of sepsis and hemorrhage in 1. In this group, a surgical procedure was considered in 2 presenting with tracheoesophageal fistula. One patient was not considered stable enough to undergo repair [8], and the other had disseminated fungal sepsis (case 4). Another patient regurgitated a necrotic segment of esophagus [15], yet the significance of a lost gullet was not recognized in time. In contrast, outcome of 12 surgically treated patients was reported in 11 of whom 3 died (27%). No evidence pointed to critical illness as a cause for this difference in mortality. Five of 12 patients in the surgical group, but only 1 of 13 patients in the medical group, were intubated and received mechanical ventilation at the time of presentation. Six patients underwent esophagectomy, 3 for bronchoesophageal fistula, 2 for perforation, and 1 for necrosis; 1 of 6 (17%) died of preexisting veno-occlusive disease of the liver, the complication of a bone marrow transplant (case 2) [23]. Esophageal stent placement was combined with mediastinal or pleural drainage in 2 patients and both survived after prolonged hospital stay. Thoracic drainage alone or salivary diversion alone was performed in 2 patients each. Individual considerations to pursue either medical or surgical therapy were not explained in most reports. In 1 patient, an attempt to repair a fistula failed before esophagectomy was performed (case 1) because wall injury surrounding the fistula had been underestimated. There were two known late deaths among 9 survivors, one after 9 months of AIDS (case 1) and the other of pneumonia in acute leukemia 2 years later [6].


   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
Complications of invasive esophagitis, just as esophageal perforation of any other cause, lead to life-threatening sepsis due to mediastinitis, aspiration pneumonia, or pleural contamination. The onset of symptoms is gradual, and some patients treated with antibiotic therapy alone had a smoldering course for days to weeks before succumbing to their infection. Despite the poor outcome of medical management, systemic sepsis requires specific antimicrobial therapy. Once characteristic endoscopic findings are observed, esophageal biopsies and washings should guide the choice of antibiotic. The organisms found in necrotizing esophagitis suggest that both bacterial and fungal cultures, and furthermore histologic examination for viral cytopathic changes and immunohistochemical stains, are required.

Necrotizing esophagitis is easily dismissed as hopeless because it affects severely ill patients in whom one additional critical illness may convince the physician that any operation is futile. Reviews of infectious esophagitis support this view by emphasizing antibiotic therapy and omitting complications from their discussion [24]. Of course, the natural history of necrotizing esophagitis cannot be reconstructed solely from individual case reports. Its complications are probably underreported, as perhaps are the failures of surgical treatment. While we admit the guarded long-term prognosis in these patients, we note that they are typically young and immunodeficient. The former indicates that they should tolerate an operation and the latter that evaluation and treatment be conducted without delay. Operative intervention succeeded in 9 of 12 selected patients, and 8 patients are confirmed to have left the hospital alive. Five of 6 patients reported by us (cases 1 to 4) or one of us and associates [6] underwent esophagectomy, and 4 survived. Surgical intervention is therefore neither hopeless nor futile.

Perforation of the esophagus due to invasive infection should be distinguished from an injury unrelated to mucosal disease. Boerhaave’s syndrome refers to perforation caused by barotrauma and should not be ascribed to a disintegrating esophagus in the presence of an immunologic disorder and systemic infection [21]. Bauer and associates [25] reported 2 cases of spontaneous esophageal perforation with subsequent candida infection different from primary esophagitis. Both patients vomited before presentation, neither had endoscopic demonstration of mucosal disease beyond the tear, and both developed invasive candidiasis outside the esophagus: one after nonoperative treatment and the other who presented with delayed presentation following operative closure. Finally, the pathology in 5 patients with acute leukemia contained in this review is distinct from leukemia infiltrates [26]. Tissue from resection or autopsy was available in all 5, and there was no evidence of leukemia.

Mycobacterial perforation of the esophagus results commonly from erosion of necrotic lymph nodes into the esophageal lumen and rarely from a mucosal ulcer [11, 27–29]. De Silva and colleagues [11] reported esophageal perforations in 5 patients with typical and 1 with atypical mycobacterial infections; mediastinal adenopathy was present in 4 and led to their exclusion from this review. Two of the 3 remaining patients with mycobacterial disease in this review had peculiar esophago-esophageal fistula without mediastinal nodal enlargement. Since there is no confirmed spontaneous closure of a tuberculosis-related transmural injury in an immunodeficient patient, the primary treatment of mycobacterial perforation due to intrinsic or extraluminal disease is repair or resection [28, 30]. The only reported instance of long-term survival occurred after esophagectomy [27].

In published reports, esophagectomy and surgical drainage succeed in controlling sepsis. These procedures are not interchangeable options. Perforation unrelated to infection is preferably treated by reinforced repair [31], whereas resection is reserved for irreparable destruction of the esophagus [32]. We did not find any report of successful esophageal repair in invasive infection, and our single attempt failed. Disease severity, not surgical aggressiveness, dictates the need for esophagectomy. A lesser procedure could be selected when the chance of success is reasonable. Two patients undergoing tube thoracostomy and stent placement did so because they were not deemed stable for thoracotomy. Both patients eventually recovered after a long hospital course. Two other patients treated with delayed drainage did not survive [18]. This approach does not remove the focus of sepsis or allow debridement of pleura and mediastinum. We therefore do not recommend leaving the esophagus in situ when resection can be accomplished.

The outcome in these patients encourages us to question whether patients with transmural esophagitis, but without perforation, should undergo esophageal resection to contain systemic sepsis. St. Onge and Bezahler [33] reported a giant ulcer due to cytomegalovirus associated with AIDS. An operation was refused due to poor patient condition. McDonald and colleagues [5] found a strong relationship between esophageal and systemic disease: in 18 of 25 patients with esophageal ulcers at autopsy, an identical organism was cultured from blood and esophageal tissue. All 8 patients with CMV esophagitis had systemic CMV infection. Most patients respond to specific therapy for viral or fungal mucosal disease, yet the distinction between giant ulcer and full-thickness necrosis is difficult to make, if not impossible. Resection or debridement should be considered in a deteriorating patient with large esophageal ulcers on maximal antibiotic or antiviral therapy.

In conclusion, the available evidence supports an aggressive attitude in the evaluation of necrotizing esophageal infection, as the mortality of local complications is high. A patient without disseminated disease or end-organ failure has a good chance to survive esophagectomy and thus recover from sepsis. Local drainage procedures and esophageal stenting or salivary diversion alone should be considered only when esophageal resection cannot be tolerated. Although we support esophagectomy for local complications including nonperforated necrosis, the strength of our recommendation is tempered by a lack of prevalent data and prospective studies.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

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