Ann Thorac Surg 2000;70:2143-2145
© 2000 The Society of Thoracic Surgeons
Case report
Successful treatment of mediastinal gas gangrene due to esophageal perforation
Jarmo A. Salo, MD, PhDa,
Jukka K. Savola, MDa,
Vesa J. Toikkanen, MDa,
Vesa J. Perhoniemi, MD, PhDa,
Ville Y.O. Pettilä, MDb,
Jorma A. Klossner, MDc,
Hannu J. Toivonen, MD, PhDb
a Department of Thoracic and Cardiovascular Surgery, Helsinki University Central Hospital, Helsinki, Finland
b Department of Anaesthesiology, Helsinki University Central Hospital, Helsinki, Finland
c Department of Anaesthesiology, Turku University Hospital, Turku, Finland
Accepted for publication February 16, 2000.
Address reprint requests to Dr Salo, Department of Thoracic and Cardiovascular Surgery, Helsinki University Central Hospital, Haartmaninkatu 4, FIN-00290 Helsinki, Finland
e-mail: jarmo.salo{at}huch.fi
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Abstract
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Esophageal perforation and mediastinal gas gangrene developed in a 55-year-old male after the endoscopic ethanol injection of a Mallory-Weiss ulcer. Initially, extensive gangrene of the esophagus and the mediastinum was treated by esophagectomy; however, an abundance of Clostridium perfringens in the Gram stain verified the presence of gas gangrene. Subsequently, the patient was transferred to a hyperbaric oxygen center, wherein a total of seven hyperbaric treatments were administered. The patient survived, and 4 months later, after having undergone several reoperations because of pleural empyema, mediastinal abscess, splenic rupture, and acalculous cholecystitis, was discharged and is still surviving.
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Introduction
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The use of endoscopic instruments is the most common cause of esophageal perforation. However, the diagnosis is often delayed, thereby worsening the prognosis and raising the mortality rate to 66% after 24 hours [1]. Aerobic bacteria of the mouth and upper gastrointestinal tract usually cause mediastinitis, but frequently the flora is a mixture of aerobic and anaerobic bacteria. Clostridium perfringens is a gram-positive obligate anaerobe normally present in the gastrointestinal tract and in soil. The presence of tissue necrosis and a low oxidation-reduction potential is essential to the development of gas gangrene by this microbe. The etiology is usually posttraumatic or postoperative, but gas gangrene has also been reported after heroin injection [2]. Mediastinal gas gangrene, after a delayed diagnosis of esophageal perforation, has a very severe prognosis. We are aware of no studies in which delayed esophageal perforation with mediastinal gas gangrene has been successfully treated.
Six years earlier, a 55-year-old male had a mitral valve replaced with a mechanical prosthesis. The subject had since then been anticoagulated with warfarin. While abroad, he vomited food and blood heavily. This was followed by severe pain in the upper abdomen, radiating to the spine and left shoulder. The local hospital diagnosed an erosive gastritis and a bleeding Mallory-Weiss ulcer, which was treated with an endoscopic ethanol injection. Thereafter, the subject’s general condition rapidly declined; he became confused and septic. He was transferred to Helsinki University Central Hospital 2 days later.
On arrival, chest roentgenogram and computed tomography scan verified mediastinal and intrapericardial gas, pleural effusion, and pneumonic infiltration of the lungs (Fig 1). The C-reactive protein was 331 mg/L (normal < 10 mg/L). Esophagography showed an esophagopleural fistula. On emergency thoracotomy, foul-smelling pus and a gangrenous, perforated (length 5 cm) esophagus were found. Additionally, mediastinal fat, pleura, parts of the pericardium, and parts of the left main bronchus were also gangrenous. Subtotal esophagectomy was performed, with cervical esophagostomy, mediastinal cleansing, debridement of the devitalized tissue, and gastrostomy. This treatment has been shown to be successful in delayed cases with mediastinal sepsis [3]. Unfortunately, some of the devitalized tissue in the vital organs could not be removed. Antibiotic treatment consisted of intravenous imipenem, vancomycin, fluconatzol, and medronidazole together with local irrigation with ceftriaxone. Emergency Gram stains revealed positive rods suggestive of an abundant growth of C perfringens. Septic shock progressed to ventricular fibrillation, which was then defibrillated. Due to the fast deterioration of the patient’s condition, and the strong suspicion of gas gangrene, he was transferred to the nearest hyperbaric oxygen treatment center: Turku University Hospital (100 miles away), where the first treatment was administered 26 hours after the initial surgery. Altogether, seven hyperbaric oxygen treatments were administered (90 minutes at 2.5 ATA (atmosphere absolute) of 100% oxygen twice a day). After three treatment sessions, the patient became afebrile. His hemodynamic situation stabilized, and supportive vasoactive drugs were withdrawn gradually as treatment continued. The patient had to be operated on, 2 days after the last session, because of bleeding from a ruptured spleen, and again, 2 days later, due to a postoperative intraabdominal hematoma. The patient was then returned to Helsinki University Central Hospital, where bilateral pleural empyema and a left mediastinal abscess were operated on. A cholecystectomy due to acalculous cholecystitis was also required. The patient was discharged from the hospital 4 months later. Seven months later, the alimentary passage was reconstructed from the isoperistaltic colon transversum. Peroral feeding began on the eighth postoperative day. A week later, the ileum was resected because of ileus due to severe adhesions. Thereafter, recovery was uneventful. At the most recent follow-up, 4 years after the original incident, the subject was well within normal weight limits and evinced no dysphagia. On endoscopy, the colon interposition was normal. No signs of infection were found in the prosthetic mitral valve, and cardiac ultrasound was normal.
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Fig 1. At admission, CT revealed mediastinal (1) and intrapericardial gas (2) and left pleural effusion. However, the presence of gas is not diagnostic of gas gangrene, because mediastinal gas is a common finding after esophageal perforation, and anaerobic bacteria other than C perfringens can also produce it.
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Comment
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Gas gangrene was not initially suspected in this case; fortunately, emergency Gram stains had been made during the session, and subsequently, a bacterial culture verified the diagnosis. Because gas gangrene progresses very rapidly, treatment including debridement of the gangrenous tissue together with antibiotic and hyperbaric oxygen therapy, has to be started based on clinical findings and Gram stains. The pure isolation of C perfringens from tissues is not indicative of gas gangrene, but foul-smelling gangrenous mediastinitis and positive Gram stains necessitate starting this treatment immediately. C perfringens is sensitive to penicillin, but because mediastinitis after esophageal perforation consists of a mixed flora, additional broad-spectrum antibiotics (ceftriaxone, imipenem, medronidazole, piperacillin, and teicoplanin) are generally required.
Hyperbaric oxygen therapy improves phagocyte-mediated bacterial killing, suppresses toxin formation, and helps create a bacteriostatic environment. It is also bactericidal for certain anaerobes, including C perfringens [4]. However, it is often unavailable because of the lack of pressurized chambers with intensive care facilities. The addition of hyperbaric oxygen to the therapy has clearly improved the survival of gas gangrene patients, even though randomized prospective studies of this therapy do not exist [5]. Our case corroborates previous experience with gas gangrene in other parts of the body, in which delayed hyperbaric oxygen therapy was still found to be effective. Nevertheless, its immediate use is strongly recommended. If surgical debridement is first performed, and antibiotic therapy then started, transport to a remote oxygen therapy center is usually feasible. The decision to transfer our critically ill patient was made after 16 hours of intensive care, during which, complete surgical debridement was impossible because of the vital mediastinal structures involved. The initial diagnostic delay had been 2 days, followed by 1 day of surgical and antibiotic therapy before hyperbaric oxygen treatment. Therefore, hyperbaric therapy, even after several hours of delay, seems highly essential to the healing of gas gangrene mediastinitis.
Although we were unable to find reports of successfully treated mediastinal gas gangrene after delayed perforation of the thoracic esophagus, in one case, an early perforation of the cervical esophagus caused C perfringens mediastinitis after the endoscopic removal of a chicken bone [6]; treatment consisted of drainage of the mediastinum via the neck without esophageal debridement, but with both hyperbaric oxygen treatment and Clostridium antitoxin serum. Both cases support the use of hyperbaric oxygen treatment in both early and delayed diagnoses of gas gangrene mediastinitis caused by esophageal perforation.
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Acknowledgments
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We thank Yvonne Sundström for skillful assistance.
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References
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Monies-Chass I., Joachims H.Z., Altman M.M. Hyperbaric oxygen in anaerobic infection of the mediastinum. J Laryng Otol 1975;89:1147-1150.
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Abstract
Introduction
