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Ann Thorac Surg 2002;73:304-306
© 2002 The Society of Thoracic Surgeons


Case report

Necrotizing soft tissue infection of the chest wall

Julian E. Losanoff, MDa, James W. Jones, MD, PhD*a, Bruce W. Richman, MAa

a Department of Surgery, University of Missouri-Columbia, Columbia, Missouri, USA

Accepted for publication March 27, 2001.

* Address reprint requests to Dr Jones, Department of Surgery, M580 Health Sciences Center, University of Missouri-Columbia, School of Medicine, 1 Hospital Dr, Columbia, MO 65212, USA
e-mail: jonesjw{at}health.missouri.edu


    Abstract
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 Abstract
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 Comment
 References
 
Necrotizing soft tissue infection of the chest wall is a relatively rare but highly lethal surgical condition that has received little attention in the literature. The case of a 21-year-old female patient affected by this rare infection is reported. Our recent experience and literature data suggest that chest wall necrotizing soft tissue infection spreads rapidly and is highly lethal. High index of suspicion, early diagnosis, and aggressive approach are essential to its successful treatment.


    Introduction
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Necrotizing soft tissue infection (NSTI) affecting the chest wall is a rare condition, with only 15 previously published reports (1973 to 1998). Forty-seven percent of reported cases showed delay in diagnosis, and there was a 67% mortality rate [18].

A 21-year-old white woman was hospitalized with a history of increasing epigastric and chest pain of several days’ duration, shortness of breath, and pyrexia. Her past medical history was significant for intermittent heartburn and multiple episodes of nausea, vomiting, and retching during the previous 2 months. She had no history of hematemesis or melena. She was moderately obese and had a history of marijuana and tobacco use.

On examination she was alert and oriented but in acute distress. Surface temperature was 38.3°C, blood pressure 106/64 mm Hg, pulse 146, and 24 respirations. Examination of the chest revealed coarse breath sounds bilaterally. The abdomen was unremarkable.

Pathology was significant for leukocytosis of 19,000/mm3. Human immunodeficiency virus testing was negative. The patient’s clinical condition deteriorated during evaluation, requiring emergency intubation and intensive medical support. Chest roentgenogram showed bilateral pleural effusions with infiltrate in the left lower lobe. Computed tomography of the chest showed bilateral pleural effusions with compressive atelectasis, mediastinitis, and subcarinal lymphadenopathy (Fig 1). Ventilatory support in the intensive care unit was required. Parenteral ampicillin/sulbactam (Unasyn, Pfizer, New York, NY) and total parenteral nutrition were started. Bilateral chest tubes drained grossly purulent, foul-smelling exudate. Cultures from this exudate and from blood grew Fusobacterium species, Prevotella oralis, and alpha-hemolytic streptococci. Barium esophagography showed no esophageal perforation, but fiberoptic esophagoscopy revealed a 1.5-cm tear in the midesophagus. A left posteromedial thoracotomy found muscles of the chest wall severely edematous; the deep fascia was necrotic. The lung was coated with thick pus and fibrin plaques; they were consolidated and difficult to manipulate to visualize the posterior mediastinum. The mediastinal pleura was opened. The esophagus was viable but coated with fibrin and pus and extremely friable. No perforation or foreign bodies were seen. Pus was evacuated, mediastinum and pleura debrided and lavaged with warm saline, and two No. 36 chest tubes placed. The thoracic cavity was closed and the subcutaneous tissues left open and drained. Because of the friability of tissues, two nasogastric tubes were left in place: one at the junction of the lower and middle thirds of the esophagus and one in the stomach. Hyperbaric oxygen therapy was instituted starting at 2.4 atmospheres absolute/90 minutes. Despite a subsequent increase to 3.0 atmospheres absolute/90 minutes oxygen, no improvement was noted.



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Fig 1. Admission computed tomographic scan demonstrating bilateral pleural effusions and mediastinitis with air bubbles.

 
Because of her poor and constantly deteriorating condition, the patient was considered a poor candidate for repeat surgery. She developed nosocomial pneumonia, and her blood culture grew Pseudomonas aeruginosa and Enterobacter cloacae. Clostridium difficile colitis and an outbreak of herpes lesions supervened and were treated accordingly. Multiple organ failure developed in the patient, and she died on postoperative day 21. Autopsy findings were consistent with severe suppurative mediastinitis, bilateral pleuritis, and multiple organ failure. The esophagus was surrounded by granulations, and no tear could be identified.


    Comment
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Significant predisposing conditions including carcinoma are common in chest wall NSTI [27]. The condition is seen more frequently in postoperative patients [37] undergoing a variety of procedures, including tube thoracostomy [3] and esophageal [4], breast [6], and pulmonary [7] surgery. More rarely, the infection may occur spontaneously, without apparent etiology [1], or simultaneously with distant infection such as paronychia [8]. In this context, the etiology of our patient’s NSTI remains obscure. Spontaneous esophageal perforation (Boerhaave syndrome) might be considered, but no evidence was found intraoperatively to confirm the indications of a transmural tear diagnosed at esophagoscopy.

Clinical features of chest wall NSTI are similar to those seen at other sites: wound pain, skin blistering, crepitus, foul-smelling watery discharge from the wound, and dramatic deterioration in the patient’s condition [35]. Because there are few early symptoms (cutaneous manifestations appear late) [28], diagnosis is difficult and may require blood culture [6], wound puncture [3], and radiographic imaging, as exemplified by the present report. The diagnosis of chest wall NSTI is usually made late [3, 4], probably contributing to the high mortality rate. Based on computed tomography results, our patient underwent emergency exploration of the mediastinum and pleura. The advanced, devastating inflammatory and destructive changes of the involved organs indicated possible earlier onset or highly virulent infection. Rapidly progressive deterioration precluded further surgery for repetitive debridement and removal of necrosis. In retrospect, a more aggressive surgical attitude, incorporating bilateral thoracotomy with multiple reexplorations, might have been more appropriate. The effectiveness of repeated debridement remains uncertain, however; survival has been described with no debridement [1], superficial debridement [5], or multiple and complex debridements [4]. The latter therapy requires reconstruction of the resulting complex chest wall defect, elimination of residual cavities, and reestablishment of chest continuity and stability.

Mortality from chest NSTI is high. Early death is usually from sepsis; patients such as ours, who survive this period, often succumb later to multiple organ system failure. Unexplainably sick thoracic postoperative patients require a high index of suspicion. Rapid diagnostic measures, including computed tomography imaging, and aggressive surgical intervention are typically the only real hope for patient survival.


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 Abstract
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 Comment
 References
 

  1. Dayal A., Gupta L.P., Patawari J., Dave K.S. The chest wall gangrene in an infant. Indian J Chest Dis Allied Sci 1979;21:102-104.[Medline]
  2. Krol J.R., Kwee K.W., Thijs L.G. Rapidly progressive septic shock, associated with necrotizing fasciitis. Intensive Care Med 1982;8:235-237.[Medline]
  3. Chen Y.M., Wu M.F., Lee P.Y., Su W.J., Perng R.P. Necrotizing fasciitis: is it a fatal complication of tube thoracostomy? Report of three cases. Respir Med 1992;86:249-251.[Medline]
  4. Urschel J.D., Horan T.A., Unruh H.W. Necrotizing chest wall infection. Comp Surg 1993;12:37-43.
  5. Viste A., Vindenes H., Gjerde S. Herniation of the stomach and necrotizing chest wall infection following laparoscopic Nissen fundoplication. Surg Endosc 1997;11:1029-1031.[Medline]
  6. Eugster T., Aeberhard P., Reist K., Sakmann K. Streptococcal necrotizing fasciitis with fatal outcome: a case report. Swiss Surg 1997;3:117-120.[Medline]
  7. Hammainen P., Kostiainen S. Postoperative necrotizing chest-wall infection. Scand Cardiovasc J 1998;32:243-245.[Medline]
  8. Banwell P.E., Pereira J., Powell B.W.E.M. Symmetrical necrotizing chest wall infection following paronychia. J Acc Emerg Med 1998;15:58-59.



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This Article
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