Successful Thoracoscopic Repair and Intrapleural Antibiotic Lavage for Delayed Boerhaave Syndrome Complicated by NDM-Producing Multidrug-Resistant Gram-Negative Empyema: A Case ReportQuanjin Li^a , Xuemei Wan^b, Chunlin Yea,Xuxing Wua,Yongchao Tanga, Da Lia ,Yang Aia , Lijuan Zhou a ,Shaohua Dai*aMail: ndyfy04060@ncu.edu.cn TEL:+86 13479165726a Department of Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.b Department of Cardiovascular and Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.Co-first author：Quanjin Li,Department of Thoracic Surgery, The First Affiliated Hospital of Nanchang University,Nanchang, Jiangxi, 330006, China.Xuemei Wan, Department of Cardiovascular and Thoracic Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China.Corresponding author: Shaohua Dai, Department of Thoracic Surgery, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17 Yongwai Zhengjie, Nanchang 330006, China..Email: ndyfy04060@ncu.edu.cn.KEY CLINICAL MESSAGE：Prompt recognition and a multimodal therapeutic approach—combining surgical repair with targeted antimicrobial therapy—are crucial for patient survival in Boerhaave syndrome, especially in delayed presentations complicated by resistant infection.ABSTRACTION:Background: Boerhaave syndrome is a rare but often fatal condition of spontaneous esophageal rupture. Early diagnosis is paramount, as delays in treatment >24–48 hours sharply increase mortality[1].Summary: We report a 40 years old man who presented two days after vomiting with persistent retrosternal pain. He came to our center because of severe chest pain. Chest CT showed a right-sided hydropneumothorax and confirmed esophageal perforation. He was emergencyly thoracoscopically primary repair of 1.5 cm esophageal laceration, gastric decompression and jejunal feeding tube. The pleural space was extensively contaminated with food debris and purulent fluid. Cultures were grown (New Delhi metallo–lactamase) NDM producing Klebsiella pneumoniae and Escherichia coli. Based on drug sensitivity test, targeted intravenous antibiotics (ceftazidime–avibactam and Eravacycline) were initiated and adjunct intrapleural antibiotic irrigation 400ml/day (gentamicin 20 μg/mL + polymyxin B 500 IU/mL) because persistent empyema.Intervention: Surgery, adequate drainage with continuous antibiotic lavage and broad-spectrum antimicrobials controlled the infection. Inflammatory markers normalized by POD 30 (post-operative day ) and serial cultures were negative. By POD 33 contrast esophagogram showed no leak at repair site and endoscopy confirmed healing. Enteral feeding resumed.Delayed esophageal rupture complicated by a multidrug-resistant infection was successfully managed with timely surgery and innovative adjuvant therapies. This case highlights that aggressive multidisciplinary management—including surgical repair, targeted combination antibiotics, and intrapleural antibiotic irrigation—can achieve full recovery even in high-risk Boerhaave syndrome cases.INTRODUCTION:Boerhaave syndrome (BS) is a spontaneous transmural perforation of the esophageal vessels (usually after forceful vomiting) caused by sudden rises in intraesophageal pressure and negative intrathoracic pressure (typically after forceful vomiting). BS is a surgical emergency (less than 3.1 per million per year) and affects middle-aged men with food and alcohol overindulgence risk factors. Classically, patients may have Mackler’s combination of forceful vomiting, chest pain and subcutaneous emphysema, but the complete trio is present only in less than 50% of cases. More frequently, patients may have severe chest/epigastric pain after retching with dyspnea or shock and presentation can mimic cardiopulmonary emergencies. These unusual presentations often lead to misdiagnosis (myocardial infarction), leading to delayed diagnosis. Mortality rises dramatically with delayed treatment. If intervention is initiated within 24 hours of rupture, survival is 75%, delays beyond 24–48 hours can lead to mortality of [1]50% or higher.The first lesion in BS occurs when acid gastric contents leak into the mediastinum (chemical mediastinum) [2]and the perforation allows bacteria from the stomach into mediastinum, which causes polymicrobial contamination (chemical mediastinum)[3]. The normal esophageal fauna includes aerobic bacteria, most commonly Viridans group streptococci, Enterobacteriaceae family (Klebsiella pneumoniae, Escherichia coli, Staphylococcus aureus) and Staphylococcus bacterium (Klebsiella pneumoniae)/The first colonization of bacteria is taken into account, and the septic phase of the disease evolves. The progression from mediastinitis to sepsis takes place within a few hours after perforation, chemical mediastinitis and polymicrobial contamination leads to [2]initial hyperinflammatory response. Mediastinal infection progresses to sepsis and organ dysfunction, and death of patients is also very high. We present a severe Boerhaave syndrome with pleural empyema with carbapenem-resistant organisms. We present a severe Boerhaave syndrome with pleural empyema with carbapenem-resistant organisms, and we illustrate the importance of surgical intervention and adjunctive treatments.CASE PRESENTATION:A 40-year-old male with no history of gastroesophageal reflux, alcoholism or other serious disease presented to our center with two days of persistent retrosternal chest pain starting after vomiting. He was hemodynamically stable and afebrile. He had no subcutaneous emphysema, abdominal exam did not show any rigidity or rebound tenderness, breath sounds decreased on right chest. Laboratory results showed leukocytosis (15.13109/L,90.8% neutrophils), and high inflammatory markers (C-reactive protein 230.42 mg/L, 8; procalcitonin 1.58 mg/mL, 0.5). Recent vomiting and chest pain, high suspicion of rupture of esophageal tubes (even though no classic emphysema was found) were maintained. A contrast-enhanced chest CT scan was carried out, showing large right hydropneumothorax with pleural fluid and free air, mediastinal air tracking from the distal esophageal tube (Figure 1) confirmed Boerhaave syndrome with right-sided empyema. The patient was taken to the operating room. The tear and pleural decorticators were repaired by thoracoscopic repair of the tear, removing the necrotic tissue and draining the infected space, a large right chest tube was placed for drainage after operation, intraoperative endoscopy was performed for stomach decompression and endoscopic feeding tube was placed for dietary support in esophageal healing. Intraoperative results include 1.5 cm longitudinal laceration of the distal thoracic esophagus. Mediastinum and right pleura are covered with food debris and thick purulent fluid. Necrotic pleural peel is observed, which was trimmed during decortication for lung expansion. Figure 2 shows the operative field with large fibrinopurulent exudate covering the pleura. The cultures of the pleural fluid produced carbapenem-resistant Klebsiella pneumoniae (CRKP positive for metallo–lactamase) and Escherichia coli. These results indicate a multidrug-resistant healthcare-associated infection in the pleural space. Based on antimicrobial susceptibility tests (and discussions with infectious disease specialists) we started the combination of ceftazidime–avibactam and eravacycline. Eravacycline was chosen for the results of the drug sensitivity test and Ceftazidime–avibactam was added for its broad spectrum of action against carbapenem resistant Gram-negatives. The patient still had high-output purulent drainage from the chest tube for the next week, suggesting pleural infection burden. To further control source, we initiated intrapleural antibiotic irrigation on POD 8, using modified double-antibiotic solution (Dialyzable antibiotic solution, DABs). gentamicin (20 μg/mL) and polymyxin B (500 IU/mL) in normal saline were injected via the chest tube (approximately 400 ml/day), dwelled, and then drained. Our aim was to obtain high local antibiotic concentrations in the pleural space, since systemic antibiotics are restricted to places empyema collections. Polymyxin was used to target CRKP (polymyxin-susceptible), and gentamicin provided additional gram-negative coverage. Both agents can be used intrapleurally with careful monitoring. The patient’s treatment gradually improved. By POD 30, the pleural fluid had cleared significantly and the chest tube output was reduced to minimal serous fluid. Inflammatory markers also normalized (WBC 7.6 109/L, CRP 5 mg/L, procalcitonin 0.1 ng/mL). Cultures of pleural fluid and sputum on POD 28 and POD 30 were negative and confirmed the infection. We de-scaled antibiotics and removed the chest tube on POD 30. On POD 33, contrast esophagography (barium swallow) was performed (controlling contrast into stomach and no leakage at the repair site). The following day, gastroscopy showed well-healed esophagus at repair site with no fistula (Figure 3). Trans jejunal feeding was stopped and gradual oral diet was started. By POD 39, the patient had fully recovered and was discharged home on oral diet. He was advised not to strain too much and was referred to follow-up. At 3 months follow-up, he was asymptomatic swallowed normally.CONCLUSIONS:Boerhaave syndrome has high mortality, but early diagnosis and treatment can improve outcomes. Delayed presentation (as in our case) raises the death risk for a severe infection.Our case shows that even a delayed esophageal rupture with multidrug resistant empyema can be successfully managed. Our key success factors were timely surgical intervention (repairing the perforation and drain infection), postoperative critical care (supporting organ function and providing nutrition) and targeted antimicrobial therapy (using new anti-CRKP antibiotics and adjunct intrapleural antibiotic irrigation for local control). We advocate for a proactive combination approach in Boerhaave syndrome: surgical debridement of infected tissue, adequate pleural drainage (like lavage) and nutritional and antimicrobial support. This strategy is the best chance for recovery and should be considered, especially in complex cases where standard management might fail. Finally, high index of suspicion for early diagnosis and involvement of multidisciplinary team are crucial for improving the prognosis of this life-threatening condition.DISCUSSION:This case illustrates several important management challenges and principles in Boerhaave syndrome. First, the time of intervention is important. Our patient’s perforation was only detected 48 hours after the symptoms and thus he is much more likely to die. A delayed diagnosis of BS is known to worsen outcomes. In one study, a delay of Historically, mortality increases from 25% with prompt treatment to more than 50% if treatment is initiated after[1] 48 hours. In this case, our patient’s survival and full recovery are due to the aggressive comprehensive care he received after the late diagnosis. It is highly recommended that patients with compatible symptoms should be highly suspect and early imaging even if classical signs (like Mackler’s triad) are absent. In practice, any uncomplained chest pain following vomiting should prompt esophageal rupture and urgent CT examination.Second, the best management strategy for BS – surgery vs endoscopy – must be individualized because there is no consensus on all cases. In our case, given the large mediastinal contamination and delay, it was clear that we would recommend primary surgical repair and debridement. In contrast, some reports have considered minimally invasive endoscopic procedures (such as temporary esophageal stenting or endoscopic vacuum therapy) for contained perforations or as bridging measures. Endoscopic stenting can seal the esophageal defect and avoid a thoracotomy in some[4] early cases. However, evidence suggests that stent therapy is often not enough to be used solely in Boerhaave syndrome. In fact, 85% of patients first treated with stents eventually required additional surgical procedures (e.g. surgical drainage) due to persistent leaks or sepsis. Mortality was [4]higher in the stent group (15% vs 5% in surgery group). These results are consistent with other series with high re-intervention rates after stenting and frequent complications such as stent migration, empyema or fistula formation. Current expert opinion favors surgical management (primary repair with wide drainage) for most spontaneous rupture syndrome (especially when diagnosis is delayed or large [5] contamination). Endoscopic techniques may be useful adjuncts/alternative therapy (small perforations detected early, or combination of stent placement with surgical drainage) for some cases (e.g. small perforations identified early), or combination therapy (including stent placement with surgical drainage). In our case, the surgical approach was chosen due to the >2 days delay and evidence of fulminant pleural infection; however, if the stent only treatment would have failed.Another aspect of this article is that of treatment of infection and sepsis caused by the leak. The pleural empyema in BS is often polymicrobial (oral flora) if early, but in hospitalized or delayed cases it can be superinfected with nosocomial multidrug resistant bacteria. In this case we isolated CRKP because carbapenem resistant K. pneumoniae infections are rarely treated [6]and mortality rates around 40–50%. CRKP usually contains carbapemase enzymes (e.g. KPC and NDM) which render most -lactams useless. Recently new antimicrobials such as ceftazidime–avibactam have been developed that inhibit many serine -lactamases (e.g. KPC) and restore activity to ceftazidime. However, ceftazidime–avibactam alone is useless against metallo–lactamase producers; [8] often combined with aztreonam or other agents. In this case, the pus was cultured to be New Delhi metallo–lactamases (NDM)–producing CRKP, and in clinical practice, ceftazidime–avibactam and aztreonam is often considered. In this case, the antimicrobial susceptibility test showed resistance to both ceftazidime–avibactam and aztreonam while still showing resistance to eravacycline. Eravacycline has activity against most MDR Gramnegative bacteria, including some carbapenemase-producing bacteria. Eravacycline is primarily bacteriostatic, and generally not recommended as monotherapy. Eravacycline is a recently developed tetracycline derivative with preserved activity against a wide array of multidrug-resistant Gram-negative pathogens, including certain carbapenemase-producing isolates. However, because eravacycline acts predominantly as a bacteriostatic agent, its use as monotherapy in severe, highly aggressive CRKP infections—where the risk of death is considerable—remains suboptimal. On this basis, combination therapy was deemed more appropriate. We therefore selected eravacycline in combination with ceftazidime–avibactam, guided by in vitro susceptibility profiles and with the intent of achieving complementary antimicrobial coverage for both CRKP and the concomitantly isolated Enterobacter species.Although appropriate systemic antibiotics, source control in post-perforation empyema can be difficult. Our patient had persistent pleural sepsis until we escalated the treatment with intrapleural antibiotic lavage. Instilling antibiotics directly into the pleural space is not new – antibiotics were used in post-pneumonectomy empyema (the modified Clagett procedure uses[7] gentamicin/polymyxin irrigation), but not spontaneous esophageal perforation with MDR organisms is reported. In our case, we used gentamicin + polymyxin-B solution, which is a regimen active against many carbapenem resistant Enterobacteriaceae (polymyxin B often a last-resort drug for CRKP) as well as surgical debridement and chest tube drainage – intrapleural antibiotics should be considered as adjunctive and not substitute for adequate drainage. No adverse effects (like systemic toxicity) were observed from the local antibiotic instillation. By the time chest tube removal the pleural cavity was sterilized, this multimodal infection control strategy (surgery + systemic + local antibiotics) can achieve source control even with a highly resistant organism. There are no standard protocols for dosing or duration of intrapleural antibiotic therapy. Decisions are made case-by-case basis, balancing potential benefits and risks. Our success adds to growing evidence that intrapleural antimicrobial therapy can be a salvage option for refractory empyema caused by MDR in combination with conventional measures.Finally, nutrition support and organ support are important support steps for Boerhaave syndrome. We fed the patient with enteral nutrition via a jejunal tube to heal, avoid malnutrition during the nil-per-os period and decrease aspiration risk. We monitored patient respiratory status due to risk of acute respiratory distress syndrome (mediastinitis or sepsis), but surgery and drainage tended to prevent significant pulmonary compromise in this case. The team (thoracic surgeons, intensivists, infectious disease physicians, nutritionist) coordinated care to address all aspects of the patient’s complex condition.In summary, our case highlights that successful treatment of delayed Boerhaave syndrome requires aggressive surgical and medical treatment. Early surgical repair (complete debridement) remains the key, but a supplementary treatment, e.g. endoscopic stents or vacuum therapy, may be considered. When severe contamination or resistance arises, tailored antibiotic therapy (new generation agents and regional therapy such as intrapleural lavage) can help improve outcomes. Each esophageal perforation case is unique and a flexible patient-specific treatment regimen is recommended, guided by surgical judgment and multidisciplinary input.CONFLICT OF TNTEREST STATEMENT:All other authors reported no conflicts of interest.AUTHORS CONTRIBUTIONS:Author Contributions• Conceptualization: Xuxing Wu, Yongchao Tang• Data Curation: Xuemei Wan,Xuxing Wu, Yongchao Tang• Clinical Management (Surgery): Shaohua Dai, Quanjin Li• Writing – Original Draft:Xuemei Wan,Quanjin Li• Writing – Review & Editing: Shaohua Dai• Supervision: Yang Ai(All authors have read and approved the final manuscript.)Conflict of InterestThe authors declare no conflicts of interest.Ethics StatementWritten informed consent was obtained from the patient for publication of this case report and the accompanying images. No potentially identifiable patient data are presented in this report. 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