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Case Report of Esophageal Rupture, Empyema, and Aortic Dissection Potentially Caused by Severe Vomiting

Huang, Jiawen1; Huang, Chengfeng2; Lin, Zhaoming2; Liu, Huanan2; Zhang, Xiaoshen2,∗

Editor(s): Xu, Tianyu; Fu, Xiaoxia

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doi: 10.1097/CD9.0000000000000046
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Abstract

Introduction

Empyema, a collection of pus in the pleural cavity, is associated with elevated mortality. Early intervention is crucial in the management of empyema because 20% to 30% of patients affected will either die or require further surgery within the first year after developing empyema.[1] Aortic dissection is a life-threatening condition caused by a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the dissection of the layers of the aortic wall. The in-house mortality has been found to be more than 30%.[2] The case described in this report was diagnosed with both severe empyema and acute type A aortic dissection, which were possibly caused by vomiting after heavy consumption of yogurt. The patient was found to have an esophageal fissure and pus from the thoracic drainage suggesting a co-infection of Granulicatella adiacens (G. adiacens) and Escherichia coli (E. coli). G. adiacens, a Gram-positive cocci and facultative anaerobe, is a normal bacterium in the human mouth, throat, intestine, and urogenital tract.[3] It can cause endocarditis,[4,5] osteomyelitis,[6,7] peritonitis,[8] and joint infection.[9] However, due to its staining variability, atypical biochemical characteristics, and poor growth on common media, it is hard to identify. Therefore, clinical reports of G. adiacens infections are very rare.[3]E. coli,a Gram-negative bacterium, is essential to the normal flora of the human gut. To date, there have been rare reported cases of mixed infection of these 2 bacteria causing empyema, particularly in patients with concurrent type A aortic dissection.

The patient has consented to the use of all his clinical data and images in this report. Written informed consent for the personal or clinical details along with any identifying images to be published in this study was obtained from the patient.

Case presentation

A 50-year-old man was referred to the department of cardiovascular surgery on an emergency basis due to sudden chest pain and a suspected diagnosis of aortic dissection. The patient complained of severe laceration pain in the chest region for more than 1 day, accompanied by chest tightness, shortness of breath, and a low fever, but no dizziness or headache. The patient recalled that he had eaten a lot of yogurt for 5 consecutive days the week before admission, then vomited. There was no obvious abdominal pain on the first day of vomiting, but the vomiting symptoms gradually worsened. On the third day of vomiting, severe pain appeared in the area near the fourth intercostal margin of the left sternum, so he sought medical attention. He had a history of hypertension and renal insufficiency for more than 10 years, and his blood pressure was well controlled with oral antihypertensive drugs.

On admission, his upper limb blood pressure was 80/40 mmHg, heart rate was 100 beats/min, respiratory rate was 30 breaths/min, temperature was 37.5°C, and oxygen saturation was 98% on room air. Initial laboratory studies showed levels of procalcitonin (PCT) of 252.7 ng/mL; levels of serum creatinine of 197 μmol/L; normal levels of leukocytes, hemoglobin, and platelets; no abnormalities in biomarkers of myocardial infarction; and normal liver enzymes. Enhanced computed tomography imaging revealed Stanford type A (DeBakey type I) aortic dissection with left renal artery involvement and moderate stenosis in the initial segment of the celiac trunk, mild stenosis in the proximal segment of superior mesenteric artery, left fluid pneumothorax, and atelectasis [Figure 1].

F1
Figure 1:
Enhanced computed tomography revealed Stanford type A (DeBakey type I) aortic dissection with left renal artery Involvement and moderate stenosis In the initial segment of celiac trunk, and mild stenosis in the proximal segment of superior mesenteric artery (A, B, and C). Left fluid pneumothorax, atelectasis (D and E).

To sedate the patient for emergency surgery, deep venous catheterization, endotracheal intubation, and ventilator assisted breathing were performed. Drainage of pleural effusion was then performed by placing a tube between the fifth and sixth ribs in the left midaxillary line. After puncture, a large amount of chest fluid was discharged from the drainage tube, which was foul smelling and thick. Chest drainage fluid and blood were collected for biochemical and etiological examination, and a diagnosis of empyema was confirmed. Because of the high risk of operation, the patient's family decided to forego the operation for conservative treatment. To investigate the cause of empyema, an endoscopic examination of the esophagus was performed. The results showed that there was a linear slit with white coating about 5 cm long from the lower esophagus to the cardia, but it did not penetrate [Figure 2]. Therefore, endoscopic clamping was performed and nasal feeding was performed with a jejunal tube. Considering that the source of the infection may have come from the digestive tract, there was a possibility of both Gram-positive and Gram-negative bacteria being present; linezolid at a dose of 0.6 g and meropenem at a dose of 1 g were administered intravenously every 12 hours for empirical anti-infection therapy.

F2
Figure 2:
Endoscopic examination showed that there was a 5 cm long linear slit in the lower esophagus from the cardia, with white coating on the surface and no penetration. (A) Linear slit with white coating; (B) Endoscopic clamping.

The volume of chest drainage fluid reached 3000 mL in the first 12 hours, then gradually decreased and became less cloudy. On day 3, it was confirmed that the sample from day one's pleural effusion grew G. adiacens. Antimicrobial susceptibility testing for G. adiacens showed susceptibility to penicillin, cephalosporins, vancomycin, and linezolid, but not macrolides. Later, another bacterium, E. coli, was identified from the same specimen. Susceptibility testing showed susceptibility to third- and fourth-generation cephalosporins, thiomycins, and quinolones, but not tetracyclines. The chest fluid sample from day 2 revealed the same results. Cultivation of the blood and subsequent samples of pleural effusion were negative for bacteria. We continued the aforementioned antimicrobial therapy and began the left pleural lavage. During the following week, the drainage fluid from the chest became clear. After 20 days of anti-infection treatment, the patient was fever-free with 5.45 × 109 leukocytes/L and PCT levels of 0.01 ng/mL. Therefore, the antibacterial drug dosage was downgraded to ceftriaxone (2 g intravenously every 12 hours). Thirty days after admission, the drainage tube was removed. The antibiotics were discontinued 1 week later.

During hospitalization, the patient's blood pressure and heart rate were well-controlled at 95–110/55–70 mmHg and 60–70 beats/min, respectively, to curb the progress of aortic dissection. Reexamination of aortic computed tomography angiography 1 month after admission indicated that the condition of aortic dissection tended to be stable. Due to family financial reasons, the patient was discharged with medicine after 40 days of hospital treatment.

Discussion

This is a rare case with severe empyema and aortic dissection. Co-infection of G. adiacens—which is difficult to identify[3]—and E. coli is very rare, let alone being comorbid with aortic dissection. Therefore, during this patient's treatment, we very much hoped to explore the cause of his disease. After admission, we found the laceration of the esophagus and cardiac orifice through endoscopy in time. However, the laceration had a white coating 3 days after the onset of the disease, and the patient was in critical condition at that time, thus we could not determine whether there had ever been a penetrating tear. Since vomiting is a common cause of esophageal rupture,[10] and the G. adiacens and E. coli that were repeatedly cultured from this patient's chest drainage fluid samples are both digestive-tract bacteria, we considered the possibility of penetrating esophageal rupture. Bacteria from the digestive tract might have entered the left thoracic cavity along with the laceration, resulting in a severe empyema. Aortic dissection may have resulted from a sudden rise in blood pressure during repeated vomiting.

On the first day of admission, the purulent pleural drainage smear from this patient showed a large number of Gram-negative bacilli and a moderate amount of Gram-positive cocci. After culture and identification by various methods in the bacteriology laboratory, the presence of the previously-mentioned 2 bacteria in multiple specimens was confirmed, suggesting a high possibility of severe empyema caused by mixed infection of G. adiacens and E. coli. Fortunately, the anti-infection treatment was very effective. During this patient's treatment, we timely and accurately identified the possible bacterial source and initiated the empirical, effective, anti-infection treatment; actively thoracic drained and flushed; actively controlled the patient's blood pressure; and gave symptomatic treatments such as analgesia, gastric care, and nutritional support; so that the patient could smoothly pass the acute phase of aortic dissection and finally be discharged in a stable condition.

For similar critically ill patients with unexplained acute pyothorax, determining the possible etiology as soon as possible and carrying out accurate, empirical, anti-infective therapy are the keys to controlling the infection effectively. Additionally, one could also gain valuable time to determine the underlying cause and pathogenic microorganisms involved in the disease.

Acknowledgments

We wish to thank Dr. Guangchao Yu and Xiaoyi Fan of Clinical Medical Laboratory, First Affiliated Hospital, Jinan University, China, for the great help in identifying the pathogenic microorganism. We also wish to thank Dr. Jingwen Liu of Endoscopy Center, First Affiliated Hospital, Jinan University, China, for the professional guidance of endoscopy in this case.

Funding

None.

Author Contributions

Jiawen Huang: Anti-infective therapy consultation and case writing.

Chengfeng Huang, Zhaoming Lin, Huanan Liu: Treatment and management of patient.

Xiaoshen Zhang: Treatment decisions.

All authors have read and approved the manuscript.

Conflicts of Interest

None.

References

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[8]. Elfessi Z, Liu E, Dukarevich Y, et al. Sepsis induced bacterial peritonitis caused by Granulicatella adiacens. Am J Emerg Med 2019;37(12). 2263.e1-2263.e3. doi: 10.1016/j.ajem.2019.158428.
[9]. Quénard F, Seng P, Lagier JC, et al. Prosthetic joint infection caused by Granulicatella adiacens: a case series and review of literature. BMC Musculoskelet Disord 2017;18(1):276. doi: 10.1186/s12891-017-1630-1.
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Keywords:

Case report; Empyema; Escherichia coli; Granulicatella adiacens; Acute aortic dissection

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