Boerhaave syndrome: A rare complication of cosmetic surgery
Síndrome de Boerhaave: uma complicação rara em pós-operatório de cirurgia estética

INTRODUCTION

This is a case report study on the rare occurrence of Boerhaave syndrome in a patient who underwent abdominoplasty with general anesthesia.

The patient presented vomiting and nausea after abdominoplasty and mastopexy under general anesthesia, which, together with the use of an abdominal binder, resulted in the syndrome. It is important to emphasize that the location and sudden onset of pain may be confused with myocardial infarction or pulmonary embolism¹.

Boerhaave syndrome or spontaneous rupture of the esophagus was first described in 1724 by Hermann Boerhaave². It is a severe life-threatening disease that requires diagnosis within 12 hours and proper treatment. It is a relatively rare syndrome, but has a high mortality rate (35%). In fact, it is considered the most lethal type of rupture in the digestive tract⁴.

Boerhaave syndrome should be considered in the postoperative period of abdominal dermolipectomy under general anesthesia, which in this study was associated with mastopexy and postoperative vomiting and nausea.

Given the information provided here, the subject of this study is extremely important, especially considering the lack of studies on the association of Boerhaave syndrome with plastic surgery.

The objective of this study was to alert plastic surgery professionals about Boerhaave syndrome, which may occur after abdominoplasty under general anesthesia.

CASE REPORT

Patient A.M.R.L.P., a 58-year-old woman, visited our clinic to undergo abdominal dermolipectomy and mastopexy.

At physical examination:

Laboratory and radiological examinations, and preanesthetic consultation showed no abnormalities, and the patient was considered eligible for surgical dermolipectomy and mastopexy.

On May 25, 2007, she underwent abdominal dermolipectomy and mastopexy using the inferior pedicle technique under spinal anesthesia. The surgery lasted 4 hours with no complications.

Four hours after the end of surgery, the patient presented several episodes of vomiting alternating with periods of improvement after antiemetic medication.

Ten hours after surgery, she reported painful swallowing, which improved with xylocaine spray, and the patient passed the night without other complications.

At 6:45 am on May 26, 2007, she reported generalized severe pain and dyspnea, which improved with administration of corticosteroids and intravenous bronchodilator. The patient was discharged at 11:30 am with no complaints.

On the same date, at 2:30 pm, the patient returned with severe dyspnea, sweating, pallor, and a 90/50 mmHg blood pressure. She received supportive care, but the condition worsened, and she was referred to the intensive care unit, where she was intubated and underwent thoracentesis. The aspirated fluid had characteristics of gastric juice, and the amylase values were increased in the biochemical test (Table 1).

Table 1 - Pleural fluid test results

The mediastinal shift worsened, but the diagnosis was not conclusive. The patient’s general condition was poor, with sepsis and severe changes in laboratory parameters (Table 2).

Table 2 - Radiological examination results

After these examinations, the general surgery team drained the left hemothorax (LHT) and requested computed tomography of the abdomen (Table 3) and chest (Table 4). After several examinations, the patient’s condition continued to deteriorate, with LHT opacity 10 days later.

Table 3 - Complete abdominal tomography result

Table 4 - Chest computed tomography results

After several radiological examinations and laboratory tests, including upper digestive endoscopy, the patient was transferred to a hospital with a thoracic surgery service, where she underwent a thoracotomy for LHT decortication and was diagnosed intraoperatively at approximately 30 days after her plastic surgery. Currently, the patient is well recovered and uses an esophageal prosthesis.

DISCUSSION

Boerhaave syndrome is characterized by secondary esophageal perforation and a sudden increase in esophageal intraluminal pressure. It is common to find an etiological factor, which is often an internal pressure trauma. Although the classic definition of spontaneous rupture is incorrect, it is universally accepted. This syndrome results from increased intra-abdominal pressure due to vomiting, vomiting efforts, or other efforts. Pressure is rapidly transmitted to the esophagus, and a perforation may occur owing to distension of the mucosa and esophageal muscles, which cannot resist high pressure⁵.

In 80% of cases, the most common cause is vomiting or effort to vomit due to excessive food or alcohol ingestion⁵.

This perforation is often longitudinal and usually occurs on the left lateral wall⁵ of the distal esophagus, above the esophagogastric transition and diaphragm. Thus, it may produce an esophageal-pleural fistula with subsequent pleural effusion and/or pneumothorax.

It is more frequent in men between 40 and 60 years of age⁶. The main symptom is severe, abrupt, progressive retrosternal pain. The classic Mackler’s triad⁷, including vomiting, chest pain, and cervical emphysema, is uncommon. Hematemesis occurs in 22% of cases. Dyspnea occurs in 61% of cases, and cyanosis is also common. When an esophageal-pleural fistula is present, the typical pleural fluid presents nonspecific findings such as low pH and increased amylase⁸, and the diagnosis can be confirmed by finding food in the fluid. Other signs and symptoms include dysphagia, tachycardia, and hypotension, which may progress to sepsis and death.

Many diagnostic tools are available, including clinical diagnosis with history, physical examination, and radiological findings. Physical examination shows decreased vesicular murmur and fever in 30% of cases, with possible cervical crepitus and decreased airborne noises. Laboratory tests may show leukocytosis in some cases, without further changes⁹.

Chest radiography is useful for initial diagnosis, and the most common finding is pleural effusion, usually on the left side. Other findings include pneumothorax, often on the left side⁵, hydropneumothorax, pneumomediastinum, and subcutaneous emphysema.

Esophagography would reveal typical contrast extravasation into the pleural cavity and provide information on the size and location of the perforation, which are useful in choosing the most adequate surgical approach⁹.

Computed tomography can confirm the diagnosis or replace esophagography in intolerant patients. Early diagnosis and proper treatment are essential to prevent mediastinitis, sepsis, and shock, often associated with the second phase of the disease

Choosing the surgical technique to treat the spontaneous esophageal perforation can be controversial, and time from onset is a decisive factor. When the diagnosis is established within the first 24 hours, cardiorespiratory stabilization, clinical support, and antibiotic therapy are recommended, as well as primary closure of the perforation through thoracotomy associated with mediastinal drainage.

After this period, the presence of edema, tissue necrosis, and mediastinal infection can make surgery extremely difficult. The most important complication of primary closure is the occurrence of fistulas.

Conservative treatment can be a choice in cases of small perforations, where the patient has minor symptoms and limited mediastinal lesions.

In addition to surgical correction, treatment with parenteral nutrition support, nasogastric tube, broad-spectrum antibiotics, and gastric acid secretion inhibitors is essential for these patients.

Late-diagnosed cases often require some form of esophageal exclusion, usually cervical esophagostomy and gastrostomy associated with jejunostomy for nutritional support.

Spontaneous esophageal rupture is reported in the literature to occur in 10% of patients with reflux esophagitis, duodenal diverticulum, and carcinoma, but can also occur in patients without previous esophageal disease¹.

CONCLUSION

Postemetic rupture of the esophagus is a serious condition that is often overlooked in the initial evaluation. Vomiting crisis, left pleural effusion, thoracentesis with fluid aspiration, and suspected digestive secretion with increased amylase levels are diagnostic factors that indicate surgical treatment. Postoperative evolution is usually complicated with vital organ failure and requires intensive support. Mortality and morbidity rates are high¹⁰.

The present case leads us to conclude that prolonged surgeries should be avoided, especially under general anesthesia, because of the risk of carbon dioxide retention, which may lead to postoperative emetic crisis, mostly in patients with a history of esophageal disease. Above all, it is important to pay attention to symptoms, not excluding the possibility of Boerhaave syndrome.

No cases of Boerhaave syndrome in the postoperative period of abdominal plastic surgery were found in the literature.