Anesth Analg 2004;98:1164-1166
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000101981.85523.82
OBSTETRIC ANESTHESIA
Boerhaave’s Syndrome After Postoperative Vomiting
Fouad N. Atallah, MD*,
Béatrice M. Riu, MD*,
Luc B. Nguyen, MD*,
Philippe O. Seguin, MD
, and
Olivier A. Fourcade, MD*
Departments of *Anesthesiology and Intensive Care and
Urology, Toulouse University Hospitals, France
Address correspondence and reprint requests to Fouad Atallah, MD, Department of Anesthesiology and Intensive Care, Urology Unit, Toulouse University Hospitals, 1, Poulhes Ave., 31403 Toulouse cedex 4, France. Address e-mail to atallah.f{at}chu-toulouse.fr
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Abstract
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Postoperative nausea and vomiting are common after general anesthesia but rarely produce life-threatening conditions. We report a case of postoperative vomiting complicated by esophageal rupture (Boerhaave’s syn- drome). As this complication is quite rare and can have varied and atypical presentations, anesthesiologists may fail to consider this diagnosis.
IMPLICATIONS: We report a case of postoperative vomiting complicated by esophageal rupture (Boerhaave’s syndrome). As this complication is quite rare, anesthesiologists may fail to consider this diagnosis.
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Introduction
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Postoperative nausea and vomiting (PONV) remains a common side effect of general anesthesia (1). Although PONV is rarely associated with serious complications, Boerhaave’s syndrome, the spontaneous rupture of the esophagus as a result of severe retching and vomiting, is an emergency situation where a delay in treatment leads to increased morbidity or mortality. However, its diagnosis is difficult because the clinical presentation is often nonspecific (2). The available literature is mainly surgical, and few articles are available in the anesthesia literature on this topic (3). However, its early diagnosis is important for anesthesiologists who are increasingly involved in postoperative patient care. We report a patient who developed Boerhaave’s syndrome after PONV.
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Case Report
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A 34-yr-old man, ASA physical status I, with a problem of infertility was scheduled for an elective inpatient surgery for an in vivo fertilization procedure.
General anesthesia was induced with midazolam, propofol, fentanyl, and atracurium. The trachea was intubated without difficulty or evident trauma. Anesthesia time was 100 min and was maintained with isoflurane in a nitrous oxide-oxygen mixture (50/50) and a total of 250 µg of fentanyl. The patient had an uneventful emergence from anesthesia and was easily tracheally extubated. Two hours later, the patient received propacetamol 2 g IV and 0.3 mg of buprenorphine SQ for postoperative analgesia. He had a light meal 6 h after tracheal extubation. Two hours later, he complained of several episodes of nausea. He finally vomited and felt better. The next day, despite refusing any food, the patient was still nauseated and started retching. Multiple injections of metoclopramide helped to reduce nausea intensity. In the afternoon, the patient complained of severe epigastric pain radiating to the left shoulder. Clinical examination revealed a rapid and regular pulse of 120 bpm, a normal arterial blood pressure, a mild fever of 38.8°C, a decreased air entry in the left lower lung field, and a firm, nontender, nondistended abdomen. The chest radiograph showed a small left basal pleural effusion with some left parenchymal opacities. Large laboratory studies just revealed a leukocytosis (16,200 white blood cell count/mm3), normal cardiac enzymes, excluding myocardial infarction, and normal serum amylase, excluding acute pancreatitis. Peptic ulcer was also excluded because there was no persistence or aggravation of the pain. The pain and vomiting then disappeared, and antibiotherapy was started to treat a pulmonary infection.
On the third day, the patient was still feeling ill, with some abdominal pain and moderate oxygen desaturation requiring supplementation with oxygen. Thoraco-abdominal computed tomographic scan revealed the presence of a mild pneumomediastinum (Fig. 1). Because esophageal rupture was suspected, an esophagogram was performed in different views but did not reveal any esophageal leak. The patient’s clinical state remained stable for the next 3 days despite a toxic picture with a low-grade fever of 38°C and a tachycardia of 100 bpm.
On the sixth day, the patient became dyspneic. The chest radiograph showed a large pleural effusion, which was drained giving 450 mL of a clear inflammatory liquid. Because esophageal rupture was still our main suspected diagnosis, another esophagogram was performed that finally revealed an intrathoracic extraesophageal leak of contrast medium from the left lower third of the esophagus, confirming the presence of an esophageal rupture (Fig. 2). An urgent thoracotomy revealed a left tear of 2 cm in the lower part of the esophagus just before the esophagogastric junction. The surgical procedure consisted of debridement and drainage of the posterior mediastinum and the left pleural cavity, a gastrostomy for gastric drainage, and a jejunostomy for enteral feeding. The patient was discharged from the intensive care unit on the seventh postoperative day and from the hospital 13 days later in satisfactory condition. A month later, a last esophagogram confirmed the absence of any leak, the gastrojejunostomy was closed, and oral intake was resumed.
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Discussion
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Although referred to as spontaneous rupture, Boerhaave’s syndrome nearly always results from an identifiable increase in the intraluminal esophageal pressure. In 90% of cases, the tear is at the left posterolateral wall of the lower third of the esophagus and communicates with the left pleural cavity in 80% of cases, as was the case for our patient (2). Boerhaave’s syndrome is usually observed in patients aged 40–60 years and is more frequently described in men than in women, with ratios ranging from 2:1 to 5:1 (4).
A classical triad of signs constitutes Boerhaave’s syndrome: forceful vomiting, chest pain, and subcutaneous emphysema. In a literature review, Brauer et al. (5) noted that the usual presenting symptom is chest or epigastric pain (83%), with an antecedent vomiting or retching (79%), associated with dyspnea (39%) and shock (32%), and subcutaneous emphysema, when present, can be palpable in the neck or chest. Lemke and Jagminas (6) reported that toxic appearance, pleural effusion, pneumothorax, leukocytosis, azotemia, and hypoxia are all positively associated with this disease. These findings may be minimal or absent, depending on the amount of pleural or peritoneal contamination. Our patient had fever, tachycardia, and leukocytosis, which are common signs of mediastinitis. These symptoms were mild because there was no leak of food material through the tear because of the empty stomach after the preoperative fasting period. This was obvious as the drained pleural liquid did not contain food particles, as frequently reported (7).
Chest radiograph shows anomalies in 90% of patients such as pleural effusion, hydropneumothorax, and pneumomediastinum. The esophagogram is used to confirm the diagnosis of Boerhaave’s syndrome. Even when properly performed, as was the case of the first esophagogram performed on our patient, the rate of false-negative results is 10%–25% (8).
In conclusion, as Boerhaave’s syndrome is uncommon, errors in diagnosis are usually caused by failure of clinicians to consider its possibility and unawareness of its varied and atypical presentations. This diagnosis should be considered early by anesthesiologists in the presence of PONV accompanied by pain, dyspnea, or subcutaneous emphysema. Because of a frequent incidence of false-negative esophagogram, a high index of suspicion must be maintained when the clinical picture is suggestive of this rare but potentially life-threatening condition. The final outcome for our patient was good because of the absence of spoliation of the pleural and the mediastinal cavities with food particles, because his stomach was empty.
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References
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- White PF, Watcha MF [Editorial]. Postoperative nausea and vomiting: prophylaxis versus treatment. Anesth Analg 1999; 89: 1337–9.[Free Full Text]
- Bjerke HS. Boerhaave’s syndrome and barogenic injuries of the esophagus. Chest Surg Clin N Am 1994; 4: 819–25.[Medline]
- Baric A. Oesophageal rupture in a patient with postoperative nausea and vomiting. Anaesth Intensive Care 2000; 28: 325–7.[Medline]
- Zwischenberger JB, Savage C, Bidani A. Surgical aspects of esophageal disease. Am J Respir Crit Care Med 2001; 164: 1037–40.
- Brauer RB, Libermann-Meffert D, Stein HJ, et al. Boerhaave’s syndrome: analysis of the literature and report of 18 new cases. Dis Esophagus 1997; 10: 64–8.[Medline]
- Lemke T, Jagminas L. Spontaneous esophageal rupture: a frequently missed diagnosis. Am Surg 1999; 65: 449–52.[Medline]
- Janjua KJ. Boerhaave’s syndrome. Postgrad Med J 1997; 73: 265–70.[Abstract]
- Pate JW, Walker WA, Cole FH Jr., et al. Spontaneous rupture of the esophagus: a 30-year experience. Ann Thorac Surg 1989; 47: 689–92.[Abstract]
Accepted for publication October 3, 2003.
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Abstract
Introduction
