Ann Thorac Surg 2009;87:1257-1258. doi:10.1016/j.athoracsur.2008.08.009
© 2009 The Society of Thoracic Surgeons
Case Reports
Cardiac Arrest Caused by Tension Pneumomediastinum in a Boerhaave Syndrome Patient
Piotr Paluszkiewicz, MDa,*,
Jaroslaw Bartosinski, MDb,
Katarzyna Rajewska-Durda, MDb,
Katarzyna Krupinska-Paluszkiewicz, MDc
a Department of Surgery and Surgical Nursing, Medical University, St. John Hospital, Lublin, Poland
b Department of Anaesthesiology and Intensive Care, St. John Hospital, Lublin, Poland
c Department of Radiology, St. John Hospital, Lublin, Poland
Accepted for publication August 6, 2008.
* Address correspondence to Dr Paluszkiewicz, Department of Surgery and Surgical Nursing, Medical University, 6 Chodzki St, Lublin, PL-20950, Poland (Email: ppalusz{at}uhc.com.pl).
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Abstract
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This report presents a 23-year-old man with esophageal perforation, tension pneumomediastinum, and subsequent cardiorespiratory arrest. Initial resuscitation by cervical and subxiphoid mediastinotomy was ineffective. Bedside decompression of the posterior mediastinum through the esophageal hiatus of the diaphragm resulted in immediate return of a normal sinus rhythm and noncompromised mechanical ventilation. The patient made a full recovery and was discharged on day 12. Transhiatal decompression of the posterior mediastinum can be recommended for the treatment of cardiorespiratory complications in patients with tension pneumomediastinum in whom the classic cervical and subxiphoid mediastinotomies are ineffective.
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Introduction
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Tension pneumomediastinum leading to acute dyspnea and subsequent cardiac arrest is an extremely rare and severe condition. Similar findings have been observed in artificially ventilated or trauma patients with concomitant damage of the tracheobronchial tree [1, 2].
Barotraumatic perforation of the esophagus (Boerhaave syndrome) usually results in left-sided hemi-pneumothorax, subcutaneous emphysema of the neck and upper trunk, and secondary sepsis due to translocation of the infected content into the mediastinum [3]. This condition is uncommon and is associated with a high mortality rate [3]. In this presented case, the high-tension air collection inside the mediastinum, as a first symptom of Boerhaave syndrome, resulted in cardiorespiratory arrest. Successful decompression of the mediastinum was accomplished by opening the esophageal hiatus of the diaphragm.
A 23-year-old man was admitted to our intensive care unit after he presented with severe vomiting, lower chest and epigastric pain, and awareness disorder (Glasgow Coma Score, 12 points) after a clozapine overdose that was confirmed by urine analysis. There was no history of illicit drug abuse. The result of a chest roentgenogram was unremarkable. A computed tomography scan demonstrated mild cerebral edema. After resuscitation with intravenous fluids, the patient stabilized.
The patient was transferred to a general medical ward and a liquid diet was commenced. The following day (third day after admission), cardiorespiratory arrest occurred after the patient drank 250 mL of soup and 150 mL of water.
Endotracheal tube ventilation was ineffective due to high airway pressure and therefore chest tubes were inserted bilaterally. No pleural air collection was found. A portable chest roentgenogram was performed. Difficulties with mechanical ventilation were attributed to a tension pneumomediastinum (Fig 1). Cervical and subxiphoid resuscitative mediastinotomies were both ineffective.
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Fig. 1. Portable chest roentgenogram of our mechanically ventilated patient during resuscitation shows a massive pneumomediastinum with extended bilateral atelectases. The patient showed no signs of neck and chest subcutaneous emphysema.
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Decompression of air under tension was achieved by opening the periesophageal space through the esophageal hiatus of the diaphragm. The patient's condition suddenly improved, with the return of normal sinus rhythm and noncompromised mechanical ventilation. The posterior mediastinum was drained using a tube inserted in the periesophageal space. Subsequent emergency water-soluble fluoroscopy did not reveal any esophageal leakage.
The patient was treated conservatively (total parenteral nutrition, nasogastric tube, wide-spectrum antibiotics) for 10 days after the arrest. Clinical examinations and laboratory tests did not reveal any rise in inflammatory markers. The third day after resuscitation the patient was breathing spontaneously. A chest roentgenogram confirmed absence of atelectasis (Fig 2), and laboratory tests demonstrated normal values of arterial blood gases; therefore, the endotracheal tube was removed. The following day, the posterior mediastinal and pleural tubes were also removed.
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Fig. 2. Chest roentgenogram of the patient 3 days after decompression of the posterior mediastinum shows reduction of mediastinal emphysema, complete regression of atelectases, and normal lungs opacity.
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Ten days later an esophagogastroduodenoscopy confirmed a healed 2.0-cm linear left-sided supracardiac perforation of the esophagus. The patient was discharged in good condition without any additional complications; however, he was monitored closely for 2 years by regular physical examinations, chest roentgenograms, and laboratory tests. During a follow-up of 2 years, there was no evidence of further abnormalities or any gastrointestinal symptoms.
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Comment
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Spontaneous perforation of the esophagus usually occurs on the left side of the distal third part at a "weak point" between clasp and oblique fibers. An increase of intraesophageal pressure and rotation of the esophagi tears the muscle layer proximally to the esophageal mucosa. This may lead to pseudovalve and air-trap formation [3]. In patients without sepsis, the perforation could heal with conservative measures [4] or by placement of a self-expanding esophageal stent [5].
We speculate that tension pneumomediastinum, which developed 3 days after admission, was related to secondary disintegration of a healing, initial tear induced by elevation of intraesophageal pressure during swallowing. It is possible that the either the mucosal or muscle layers tore initially, followed later by the other layer. A similar case of incomplete rupture related to barotrauma has been discussed [6].
An air collection in the mediastinum as a result of esophageal wall rupture may spontaneously relocate into pleural, retroperitoneal, or subcutaneous spaces. When natural decompression into these spaces does not occur, the pressure of retained air may reduce lung capacity with secondary atelectasis and may cause compression of the right atrium and vena cava confluence. All these effects, either solely or in combination, may cause sudden hemodynamic and respiratory distress [1, 2, 4].
In a tension pneumomediastinum resulting in cardiorespiratory distress, a successful decompression is usually achieved by opening the upper or lower retrosternal space [1, 2, 4]. When the pneumomediastinum is due to alveolar rupture, the air collection is usually retrosternal and these measures are effective. Our initial approaches had been based on this premise but were ineffective, as was pleural space drainage to exclude tension pneumothorax. In this patient, the air was trapped in the periesophageal space. Successful decompression of the mediastinum was achieved by opening the lower periesophageal space during an urgent bedside minilaparotomy.
To conclude, delayed life-threatening events may be associated with suspected Boerhaave syndrome. Decompression of the posterior pneumomediastinum through the esophageal hiatus is effective in those patients where other more classic approaches are ineffective.
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References
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Abstract
Introduction
