Postemetic Rupture Research Articles

Post-operative pneumothorax with subcutaneous emphysema in a pre-eclamptic patient.

Sir, A 30-year-old female patient presented with severe pre-eclampsia for emergency caesarean section. On the operating table, she had a blood pressure (BP) of 176/98 mm Hg, pulse rate 102/min, oxygen saturation (SpO2) 99% and air entry was equal bilaterally. Rapid sequence induction and intubation were performed; gentle laryngoscopy was performed and cuffed endotracheal tube (ETT), 7.5 internal diameter was inserted aided by a stylet. The depth of anaesthesia was maintained with O2, nitrous oxide, isoflurane and muscle relaxant vecuronium (total dose of 6 mg) was used. The monitors used were electrocardiograph, pulse oximeter, non-invasive BP, and end-tidal carbon dioxide (CO2) monitor. The patient was ventilated on closed circuit with mechanical ventilation (volume control mode with respiratory rate [RR] 12/min, tidal volume of 450 ml, without positive end-expiratory pressure (PEEP), with mean airway pressure of 14 cm H2O). Intra-operative period was uneventful. The surgery was completed in 1 h. Postoperatively, the neuromuscular blockade was reversed with neostigmine 2.5 mg intravenous (iv), glycopyrrolate 0.5 mg iv. Due to inadequate reversal of neuromuscular blockade as suspected by poor respiratory efforts, the reversal drugs were supplemented. Arterial blood gas report showed normal partial pressure of oxygen and potential of hydrogen. However, CO2 retention was present, so we continued to manually assist her ventilation. After 10 min, her respiratory efforts were adequate, but her protective airway reflexes were blunted and she was tolerating the ETT well. Therefore, we decided not to extubate the trachea. While shifting the patient to recovery room on T piece, she had a violent coughing and retching episode after which she became restless and developed bradycardia with SpO2 decreasing to 82%. We then noticed palpable crepitus all over the chest, face and doubtful air entry on chest auscultation. As we suspected displacement of ETT, we extubated the trachea. She was unable to maintain adequate respiratory efforts. Hence, we paralysed her and reintubated her trachea. Thereafter, her vital signs stabilised. Air entry on the left side was decreased. She was shifted to the Intensive Care Unit (ICU) for mechanical ventilation. A chest X-ray was done in the ICU, which showed left-sided pneumothorax with subcutaneous emphysema. An intercostal chest drain was inserted and patient. The patient was maintained ventilatory support without delay (volume control mode with RR 14/min, TV 450 ml, PEEP of 0 cm H2O, inspiratory to expiratory ratio (I: E ratio) of 1:2 and peak airway pressures limited to 24 cm H2O). We could not find any obvious airway rent as assessed by fibreoptic bronchoscopy. The patient's relative did not give consent for computed tomography of thorax. After 24 h of stay in the ICU, the patient's vital signs got stabilised with normal respiratory parameters. The patient's trachea was extubated. After 24 h of cessation of air column movement, the intercostal chest drain was removed. Pneumothorax with subcutaneous emphysema in the immediate postoperative period can be spontaneous or iatrogenic. Spontaneous causes include rupture of undiagnosed bullae, spontaneous post-violent cough airway tear, alveolar rupture and post-emetic rupture of the oesophagus.[1,2,3] Iatrogenic causes include trauma to the pharynx, trachea during traumatic intubation, over inflation of ETT cuff, repeated intubation attempts, re-positioning of ETT without deflating the cuff, stylet protruding beyond ETT tip, patient movement or coughing during intubation/extubation and patient head and neck movement after intubation.[4] In our patient, adequate precautions were taken to prevent these iatrogenic causes. Decrease in SpO2 and bradycardia did not occur in the intra-operative period during which positive pressure ventilation was provided, so the aetiology being rupture of undiagnosed bullae due to positive pressure ventilation is unlikely. There are patient and surgical factors such as congenital tracheal anomalies, chronic use of steroids, chronic obstructive pulmonary disease, thoracic and laparoscopic surgeries.[4] None of these factors are involved in our case. Even though, we could not find any obvious airway rent while doing fibreoptic bronchoscopy, a possibility of airway injury cannot be completely ruled out. There is a high probability that either the violent coughing or retching episode in the post-operative period or ETT displacement due to violent head and neck movement during transfer to the recovery room could have led to an airway or oesophageal rent. We would like to create an awareness that airway trauma can lead to pneumothorax with subcutaneous emphysema in a pregnant patient due to fragile oedematous airway mucosa. We, therefore, reemphasise the importance of gentle laryngoscopy and intubation, maintenance of cuff pressure, administration of anti-emetics, smooth reversal, extubation and care of ETT while shifting the patient. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Single Procedure Esophageal Bypass: A Valid Option In Delayed Surgical Intervention For Complicated Esophageal Perforation

We present a case report of Boerhaave syndrome or spontaneous post-emetic rupture of the esophagus complicated with an esophagopleural fistula of which the diagnosis was missed at the initial presentation in the emergency. Surgical intervention was delayed for more than two weeks until the esophageal perforation was recognized. The patient was optimized for surgery and a single-stage esophageal bypass surgery was done where the esophagus was left in situ, the stomach was pulled up through the substernal route and a cervical esophagogastric anastomosis was made to restore the gastrointestinal continuity; thus avoiding the morbidity associated with an esophagostomy and a second procedure for delayed reconstruction.

Boerhaave’s syndrome: a pain in the neck

Boerhaave’s syndrome, or post-emetic rupture of the oesophagus, classically presents with vomiting, chest pain and subcutaneous emphysema. Mortality in this condition is very high and increases dramatically with delayed diagnosis...

Ruptura pós-emética do esôfago: a síndrome de Boerhaave

Postemetic rupture of the esophagus, also known as spontaneous rupture or Boerhaave's syndrome, was first described by Herman Boerhaave in 1724. This is a severe disease that causes high mortality rates and is difficult to diagnose not only because it is rare but also because it is frequently confused with other severe clinical conditions, such as acute myocardial infarction, perforated peptic ulcer, and acute pancreatitis. Herein, we describe three cases of patients with this syndrome. Two underwent primary repair of the rupture, and one underwent esophagectomy followed by reconstruction. There was one death due to septic shock in the immediate postoperative period. The other two patients presented favorable long-term evolution.

Boerhaave's syndrome: CT diagnosis

Boerhaave's syndrome is the postemetic rupture of a normal oesophagus, the diagnosis of which is not always immediately apparent. We present here a case report which illustrates the value of computed tomography (CT) scanning in making this often difficult diagnosis.

Postemetic Rupture of Herniated Cardia of the Stomach

To the Editor.— I refer to the Letter to the Editor by Gallivan 1 commenting on our article entitled Postemetic Rupture of Herniated Cardia of the Stomach. 2 Although this is a somewhat delayed response to that letter, I believe that there still may be something new above the diaphragm after all. Our case represents a classic postemetic or spontaneous rupture similar to that reported by Boerhaave 3 in 1724 with the exception that the anatomic site of rupture occurred in a herniated cardia of the stomach rather than in the lower esophagus. In postemetic rupture, the cause remains unclear, but it is postulated that the extension of smooth-muscle fibers from the esophagus onto the stomach wall results in a defective or weakened muscular zone. As we mentioned in our article, the perforation is almost always in the lower third of the esophagus, and about 90% occur on the left

Postemetic Rupture of Herniated Cardia of the Stomach-Reply

In Reply.— Comments by E. C. James, MD, reiterating some points of his excellent article entitled Postemetic Rupture of Herniated Cardia of the Stomach: A Variant of Boerhaave's Syndrome are noted and appreciated. His conjectures concerning the case described in my Letter to the Editor are not precisely accurate, but his remarks about Belsey and Nissen procedures are cogent. To set the record straight, the modified Belsey repair of my patient's hiatal hernia was done in August 1972. It was done through a right transthoracic approach at the time of pulmonary surgery, leaving the left hemidiaphragm unscathed. Her singular postemetic rupture into the left pleural cavity of a herniated cardia of her stomach occurred almost three years later , in 1975. After she had vomited all ingested materials for three days in 1975, a stat barium swallow examination disclosed an intact hiatal hernia repair with no esophagogastric abnormalities noted. Her continued

Postemetic rupture of herniated cardia of the stomach

Postemetic rupture of herniated cardia of the stomach

Postemetic rupture of herniated cardia of the stomach

Postemetic rupture of herniated cardia of the stomach

Postemetic Rupture of Herniated Cardia of the Stomach

To the Editor.— Indeed, there is nothing new under the sun nor above the diaphragm. The article by Gapp et al (1982;247:811) indicated that isolated rupture through a herniated gastric cardia owing to forceful emesis had not been identified in their review of the literature. I have treated surgically a similar case in 1975. Report of a Case.— A 60-year-old woman had previously undergone a right transthoracic ligation of blebs with pleurodesis and a simultaneous modified Belsey repair of a symptomatic hiatal hernia. Three years later, she was seen for a three-day history of acute left submammary, retrosternal, and subscapular pleuritic chest pains, which were associated with vomiting of all ingested materials. Because of a history of phlebitis, she was treated with intravenous heparin sodium for three days for possible pulmonary emboli. She was subsequently treated with warfarin sodium, tetracycline, and intermittent positive-pressure breathing. A left pleural effusion was treated

Postemetic rupture of herniated cardia of the stomach. A variant of Boerhaave's syndrome

Postemetic rupture of herniated cardia of the stomach. A variant of Boerhaave's syndrome

Postemetic Rupture of Herniated Cardia of the Stomach

THE CLASSIC description of postemetic or spontaneous rupture of the esophagus was recorded by a distinguished Dutch physician, Herman Boerhaave, in 1724.¹His patient, the Grand Admiral Baron van Wassenauer, experienced intense chest pain during induced vomiting at the conclusion of an eating and drinking episode. His general condition deteriorated rapidly and he died 18 hours later. At postmortem examination, Boerhaave found a rent in the lower third of the esophagus with a large quantity of gastric contents and air in the mediastinum and pleural cavity. In postemetic rupture of the esophagus, the perforation almost always occurs in the lower third, and in 90% of patients it is located posterolaterally on the left side. The etiology remains enigmatic, but it is conjectured that the extension of smoothmuscle fibers from the esophagus onto the stomach wall results in a defective or weakened muscular zone. The insufflation of air into the

The Management of Nonmalignant Intrathoracic Esophageal Perforations

Eight patients with nonmalignant intrathoracic esophageal perforations recognized more than 48 hours (48 hours to 14 days) after rupture were treated at Toronto General Hospital between 1973 and 1978. Perforation was due to postemetic rupture in 7 patients and to instrumentation in 1. The patients were seen with pain (8), vomiting (7), fever (7), shock (4), respiratory insufficiency (5), pleural effusion (7), pulmonary infiltrates (7), and leukocytosis (6). All patients were managed with thoracotomy. Direct suture closure of the perforation was carried out in 4 patients with midesophageal perforations. Postoperative localized leaks developed in 2 of these patients but healed with conservative management. Cervical esophagostomy and esophageal diversion were used in 1 patient in whom a severe empyema developed in the postoperative period. Direct suture closure, reinforced with a gastric patch, was used to close three lower esophageal perforations. None of these patients had a postoperative leak but all developed subsequent reflux esophagitis. All 8 patients survived. In patients with delayed recognition of a nonmalignant intrathoracic esophageal perforation, elimination of continued chemical and bacterial contamination can be achieved by a clear definition and closure of the esophageal mucosal margins. The obliteration of potential pleural spaces by good tube drainage, lung decortication, and the elective use of mechanical ventilation with positive end-expiratory pressure decreases the incidence of uncontrolled intrapleural sepsis.

Esophageal perforation following use of the esophageal obturator airway

Four cases of esophageal rupture associated with the use of the esophageal obturator airway are presented and added to the fifteen cases already in the literature. The incidence of this complication may be greater than previously suspected since a systematic search for this complication has not been made in cardiac arrest patients. The mechanism of rupture of the occluded esophagus may be similar to that seen in postemetic rupture. Endotracheal intubation remains the procedure of choice in airway control of cardiac arrest patients, although the modified esophageal obturator airway with gastric tube may prevent the occurrence of esophageal rupture by allowing decompression of the esophagus.

Boerhaave's Prescience

To the Editor.— The recent CLINICAL NOTE by Brown and Cohen (240:140, 1978) is the latest of several recent case reports wherein nutritional support by means of total parenteral nutrition permitted successful nonoperative management of spontaneous postemetic rupture of the esophagus, the so-called Boerhaave's syndrome. Treatment of this disease is associated with considerable postoperative morbidity and even mortality despite the most favorable of circumstances such as early diagnosis, prompt operative intervention, and minimal tissue contamination and necrosis. It is therefore likely that total parenteral nutrition will be used more frequently in such cases and may in fact facilitate the conservative treatment of those carefully selected patients in whom the diagnosis is not made until late in the course of the disease and whose clinical condition is stable. Hermann Boerhaave, professor of the theory and practice of physic at the University of Leyden and the leading physician of his time, anticipated

SPONTANEOUS PERFORATION OF THE ESOPHAGUS: REVIEW OF THE LITERATURE AND REPORT OF A CASE

Excerpt Spontaneous perforation of the esophagus is a rare condition with a high mortality rate when untreated. The following patient illustrates the need for an early diagnosis and immediate surgi...

Postemetic rupture of the esophagus: a report of three cases.

The purpose of this paper is to discuss briefly one of medicine's catastrophic conditions; namely, post-emetic rupture of the esophagus, a rather uncommon accident, but by no means a rarity. Although the history, clinical, and roentgen findings are characteristic, the diagnosis is frequently missed and the condition terminates fatally. Prompt surgical treatment is necessary if the patient is to survive. This condition, sometimes spoken of as spontaneous rupture of the esophagus, is to be differentiated from perforation secondary to intrinsic or extrinsic disease, as well as from traumatic rupture of the esophagus from intrinsic or extrinsic causes or agents. By definition, post-emetic rupture of the esophagus is a tear through all layers of the wall of a normal esophagus as a result of vomiting. The 3 cases to be presented here, seen during the past two and one-half years, have all ended fatally. Spontaneous rupture of the esophagus was first described by Boerhaave in 1724. His patient was the Grand Admiral of the Netherlands Navy, and the rupture occurred as a result of vomiting and retching following ingestion of large quantities of food and alcoholic beverages. Until the 1940's, the disease was almost invariably fatal. The first successful surgical treatment was performed in 1946. The reported cases have been predominantly in males, by a ratio of 5 to 1. The average age is forty-five to fifty years. The history often reveals overindulgence in eating and/or drinking followed by vomiting and the sudden onset of severe pain in the epigastric or substernal area. The patient becomes critically ill and the course is rapidly downhill. Physical findings will vary depending on the time elapsed following the rupture. Generally the patient is suffering from extreme chest or upper abdominal pain and is restless, dyspneic, and cyanotic. Often there is a nasal twang to the voice. Subcutaneous emphysema may be present in the soft tissues of the upper chest and neck. There may be evidence of hydropneumo-thorax either unilaterally or bilaterally. Upper abdominal rigidity may be present. It is again emphasized that the course is rapidly downhill. Sooner or later the patient goes into shock due to pain, contamination, and anoxia. The possibility of esophageal rupture must be kept in mind if an early diagnosis is to be made. Among the conditions to be differentiated are perforated peptic ulcer, acute pancreatitis, empyema of the gallbladder, acute coronary occlusion, pulmonary embolism, and spontaneous pneumothorax. The most commonly confused condition is ruptured peptic ulcer. Many patients operated upon with this diagnosis in mind have been found to have no abdominal lesion. The rupture is generally considered to be the result of increased intraluminal pressure, due to spasm of the pyloric and crico-pharyngeus muscles with associated vomiting and retching.