Reevaluation of the Boerhaave Syndrome A Review of Fourteen Cases
Anthony S. Patton, MD, Salem, Massachusetts Dexter W. Lawson, MD, Salem, Massachusetts James M. Shannon, MD, Salem, Massachusetts Thomas S. Risley, MD, Beverly, Massachusetts Frank E. Bixby, MD, Beverly, Massachusetts
Esophageal perforation is usually associated with ingestion of a foreign body, surgical instrumentation, or disrupted esophageal intestinal anastomoses. So-called spontaneous esophageal perforation is unusual, and most cases are single reports. Despite its relative rarity, it is an important entity to be recognized because of the ease of cure if treated early [1,2]. In 1724 Boerhaave described a case of esophageal perforation in a Dutch admiral, Baron Von Wassenaer. His paper discussed the classic parade of symptoms and signs: acute gastric distress secondary to overindulgence followed by forceful vomiting and severe pain in the chest with resulting collapse, hypotension, and death [3]. It is logical that most textbooks and teachings describe “spontaneous” esophageal perforation emphasizing the classic symptoms [4,5]. Most case reports also have fit the classic mold [1,2,6-g]. In a review of our own experience with “spontaneous” esophageal perforation, we were surprised to find that the classic progression of symptoms and signs does not always occur. The diagnosis can be obscure and may be missed for many days and even weeks. Patients may present with pain without vomiting, vomiting without pain, constrictive pericarditis, pneumothorax, pleural effusion, or empyema. Diagnostic possibilities include almost all upper abdominal and thoracic emergency conditions. The only consistent feature seems to be perforation of the esophagus just above the cardia of the stomach. Despite this difficulty in diagnosis, even late cases can From the Departments of Surgery, Salem Hospital, Salem, Massachusetts, and Beverly Hospital, Beverly, Massachusetts. Reprint requests should be addressed to Anthony S. Patton, MD, North Shore Medical Park, Essex Center Drive, Peabody,Massachusetts 01960. Presented at the Fifty-Ninth Annual Meeting of the New England Surgical Society, Dixville Notch, New Hampshire, September 29-October 1, 1978.
560
be treated successfully. Of our fourteen patients, eleven survived; one died before operation. In six patients, treatment was delayed more than eight days because of unusual presentation. Material and Methods
Fourteen cases over a period of twenty-five years were found in the records of two hospitals, Salem Hospital and Beverly Hospital, on the North Shore of Boston. At present there are 400 medical-surgical beds at Salem Hospital and 200 medical-surgical beds at Beverly Hospital. All but one patient had proved “spontaneous” esophageal perforation as determined by either x-ray film or operation. One patient, who died an hour after admission, had a highly suspicious history with suggestive physical and x-ray findings. Histories were reviewed for age, symptoms, location of pain, vomiting, relation of pain to vomiting, associated diseases, initial presenting problem, preliminary diagnoses, time of initial diagnosis to treatment, time of treatment to discharge from hospital, treatment, and survival. Results
The results are shown in Tables I, II, and III. Patients’ ages ranged from 53 to 78 years; there were twelve men and two women. Analysis of symptoms showed that eleven of fourteen patients had severe pain. The other three had pain that was not excruciating or severe. Nine of the fourteen patients had abdominal pain with radiation to the costal margins. Seven of the fourteen patients primarily had chest pain or radiation to the left side of the chest. Three patients had radiation to the back. All fourteen patients, including the patient with a small chronic perforation, had a pleuritic comDonent to their Dain. Vomiting or hiccoughing was a significant symptom in eleven of the fourteen patients. In six of these
The American Journal oi Surgery
Boerhaave Syndrome
TABLE I
Case No. 1 2
10 11
12
13 14
Associated Disease or Conditions in Fourteen Patients
TABLE II Case No.
Associated Disease or Conditions Long-standing history of duodenal ulcer; one year after perforation patient underwent ulcer operation Recent history of weight loss and indigestion; carcinoma of stomach found on laparotomy after healed perforation of esophagus Recent history of gastric distress of few days’ duration No known history of previous abdominal complaints; recent alcohol ingestion Long-standing duodenal ulcer disease; possible pancreatitis Intermittent indigestion for days, chronic aspirin intake, large dose of soda before perforation History of indigestion of three weeks’ duration Found to have partial small bowel obstruction at postmortem examination Vague indigestion with burning and dysphagia for months; one year after successful healing of perforation, reticulum cell sarcoma in neck was found Known hiatus hernia for years with symptoms such as reflux and regurgitation lleus and small bowel contents in vomitus ten days after inguinal hernia repair; presented with uremia and dehydration Known hiatus hernia, previous repair three years earlier, symptoms of increasing substernal pain, chronic alcohol misuse Known hiatus hernia for years; high esophageal stricture, reflux esophagitis; chronic alcoholism Known hiatus hernia for years
patients, vomiting occurred at the time of the pain. In five of the eleven, there was no relation whatsoever between vomiting and pain. In the other three patients, there was no vomiting and thus no relation between vomiting and pain. Therefore, six of the fourteen patients appeared to fit the classic Boerhaave syndrome of gastric distress, that is, forceful vomiting and pain. Patients were analyzed for associated significant diagnoses, diseases, or complaints. All patients but one had some form of previous abdominal complaints, and seven patients had complaints related to the gastrointestinal tract for many months. Only one patient had no documentation of chronic or recent gastric distress. Deviation from the classic syndrome often caused difficulty in diagnosis and delay in treatment. In an analysis of the lapse of time between initial symptoms and diagnosis and treatment, it became obvious that those patients who had a classic association of pain with vomiting also usually had rapid recognition of the perforation with early treatment. Of the six patients with strong correlation of pain with vomiting, the diagnostic delay was from 0 to 30 hours. Of those seven patients with poor correlation of pain
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10 11 12 13 14
Initial Presenting Problem and Diagnoses
Presenting Problem Pain in upper abdomen, air in neck Pain in upper abdomen, air in neck Pain with air in neck Severe pain in mid chest and back, widened mediastinum on x-ray film Severe abdominal pain Pain with bilateral chest fluid, left Left pleural pain with effusion Severe pain in left flank with effusion Pain with pneumdthorax and effusion on second day Pain with pleural effusion Vomiting and ileus Increasing substernal pain, severe Increasing substernal pain, air in mediastinum Severe pain in left chest with pneumothorax and fluid
Initial Diagnosis Perforated esophagus Perforated esophagus Perforated esophagus Dissecting aneurysm
Perforated ulcer Perforated ulcer Pneumothorax with effusion Ureteral stone, pulmonary embolus Pneumothorax, questionable myocardial infarction Pulmonary embolus Uremia, unknown cause Esophagitis, severe Esophagitis, severe Perforated esophagus
with vomiting, there was delay in treatment from 8 days to months. One patient died before treatment could be given. Delay of diagnosis and treatment naturally affected final outcome. Of those patients who had the classic syndrome and early diagnosis, the hospital stay ranged from ten days to eight weeks. In those patients who had a nonclassic syndrome and delayed diagnosis, the hospital stay was increased accordingly. One of these patients died immediately, another in 9 days, and a third died in 8 weeks. Those who survived had a hospital stay of four to twelve weeks. Diagnosis was made by barium swallow in all patients but one. Other diagnostic clues were helpful. There were four patients with air in the neck. All patients eventually had air shown on chest film, either free in the pleural cavity or in the mediastinum. Two patients had obvious gastric contents on thoracentesis. One patient had a high amylase value on analysis of the pleural fluid. It is noteworthy that the amylase value of saliva is usually very high, and therefore if there is an esophageal perforation with effusion, the amylase value of this fluid will also be very high. Ofthe fourteen patients, thirteen received treat-
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TABLE III
Case No.
Summary of Treatment and Results
Time Lapse from First Symptoms to Treatment
Direct Suture
Gastrostomy
Jejunostomy
Hyperalimentation
Rib Resection
No No No No Yes Yes No No Yes
No No No No Yes Yes No Yes Decortication Yes Yes (2)
Result
1 2 3 4 5 6 7 6 9
None 6 hr 6 hr 6 hr 12hr 30 hr 24 hr 30 days 6 days
Yes Yes Yes Yes Yes Yes Yes No With lung patch
No Yes No No Yes Yes No Yes Yes
No Yes No No Yes Yes No Yes Yes
10 11
10 days 19 days
No No
Yes Yes
Yes Yes
12
Months
No
No
No
No
13 14
6 days Died on admission
Thal patch Nissen fundoplication No No
Healed in 8 wk Healed in 12 wk, pharyngostomy, pericardiectomy Healed primarily
Yes No
Yes No
Yes No
Yes No
Healed in 4 wk Died before operation
9
8
8
6
7
11 lived
Total (13 treated)
Healed Healed Healed Healed Healed Healed Died of Died of Healed
primarily primarily primarily primarily primarily in 7 wk sepsis small bowel obstruction in 6 wk
Note: No primary suture worked after 24 hours. No cervical esophagotomy was performed in this series. There was one decortication and one pericardiectomy. One attempt to repair with lung patch was unsuccessful. One Thal patch and Nissen fundoplication was performed for chronic local abscess secondary to leak.
ment. One entered the hospital with a history of severe chest pain of 12 hours’ duration. She had air in the neck and air and fluid on chest film. She died before any treatment could be given but was assumed to have esophageal rupture. She had no vomiting but had done extremely heavy lifting in the days before her pain. Thirteen other patients had various forms of surgical intervention depending on their clinical situation and delay in diagnosis. In general, those patients diagnosed early had direct repair and those with a delay of over 24 hours had some form of esophageal exclusion. Of those patients operated on, eleven survived. As noted, six patients had the usual parade of symptoms and early operation. An analysis of the seven patients with unusual symptoms and delay in diagnosis follows. Patient
7, a sixty-two
year old man (PO), entered with
chronic abdominal pain. He had only one episode of vomiting in the hospital. For 3 to 4 hours, while in the hospital, he had severe pain in the chest. Twenty-four hours later gastric fluid was noted on thoracentesis. An esophageal leak was seen on barium swallow just above the diaphragm. A few hours later attempted suture of the esophageal perforation was carried out, but the patient died of further leak and empyema nine days later. Patient 8, a seventy-five year old man (CB), entered an outside hospital with severe flank and pleural pain. He had no known vomiting. Pleural effusion was found and the patient was treated for pulmonary embolus. He was transferred to Salem Hospital one month later, where he
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found to have a pneumothorax and fluid and a leak of the esophagus just above the diaphragm was seen on barium swallow. A chest tube, rib resection, gastrostomy, and jejunostomy feedings were instituted, but the patient died two months after the initial episode. Unexpected small bowel obstruction was found at postmortem examination. Patient 9, a seventy-one year old man (JD), entered with a long, vague history of mild dysphagia and belching. Severe pain had occurred recently in the left side of the chest. Pneumothorax was not seen until a film was taken on the second day. A chest tube was inserted and the patient was better. On the seventh day, fluid in drainage seemed excessive and the amylase in the fluid was found to be near 2,000 Bodansky units. A barium swallow showed an esophageal leak just above the diaphragm into the pleural space. Decortication, wide drainage, gastrostomy, jejunostomy, and parent& hyperalimentation were carried out with recovery and discharge 8 weeks after admission. Patient 10, a seventy-eight year old woman (DG), entered another hospital with pain in the left side of the chest. She had a known small hiatus hernia. Vomiting had occurred but was not forceful and not related to pain. Pain increased and fluid and pneumothorax were seen after five days. A barium swallow on the ninth day showed esophageal leak. The patient was transferred to Salem Hospital, and ten days after the initial episode, she had tube thoractomy with rib resection, gastrostomy, jejunostomy, and parenteral hyperalimentation. Her condition improved and the leak healed after two months. Patient 11, a fifty-four year old man (RP), experienced vomiting and severe ileus one week after inguinal hernia was
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Boerhaave Syndrome
repair. He reentered the hospital with a high blood urea nitrogen level and dehydration which responded to fluid replacement. Pain was minimal. Seventeen days after admission, an air level was noted behind the heart and was thought to be an abscess in the lung. In the next two days pericardial tamponade developed with markedly elevated central venous pressure. Review of barium swallow revealed esophageal perforation. Pericardial exploration through the left anterior part of the chest revealed purulent pericardial tamponade which responded to wide removal of the pericardium and drainage into the left side of the chest. Rib removal was performed posteriorly through a separate incision to drain the esophageal perforation. A Levine tube was positioned above the perforation. In two days gastrostomy, jejunostomy, and pharyngostomy were carried out. Hyperalimentation was started through a central venous line. Further rib resection was needed, but the patient had slow healing over a twelve week period and has had no further problem. Patient 12, a sixty year old man (JM), had repair of a hiatus hernia four years earlier. He had a normal barium swallow postoperatively and had been well for three and a half years. Increasing amounts of substernal and pleural pain then developed with no vomiting. He had a known history of alcohol abuse. Barium swallow revealed a small perforation of the esophagus. He had a Thal patch with Nissen repair of the hiatus hernia. No true ulcer of the esophagus was seen. He did well postoperatively. Patient 13, a sixty-six year old man (RM), had a known hiatus hernia with esophagitis and soft stricture in the esophagus at the aortic arch. He had increasing amounts of substernal pain, which he thought was due to an increase in his usual large intake of alcohol and his severe chronic lung disease. There was one episode of vomiting after the pain had begun. Approximately eight days after the initial pain, barium swallow revealed esophageal perforation just above the diaphragm. He responded to tube drainage, rib resection, gastrostomy, jejunostomy, parenteral hyperalimentation, and drainage with a Levine tube. Discharge was in four weeks after initial treatment. Comments
Esophageal perforations are usually classified by their etiology. Perforations can be caused by trauma, instrumentation, foreign bodies, or surgical misadventures [6-8,101. Perforations that do not easily fall into these categories are usually called “spontaneous.” The classic case of spontaneous perforation was described in a lengthy monograph by Boerhaave in 1724. He outlined in vivid detail the postmortem findings of an aristocratic Dutch admiral who had rupture of the esophagus during an episode of retching after a debauchery of food and drink. Although in a sense the Baron’s misfortune was hardly “spontaneous,” the literature tends to refer to Boerhaave’s case as the first reported spontaneous
Volume 137, *prlll879
perforation. Most case reports tend to emphasize the progression from overindulgence to forceful vomiting followed by severe pleural pain, shock, and death. Certainly some cases do follow the classic pattern, and in our series six of the fourteen seemed to fit Boerhaave’s description. The remaining eight, however, were not classic and this lack of obvious correlation between pain and vomiting probably caused delay in treatment in seven patients. It was also striking that almost all patients (thirteen of fourteen) had a prolonged or recent history of some form of indigestion and gastric distress; also a large number of patients had chronic diseases of the gastrointestinal tract. This strong correlation suggests that esophageal perforation is probably never truly spontaneous except in the apparently unusual circumstances of no proved gastrointestinal illness. Even if Baron Von Wassenaer had no previous stomach trouble, it seems unlikely that Boerhaave himself would call such an episode truly spontaneous since it can easily be traced to “the immoralities of excessive personal indulgence.” The most important conclusion is that esophageal perforation can occur in an obscure fashion, and it should be included in the differential diagnosis of patients with catastrophic illnesses with upper abdominal and pleuritic pain. It should also be considered in patients having less than catastrophic illnesses but having pleural and mediastinal air and fluid without obvious cause. It can occur without the dramatic explosion frequently described. Early recognition in any case will lead to earlier treatment and less hospital time. Barrett’s [1] case was the first case of successful repair. It was successful despite some obvious postoperative drainage. Although early suture or patches are important in early cases such as those seen in the first few hours [2,11], late cases often require some form of esophageal exclusion and supplemental feeding [6-8,121. In our series, exclusion was accomplished by a Levine tube or pharyngostomy to control salivary secretions and gastrostomy to control gastric secretions and reflux. Tube drainage, rib resection, or both are needed for control of the esophageal leak and empyema. In one of our cases decortication was helpful, and this was also noted by Grill0 and Wilkins [II]. Supplemental feeding is effective by jejunostomy and central venous hyperalimentation. Other methods such as cervical esophagostomy for salivary control [8,12], distal taps or suturing for control of reflux from the stomach [8], T tubes for esophageal drainage [IO], various flaps [II], and patches [13] have been used. Late direct repair can occasionally be successful as noted in two cases of Grill0 and Wilkins
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Patton et al
CONTROL
OF SALIVA
LEVINETUBE PHARYNGOSTOMY CERVICAL ESOPHAGOSTOMY ATROPINE
DRAINAGE
OR CONTROL
OF PERFORATION PRlMARY
SUTURE.
FIRST 24 HOURS
TUBETHORACOTOMY DECORTICATION PLEURAL FLAP GASTRIC FLAP LUNG INTERCOSTALFLAP T-TUBE IN ESOPHAGUS RESECTION
CONTROL
OF GASTRIC
SECRETIONS GASTROSTOMY ESOPHAGEAL TAPE ESOPHAGEAL SUTURE
NUTRITIONAL
CONTROL
JEJEUNOSTOMY ,NTRA”ENOUSHYPERAlLlMENTATlON
Figure 1. esophagus.
Opfions of treafment for perforation
of the
important, have tended to obscure the search for etiologic mechanisms. Certainly, in our series, the high incidence of previous gastrointestinal disease seems significant. (Table I.) There appeared to be a large number of patients with either symptoms of esophagitis or gastritis and four with hiatus hernia. It is only conjecture that the esophagus may have been weakened by chronic inflammation and became more susceptible to rupture. Rupture in the acute cases by the pressure exerted by retching or vomiting against a closed glottis seems to be an attractive hypothesis. It is much more difficult to explain the cases with a more indolent course with late recognition. Perhaps chronic inflammation without fibrosis has a role. There appears to be a difference between the patients who have the classic syndrome and early operation and those with a slower course and late operation. This contrast suggests two different disease entities, perhaps because of the type of pleural insult and soilage. In the sudden tear with a full stomach, as described by Boerhaave, the amount of spillage is massive and would seem to be very irritating; the more subtle perforation might be less of a chemical insult to the pleura and mediastinum and might give the person more time to adjust physiologically. The classic case, in which the disease is more serious, would naturally attract more medical attention and earlier treatment. Summary
[11] utilizing a pleural flap. In general, however, friability and massive inflammation make such repairs difficult and often unsuccessful. Certainly, in our series, patients who were treated eight days or longer could not be expected to have a successful primary repair. An exception to this was the patient with small localized perforation repaired by a Thal patch. Triggiani and Belsey [6] have suggested esophagectomy in such cases. In our series such measures were not necessary, but convalescence was prolonged and careful nutritional, fluid, and antibiotic management was necessary. It is difficult to compare results with only fourteen cases, but this series has a survival rate among operative cases (eleven of thirteen) that compares favorably with most other reports [6,7,9,10]. There have been no deaths in recent years. The only approach used in these cases was early repair for early cases and esophageal exclusion via adequate drainage of leak, saliva, and gastric secretions. Adequate nutrition via central venous hyperalimentation and jejunostomy was emphasized also. (Figure 1.) Preoccupation with methods and results, although
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Fourteen cases of “spontaneous” esophageal perforation from two hospitals over a twenty-five year period are reviewed. The classic syndrome, as described by Boerhaave, included overindulgence, forceful vomiting, and severe pleuritic pain followed by collapse and death. In our series, six patients appeared to follow a classic pattern, and in five of these, treatment was primary suture and healing occurred early. Eight cases did not follow the usual syndrome. In one of these cases, the patient died before treatment could be given, one patient presented with localized chronic perforation and responded to a gastric Thal patch, six required prolonged treatment including tube thoracotomy, rib resection, decortication, pharyngostomy, jejunostomy, gastrostomy, parenteral hyperalimentation, and pericardiectomy. Diagnosis was often confused by total lack of correlation between vomiting and pain. Almost all patients had some other abdominal problem or symptoms long before esophageal perforation. Diagnosis was confused with that of dissecting aneurysm, perforated ulcer, myocardial infarction, renal stone, and The American
Journal
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Boerhaave
pleural effusion of unknown cause. One case presented nineteen days after perforation with constrictive purulent pericarditis. Of fourteen patients, one died almost immediately on arrival at the hospital, thirteen patients underwent operation, and eleven survived. Even in cases in which treatment is delayed by confusing presentations, the patient can survive, but vigorous treatment is needed and convalescence is prolonged. Although recognition of the classic Boerhaave syndrome is important, cases will be missed if reliance is placed solely on the usual criteria. References 1. Barrett NR: Report of a case of spontaneous perforation of the esophagus successfully treated by operation. Br J Surg 35: 216, 1947. 2. Alt RE, Bixby FE, Rowell RJ: Spontaneous rupture of the normal esophagus. N Engl J Med 249: 1060, 1953. 3. Boerhaave H: Atrocis, net descripti pius, morbi historia: secundum medicae artes leges conscripta, Lugd. Bat., Boutesteniana, 1724. Translated in Bull Med Libr Ass 43: 217, 1955. 4. d’Abreu AL, Taylor AB, Clarke DB: lntrathoracic Crises, p 66-69. London, Butterworths, 1968. 5. Sabiston DC, Spencer F: Gibbons Surgery of the Chest (3rd ed). Chapter by Ellis RH, p 715-718. Philadelphia, Saunders, 1976. 6. Triggiani E, Belsey R: Esophageal trauma; incidence, diagnosis and management. Thorax32: 241, 1977. 7. Lyons WS, Seremetis MG, de Guzman VC, Peabody JW: Ruptures and perforations of the esophagus: the case for conservative supportive management. Ann Thorac Surg 4: 346, 1978. 8. Urschel HC, Razzuk MA, Wood RE, et al: Improved management of esophageal perforation: exclusion and diversion in continuity. Ann Surg 179: 587, 1974. 9. Hadin WJ, Hardy JD, Conn JH: Esophageal perforations. Surg Gynecol Obstet 136: 325, 1967. 10. Abbott OA, Mansour KA, Logan WD, et al: Atraumatic so-called “spontaneous” rupture of the esophagus. J. Thorac Cafdiovasc Surg 59: 67, 1970. 11. Grill0 HC, Wilkins EW: Esophageal repair following late diagnosis of intrathoracic perforation. Ann Thorac Surg 4: 387, 1975. 12. Johnson J, Schwegman CW, Kirby CK: Esophageal exclusion for persistent fistula following spontaneous rupture of the esophagus. J Thorac Cardiovasc Surg 32: 827, 1956. 13. Thal AP, Hatafukw T: Improved operation for esophageal rupture. JAMA 188: 826, 1964.
Discussion John Head (Boston, MA): This may not be the burp heard around the world, but it certainly is the burp that made Boerhaave famous. The first classic case I heard about was a bit like the admiral’s. A man coming to Boston on the old New Haven Railroad spent the evening in the dining and parlor cars before going to bed. During the night as he heaved his considerable bulk in order to turn over, he felt sharp substernal pain, and by the time he reached South Station in Boston he was in shock. The fact that Doctor Patton and his colleagues have been able to collect fourteen cases of this rare entity might be construed as a comment on North Shore habits. At the
VebJme 137, April 1979
Syndrome
Massachusetts General Hospital we also have seen a wide spectrum of clinical behavior with a few delayed and chronic perforations, presumably starting with localized mediastinitis, abscess formation, and secondary rupture into the pericardium, pleural space, or bronchial tree. A valuable observation the authors made is that lower esophageal perforations do at times cause upper abdominal or mid-back pain rather than substernal pain. The other important point is the high incidence of preexisting upper gastrointestinal disease. I would add only one observation from our own experience in the surgical repair of these lesions. Even during the first 24 hours the quality of the esophageal wall may be very poor. These tears will not hold sutures well. We have found that wrapping with a large pleural flap is helpful as is visceral serosal covering a la Thal. I have two questions for Dr. Patton. Does he believe that the similar Mallory-Weiss syndrome is part of the spectrum of this disease, and if so, why is there no bleeding in cases of the Boerhaave syndrome? Second, are delayed development and poor correlation with vomiting related to a smaller perforation than that seen in the classic cases? John R. Brooks
(Boston, MA): It seems that the concept of a fundic wraparound is made to order as protection for the precarious esophageal suture line. I wonder why that has not been emphasized more. Anthony S. Patton (closing): I appreciate the comments of Dr. Head and the pertinent question raised by Dr. Brooks. Dr. Head was a close associate of Dr. Richard Sweet, one of the world’s most talented thoracic surgeons. There are two main questions or comments. One concerns the method of closure. In a case of early recognition and operation, any method such as a pleural or gastric patch is most acceptable if such material is readily available. Pleura can be used to buttress a suture line at almost any time after perforation. However, in most cases the amount of chemical and bacterial contamination after a few hours is usually so great that any extensive dissection in the chest outside the immediate area seems inappropriate. One often encounters a situation not unlike that described by Boorhaave in the postmortem examination of Baron Von Wassenaer. There are usually bits of decomposing food, saliva, and gastric juices washing around in the pleural cavity. The second question concerns the relation of a Mallory-Weiss tear to this phenomenon, spontaneous esophageal perforation. We found a number of such cases in the record rooms mixed with those of spontaneous esophageal perforation. The often bloody Mallory-Weiss tears are usually lower in position and occur both in the stomach and at the lowest edge of the esophagus. They seldom penetrate the gastric serosa and are associated with severe vomiting. A spontaneous esophageal perforation occurs higher and may or may not be associated with forceful vomiting but often with some chronic gastrointestinal complaint. The real heroes in the care of these patients are the nurses who must tally the various losses and look after the tubes with great diligence.
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Anthony S. Patton, MD, Salem, Massachusetts Dexter W. Lawson, MD, Salem, Massachusetts James M. Shannon, MD, Salem, Massachusetts Thomas S. Risley, MD, Beverly, Massachusetts Frank E. Bixby, MD, Beverly, Massachusetts
Esophageal perforation is usually associated with ingestion of a foreign body, surgical instrumentation, or disrupted esophageal intestinal anastomoses. So-called spontaneous esophageal perforation is unusual, and most cases are single reports. Despite its relative rarity, it is an important entity to be recognized because of the ease of cure if treated early [1,2]. In 1724 Boerhaave described a case of esophageal perforation in a Dutch admiral, Baron Von Wassenaer. His paper discussed the classic parade of symptoms and signs: acute gastric distress secondary to overindulgence followed by forceful vomiting and severe pain in the chest with resulting collapse, hypotension, and death [3]. It is logical that most textbooks and teachings describe “spontaneous” esophageal perforation emphasizing the classic symptoms [4,5]. Most case reports also have fit the classic mold [1,2,6-g]. In a review of our own experience with “spontaneous” esophageal perforation, we were surprised to find that the classic progression of symptoms and signs does not always occur. The diagnosis can be obscure and may be missed for many days and even weeks. Patients may present with pain without vomiting, vomiting without pain, constrictive pericarditis, pneumothorax, pleural effusion, or empyema. Diagnostic possibilities include almost all upper abdominal and thoracic emergency conditions. The only consistent feature seems to be perforation of the esophagus just above the cardia of the stomach. Despite this difficulty in diagnosis, even late cases can From the Departments of Surgery, Salem Hospital, Salem, Massachusetts, and Beverly Hospital, Beverly, Massachusetts. Reprint requests should be addressed to Anthony S. Patton, MD, North Shore Medical Park, Essex Center Drive, Peabody,Massachusetts 01960. Presented at the Fifty-Ninth Annual Meeting of the New England Surgical Society, Dixville Notch, New Hampshire, September 29-October 1, 1978.
560
be treated successfully. Of our fourteen patients, eleven survived; one died before operation. In six patients, treatment was delayed more than eight days because of unusual presentation. Material and Methods
Fourteen cases over a period of twenty-five years were found in the records of two hospitals, Salem Hospital and Beverly Hospital, on the North Shore of Boston. At present there are 400 medical-surgical beds at Salem Hospital and 200 medical-surgical beds at Beverly Hospital. All but one patient had proved “spontaneous” esophageal perforation as determined by either x-ray film or operation. One patient, who died an hour after admission, had a highly suspicious history with suggestive physical and x-ray findings. Histories were reviewed for age, symptoms, location of pain, vomiting, relation of pain to vomiting, associated diseases, initial presenting problem, preliminary diagnoses, time of initial diagnosis to treatment, time of treatment to discharge from hospital, treatment, and survival. Results
The results are shown in Tables I, II, and III. Patients’ ages ranged from 53 to 78 years; there were twelve men and two women. Analysis of symptoms showed that eleven of fourteen patients had severe pain. The other three had pain that was not excruciating or severe. Nine of the fourteen patients had abdominal pain with radiation to the costal margins. Seven of the fourteen patients primarily had chest pain or radiation to the left side of the chest. Three patients had radiation to the back. All fourteen patients, including the patient with a small chronic perforation, had a pleuritic comDonent to their Dain. Vomiting or hiccoughing was a significant symptom in eleven of the fourteen patients. In six of these
The American Journal oi Surgery
Boerhaave Syndrome
TABLE I
Case No. 1 2
10 11
12
13 14
Associated Disease or Conditions in Fourteen Patients
TABLE II Case No.
Associated Disease or Conditions Long-standing history of duodenal ulcer; one year after perforation patient underwent ulcer operation Recent history of weight loss and indigestion; carcinoma of stomach found on laparotomy after healed perforation of esophagus Recent history of gastric distress of few days’ duration No known history of previous abdominal complaints; recent alcohol ingestion Long-standing duodenal ulcer disease; possible pancreatitis Intermittent indigestion for days, chronic aspirin intake, large dose of soda before perforation History of indigestion of three weeks’ duration Found to have partial small bowel obstruction at postmortem examination Vague indigestion with burning and dysphagia for months; one year after successful healing of perforation, reticulum cell sarcoma in neck was found Known hiatus hernia for years with symptoms such as reflux and regurgitation lleus and small bowel contents in vomitus ten days after inguinal hernia repair; presented with uremia and dehydration Known hiatus hernia, previous repair three years earlier, symptoms of increasing substernal pain, chronic alcohol misuse Known hiatus hernia for years; high esophageal stricture, reflux esophagitis; chronic alcoholism Known hiatus hernia for years
patients, vomiting occurred at the time of the pain. In five of the eleven, there was no relation whatsoever between vomiting and pain. In the other three patients, there was no vomiting and thus no relation between vomiting and pain. Therefore, six of the fourteen patients appeared to fit the classic Boerhaave syndrome of gastric distress, that is, forceful vomiting and pain. Patients were analyzed for associated significant diagnoses, diseases, or complaints. All patients but one had some form of previous abdominal complaints, and seven patients had complaints related to the gastrointestinal tract for many months. Only one patient had no documentation of chronic or recent gastric distress. Deviation from the classic syndrome often caused difficulty in diagnosis and delay in treatment. In an analysis of the lapse of time between initial symptoms and diagnosis and treatment, it became obvious that those patients who had a classic association of pain with vomiting also usually had rapid recognition of the perforation with early treatment. Of the six patients with strong correlation of pain with vomiting, the diagnostic delay was from 0 to 30 hours. Of those seven patients with poor correlation of pain
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10 11 12 13 14
Initial Presenting Problem and Diagnoses
Presenting Problem Pain in upper abdomen, air in neck Pain in upper abdomen, air in neck Pain with air in neck Severe pain in mid chest and back, widened mediastinum on x-ray film Severe abdominal pain Pain with bilateral chest fluid, left Left pleural pain with effusion Severe pain in left flank with effusion Pain with pneumdthorax and effusion on second day Pain with pleural effusion Vomiting and ileus Increasing substernal pain, severe Increasing substernal pain, air in mediastinum Severe pain in left chest with pneumothorax and fluid
Initial Diagnosis Perforated esophagus Perforated esophagus Perforated esophagus Dissecting aneurysm
Perforated ulcer Perforated ulcer Pneumothorax with effusion Ureteral stone, pulmonary embolus Pneumothorax, questionable myocardial infarction Pulmonary embolus Uremia, unknown cause Esophagitis, severe Esophagitis, severe Perforated esophagus
with vomiting, there was delay in treatment from 8 days to months. One patient died before treatment could be given. Delay of diagnosis and treatment naturally affected final outcome. Of those patients who had the classic syndrome and early diagnosis, the hospital stay ranged from ten days to eight weeks. In those patients who had a nonclassic syndrome and delayed diagnosis, the hospital stay was increased accordingly. One of these patients died immediately, another in 9 days, and a third died in 8 weeks. Those who survived had a hospital stay of four to twelve weeks. Diagnosis was made by barium swallow in all patients but one. Other diagnostic clues were helpful. There were four patients with air in the neck. All patients eventually had air shown on chest film, either free in the pleural cavity or in the mediastinum. Two patients had obvious gastric contents on thoracentesis. One patient had a high amylase value on analysis of the pleural fluid. It is noteworthy that the amylase value of saliva is usually very high, and therefore if there is an esophageal perforation with effusion, the amylase value of this fluid will also be very high. Ofthe fourteen patients, thirteen received treat-
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TABLE III
Case No.
Summary of Treatment and Results
Time Lapse from First Symptoms to Treatment
Direct Suture
Gastrostomy
Jejunostomy
Hyperalimentation
Rib Resection
No No No No Yes Yes No No Yes
No No No No Yes Yes No Yes Decortication Yes Yes (2)
Result
1 2 3 4 5 6 7 6 9
None 6 hr 6 hr 6 hr 12hr 30 hr 24 hr 30 days 6 days
Yes Yes Yes Yes Yes Yes Yes No With lung patch
No Yes No No Yes Yes No Yes Yes
No Yes No No Yes Yes No Yes Yes
10 11
10 days 19 days
No No
Yes Yes
Yes Yes
12
Months
No
No
No
No
13 14
6 days Died on admission
Thal patch Nissen fundoplication No No
Healed in 8 wk Healed in 12 wk, pharyngostomy, pericardiectomy Healed primarily
Yes No
Yes No
Yes No
Yes No
Healed in 4 wk Died before operation
9
8
8
6
7
11 lived
Total (13 treated)
Healed Healed Healed Healed Healed Healed Died of Died of Healed
primarily primarily primarily primarily primarily in 7 wk sepsis small bowel obstruction in 6 wk
Note: No primary suture worked after 24 hours. No cervical esophagotomy was performed in this series. There was one decortication and one pericardiectomy. One attempt to repair with lung patch was unsuccessful. One Thal patch and Nissen fundoplication was performed for chronic local abscess secondary to leak.
ment. One entered the hospital with a history of severe chest pain of 12 hours’ duration. She had air in the neck and air and fluid on chest film. She died before any treatment could be given but was assumed to have esophageal rupture. She had no vomiting but had done extremely heavy lifting in the days before her pain. Thirteen other patients had various forms of surgical intervention depending on their clinical situation and delay in diagnosis. In general, those patients diagnosed early had direct repair and those with a delay of over 24 hours had some form of esophageal exclusion. Of those patients operated on, eleven survived. As noted, six patients had the usual parade of symptoms and early operation. An analysis of the seven patients with unusual symptoms and delay in diagnosis follows. Patient
7, a sixty-two
year old man (PO), entered with
chronic abdominal pain. He had only one episode of vomiting in the hospital. For 3 to 4 hours, while in the hospital, he had severe pain in the chest. Twenty-four hours later gastric fluid was noted on thoracentesis. An esophageal leak was seen on barium swallow just above the diaphragm. A few hours later attempted suture of the esophageal perforation was carried out, but the patient died of further leak and empyema nine days later. Patient 8, a seventy-five year old man (CB), entered an outside hospital with severe flank and pleural pain. He had no known vomiting. Pleural effusion was found and the patient was treated for pulmonary embolus. He was transferred to Salem Hospital one month later, where he
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found to have a pneumothorax and fluid and a leak of the esophagus just above the diaphragm was seen on barium swallow. A chest tube, rib resection, gastrostomy, and jejunostomy feedings were instituted, but the patient died two months after the initial episode. Unexpected small bowel obstruction was found at postmortem examination. Patient 9, a seventy-one year old man (JD), entered with a long, vague history of mild dysphagia and belching. Severe pain had occurred recently in the left side of the chest. Pneumothorax was not seen until a film was taken on the second day. A chest tube was inserted and the patient was better. On the seventh day, fluid in drainage seemed excessive and the amylase in the fluid was found to be near 2,000 Bodansky units. A barium swallow showed an esophageal leak just above the diaphragm into the pleural space. Decortication, wide drainage, gastrostomy, jejunostomy, and parent& hyperalimentation were carried out with recovery and discharge 8 weeks after admission. Patient 10, a seventy-eight year old woman (DG), entered another hospital with pain in the left side of the chest. She had a known small hiatus hernia. Vomiting had occurred but was not forceful and not related to pain. Pain increased and fluid and pneumothorax were seen after five days. A barium swallow on the ninth day showed esophageal leak. The patient was transferred to Salem Hospital, and ten days after the initial episode, she had tube thoractomy with rib resection, gastrostomy, jejunostomy, and parenteral hyperalimentation. Her condition improved and the leak healed after two months. Patient 11, a fifty-four year old man (RP), experienced vomiting and severe ileus one week after inguinal hernia was
The American Journal
of Surgery
Boerhaave Syndrome
repair. He reentered the hospital with a high blood urea nitrogen level and dehydration which responded to fluid replacement. Pain was minimal. Seventeen days after admission, an air level was noted behind the heart and was thought to be an abscess in the lung. In the next two days pericardial tamponade developed with markedly elevated central venous pressure. Review of barium swallow revealed esophageal perforation. Pericardial exploration through the left anterior part of the chest revealed purulent pericardial tamponade which responded to wide removal of the pericardium and drainage into the left side of the chest. Rib removal was performed posteriorly through a separate incision to drain the esophageal perforation. A Levine tube was positioned above the perforation. In two days gastrostomy, jejunostomy, and pharyngostomy were carried out. Hyperalimentation was started through a central venous line. Further rib resection was needed, but the patient had slow healing over a twelve week period and has had no further problem. Patient 12, a sixty year old man (JM), had repair of a hiatus hernia four years earlier. He had a normal barium swallow postoperatively and had been well for three and a half years. Increasing amounts of substernal and pleural pain then developed with no vomiting. He had a known history of alcohol abuse. Barium swallow revealed a small perforation of the esophagus. He had a Thal patch with Nissen repair of the hiatus hernia. No true ulcer of the esophagus was seen. He did well postoperatively. Patient 13, a sixty-six year old man (RM), had a known hiatus hernia with esophagitis and soft stricture in the esophagus at the aortic arch. He had increasing amounts of substernal pain, which he thought was due to an increase in his usual large intake of alcohol and his severe chronic lung disease. There was one episode of vomiting after the pain had begun. Approximately eight days after the initial pain, barium swallow revealed esophageal perforation just above the diaphragm. He responded to tube drainage, rib resection, gastrostomy, jejunostomy, parenteral hyperalimentation, and drainage with a Levine tube. Discharge was in four weeks after initial treatment. Comments
Esophageal perforations are usually classified by their etiology. Perforations can be caused by trauma, instrumentation, foreign bodies, or surgical misadventures [6-8,101. Perforations that do not easily fall into these categories are usually called “spontaneous.” The classic case of spontaneous perforation was described in a lengthy monograph by Boerhaave in 1724. He outlined in vivid detail the postmortem findings of an aristocratic Dutch admiral who had rupture of the esophagus during an episode of retching after a debauchery of food and drink. Although in a sense the Baron’s misfortune was hardly “spontaneous,” the literature tends to refer to Boerhaave’s case as the first reported spontaneous
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perforation. Most case reports tend to emphasize the progression from overindulgence to forceful vomiting followed by severe pleural pain, shock, and death. Certainly some cases do follow the classic pattern, and in our series six of the fourteen seemed to fit Boerhaave’s description. The remaining eight, however, were not classic and this lack of obvious correlation between pain and vomiting probably caused delay in treatment in seven patients. It was also striking that almost all patients (thirteen of fourteen) had a prolonged or recent history of some form of indigestion and gastric distress; also a large number of patients had chronic diseases of the gastrointestinal tract. This strong correlation suggests that esophageal perforation is probably never truly spontaneous except in the apparently unusual circumstances of no proved gastrointestinal illness. Even if Baron Von Wassenaer had no previous stomach trouble, it seems unlikely that Boerhaave himself would call such an episode truly spontaneous since it can easily be traced to “the immoralities of excessive personal indulgence.” The most important conclusion is that esophageal perforation can occur in an obscure fashion, and it should be included in the differential diagnosis of patients with catastrophic illnesses with upper abdominal and pleuritic pain. It should also be considered in patients having less than catastrophic illnesses but having pleural and mediastinal air and fluid without obvious cause. It can occur without the dramatic explosion frequently described. Early recognition in any case will lead to earlier treatment and less hospital time. Barrett’s [1] case was the first case of successful repair. It was successful despite some obvious postoperative drainage. Although early suture or patches are important in early cases such as those seen in the first few hours [2,11], late cases often require some form of esophageal exclusion and supplemental feeding [6-8,121. In our series, exclusion was accomplished by a Levine tube or pharyngostomy to control salivary secretions and gastrostomy to control gastric secretions and reflux. Tube drainage, rib resection, or both are needed for control of the esophageal leak and empyema. In one of our cases decortication was helpful, and this was also noted by Grill0 and Wilkins [II]. Supplemental feeding is effective by jejunostomy and central venous hyperalimentation. Other methods such as cervical esophagostomy for salivary control [8,12], distal taps or suturing for control of reflux from the stomach [8], T tubes for esophageal drainage [IO], various flaps [II], and patches [13] have been used. Late direct repair can occasionally be successful as noted in two cases of Grill0 and Wilkins
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Patton et al
CONTROL
OF SALIVA
LEVINETUBE PHARYNGOSTOMY CERVICAL ESOPHAGOSTOMY ATROPINE
DRAINAGE
OR CONTROL
OF PERFORATION PRlMARY
SUTURE.
FIRST 24 HOURS
TUBETHORACOTOMY DECORTICATION PLEURAL FLAP GASTRIC FLAP LUNG INTERCOSTALFLAP T-TUBE IN ESOPHAGUS RESECTION
CONTROL
OF GASTRIC
SECRETIONS GASTROSTOMY ESOPHAGEAL TAPE ESOPHAGEAL SUTURE
NUTRITIONAL
CONTROL
JEJEUNOSTOMY ,NTRA”ENOUSHYPERAlLlMENTATlON
Figure 1. esophagus.
Opfions of treafment for perforation
of the
important, have tended to obscure the search for etiologic mechanisms. Certainly, in our series, the high incidence of previous gastrointestinal disease seems significant. (Table I.) There appeared to be a large number of patients with either symptoms of esophagitis or gastritis and four with hiatus hernia. It is only conjecture that the esophagus may have been weakened by chronic inflammation and became more susceptible to rupture. Rupture in the acute cases by the pressure exerted by retching or vomiting against a closed glottis seems to be an attractive hypothesis. It is much more difficult to explain the cases with a more indolent course with late recognition. Perhaps chronic inflammation without fibrosis has a role. There appears to be a difference between the patients who have the classic syndrome and early operation and those with a slower course and late operation. This contrast suggests two different disease entities, perhaps because of the type of pleural insult and soilage. In the sudden tear with a full stomach, as described by Boerhaave, the amount of spillage is massive and would seem to be very irritating; the more subtle perforation might be less of a chemical insult to the pleura and mediastinum and might give the person more time to adjust physiologically. The classic case, in which the disease is more serious, would naturally attract more medical attention and earlier treatment. Summary
[11] utilizing a pleural flap. In general, however, friability and massive inflammation make such repairs difficult and often unsuccessful. Certainly, in our series, patients who were treated eight days or longer could not be expected to have a successful primary repair. An exception to this was the patient with small localized perforation repaired by a Thal patch. Triggiani and Belsey [6] have suggested esophagectomy in such cases. In our series such measures were not necessary, but convalescence was prolonged and careful nutritional, fluid, and antibiotic management was necessary. It is difficult to compare results with only fourteen cases, but this series has a survival rate among operative cases (eleven of thirteen) that compares favorably with most other reports [6,7,9,10]. There have been no deaths in recent years. The only approach used in these cases was early repair for early cases and esophageal exclusion via adequate drainage of leak, saliva, and gastric secretions. Adequate nutrition via central venous hyperalimentation and jejunostomy was emphasized also. (Figure 1.) Preoccupation with methods and results, although
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Fourteen cases of “spontaneous” esophageal perforation from two hospitals over a twenty-five year period are reviewed. The classic syndrome, as described by Boerhaave, included overindulgence, forceful vomiting, and severe pleuritic pain followed by collapse and death. In our series, six patients appeared to follow a classic pattern, and in five of these, treatment was primary suture and healing occurred early. Eight cases did not follow the usual syndrome. In one of these cases, the patient died before treatment could be given, one patient presented with localized chronic perforation and responded to a gastric Thal patch, six required prolonged treatment including tube thoracotomy, rib resection, decortication, pharyngostomy, jejunostomy, gastrostomy, parenteral hyperalimentation, and pericardiectomy. Diagnosis was often confused by total lack of correlation between vomiting and pain. Almost all patients had some other abdominal problem or symptoms long before esophageal perforation. Diagnosis was confused with that of dissecting aneurysm, perforated ulcer, myocardial infarction, renal stone, and The American
Journal
of Surgery
Boerhaave
pleural effusion of unknown cause. One case presented nineteen days after perforation with constrictive purulent pericarditis. Of fourteen patients, one died almost immediately on arrival at the hospital, thirteen patients underwent operation, and eleven survived. Even in cases in which treatment is delayed by confusing presentations, the patient can survive, but vigorous treatment is needed and convalescence is prolonged. Although recognition of the classic Boerhaave syndrome is important, cases will be missed if reliance is placed solely on the usual criteria. References 1. Barrett NR: Report of a case of spontaneous perforation of the esophagus successfully treated by operation. Br J Surg 35: 216, 1947. 2. Alt RE, Bixby FE, Rowell RJ: Spontaneous rupture of the normal esophagus. N Engl J Med 249: 1060, 1953. 3. Boerhaave H: Atrocis, net descripti pius, morbi historia: secundum medicae artes leges conscripta, Lugd. Bat., Boutesteniana, 1724. Translated in Bull Med Libr Ass 43: 217, 1955. 4. d’Abreu AL, Taylor AB, Clarke DB: lntrathoracic Crises, p 66-69. London, Butterworths, 1968. 5. Sabiston DC, Spencer F: Gibbons Surgery of the Chest (3rd ed). Chapter by Ellis RH, p 715-718. Philadelphia, Saunders, 1976. 6. Triggiani E, Belsey R: Esophageal trauma; incidence, diagnosis and management. Thorax32: 241, 1977. 7. Lyons WS, Seremetis MG, de Guzman VC, Peabody JW: Ruptures and perforations of the esophagus: the case for conservative supportive management. Ann Thorac Surg 4: 346, 1978. 8. Urschel HC, Razzuk MA, Wood RE, et al: Improved management of esophageal perforation: exclusion and diversion in continuity. Ann Surg 179: 587, 1974. 9. Hadin WJ, Hardy JD, Conn JH: Esophageal perforations. Surg Gynecol Obstet 136: 325, 1967. 10. Abbott OA, Mansour KA, Logan WD, et al: Atraumatic so-called “spontaneous” rupture of the esophagus. J. Thorac Cafdiovasc Surg 59: 67, 1970. 11. Grill0 HC, Wilkins EW: Esophageal repair following late diagnosis of intrathoracic perforation. Ann Thorac Surg 4: 387, 1975. 12. Johnson J, Schwegman CW, Kirby CK: Esophageal exclusion for persistent fistula following spontaneous rupture of the esophagus. J Thorac Cardiovasc Surg 32: 827, 1956. 13. Thal AP, Hatafukw T: Improved operation for esophageal rupture. JAMA 188: 826, 1964.
Discussion John Head (Boston, MA): This may not be the burp heard around the world, but it certainly is the burp that made Boerhaave famous. The first classic case I heard about was a bit like the admiral’s. A man coming to Boston on the old New Haven Railroad spent the evening in the dining and parlor cars before going to bed. During the night as he heaved his considerable bulk in order to turn over, he felt sharp substernal pain, and by the time he reached South Station in Boston he was in shock. The fact that Doctor Patton and his colleagues have been able to collect fourteen cases of this rare entity might be construed as a comment on North Shore habits. At the
VebJme 137, April 1979
Syndrome
Massachusetts General Hospital we also have seen a wide spectrum of clinical behavior with a few delayed and chronic perforations, presumably starting with localized mediastinitis, abscess formation, and secondary rupture into the pericardium, pleural space, or bronchial tree. A valuable observation the authors made is that lower esophageal perforations do at times cause upper abdominal or mid-back pain rather than substernal pain. The other important point is the high incidence of preexisting upper gastrointestinal disease. I would add only one observation from our own experience in the surgical repair of these lesions. Even during the first 24 hours the quality of the esophageal wall may be very poor. These tears will not hold sutures well. We have found that wrapping with a large pleural flap is helpful as is visceral serosal covering a la Thal. I have two questions for Dr. Patton. Does he believe that the similar Mallory-Weiss syndrome is part of the spectrum of this disease, and if so, why is there no bleeding in cases of the Boerhaave syndrome? Second, are delayed development and poor correlation with vomiting related to a smaller perforation than that seen in the classic cases? John R. Brooks
(Boston, MA): It seems that the concept of a fundic wraparound is made to order as protection for the precarious esophageal suture line. I wonder why that has not been emphasized more. Anthony S. Patton (closing): I appreciate the comments of Dr. Head and the pertinent question raised by Dr. Brooks. Dr. Head was a close associate of Dr. Richard Sweet, one of the world’s most talented thoracic surgeons. There are two main questions or comments. One concerns the method of closure. In a case of early recognition and operation, any method such as a pleural or gastric patch is most acceptable if such material is readily available. Pleura can be used to buttress a suture line at almost any time after perforation. However, in most cases the amount of chemical and bacterial contamination after a few hours is usually so great that any extensive dissection in the chest outside the immediate area seems inappropriate. One often encounters a situation not unlike that described by Boorhaave in the postmortem examination of Baron Von Wassenaer. There are usually bits of decomposing food, saliva, and gastric juices washing around in the pleural cavity. The second question concerns the relation of a Mallory-Weiss tear to this phenomenon, spontaneous esophageal perforation. We found a number of such cases in the record rooms mixed with those of spontaneous esophageal perforation. The often bloody Mallory-Weiss tears are usually lower in position and occur both in the stomach and at the lowest edge of the esophagus. They seldom penetrate the gastric serosa and are associated with severe vomiting. A spontaneous esophageal perforation occurs higher and may or may not be associated with forceful vomiting but often with some chronic gastrointestinal complaint. The real heroes in the care of these patients are the nurses who must tally the various losses and look after the tubes with great diligence.
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