Selective Nonoperative Management of Contained Intrathoracic Esophageal Disruptions
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1 Selective Nonoperative Management of Contained Intrathoracic Esophageal Disruptions John L. Cameron, M.D., Richard F. Kieffer, M.D., Thomas R. Hendrix, M.D., Denis G. Mehigan, M.., and R. Robinson aker, M.D. ASTRACT Eight patients with intrathoracic esophageal disruptions were managed nonoperatively and without pleural drainage. Criteria for nonoperative treatment included the following: disruption contained in the mediastinum or between the mediastinum and visceral lung pleura; drainage of the cavity back into the esophagus; minimal symptoms; and minimal signs of clinical sepsis. Cause of the esophageal perforation was pneumostatic dilatation (1 patient), vomiting (2), and a leak following esophageal operation (5). Antibiotics were administered intravenously to all patients; hyperalimentation was accomplished intravenously in 5, and nasogastric suction was used in only 1. The cavities contracted and the esophageal leaks sealed in all instances. Time before oral intake was resumed ranged from 7 to 38 days (average, 18 days). Days until discharge ranged from 15 to 52 days (average, 28 days). An intrathoracic esophageal disruption can occur in a variety of circumstances. Forceful vomiting can produce the lesion, as in oerhaave's syndrome, as can endoscopy, esophageal dilatation, a swallowed foreign body, thoracic trauma, or an anastomotic leak following esophageal operation. Intrathoracic esophageal disruptions often are seen as catastrophes and can require prompt surgical intervention if survival is to be achieved. Recently, however, some authors 12, 3, 51 suggested that not every patient with an esophageal leak requires operation and that some are actually better off not undergoing thoracotomy. In this paper, 8 patients with intrathoracic esophageal From the Departments of Surgery and Medicine, The Johns Hopkins Medical Institutions, altimore, MD. Presented at the Twenty-fifth Annual Meeting of the Southern Thoracic Surgical Association, Nov 2-4, 1978, Marco Island, FL. Address reprint requests to Dr. Cameron, Department of Surgery, The Johns Hopkins Hospital, altimore, MD disruptions managed nonoperatively and without pleural drainage are reported. Guidelines for selecting patients with esophageal disruptions for nonoperative management are presented. Material Eight patients with intrathoracic esophageal disruptions were managed nonoperatively and without pleural drainage between 1969 and 1978 (Table 1). Seven of the 8 patients were treated during the last 5 years of this study. Five of the patients were men and 3 were women. They ranged from 35 to 64 years old (average, 54 years). In 1 patient with achalasia the esophageal disruption occurred after pneumostatic dilatation. In 2 patients the disruption followed forceful vomiting. The remaining 5 patients had undergone esophageal operation and subsequently experienced a leak from an esophageal suture line. The 5 surgical procedures included a Thal fundic patch and Nissen fundoplication for a benign stricture; a colon interposition for a benign stricture; an esophagogastrectomy for esophageal cancer; resection of an esophageal diverticulum with esophagomyotomy; and closure of an endoscopic esophageal perforation. The esophageal perforation was identified 8 hours after pneumostatic dilatation in the patient with achalasia. In the remaining 7 patients the disruption was detected 2 to 9 days after injury (mean, 6 days). Despite the esophageal leak and mediastinal collection, 4 of the 8 patients were asymptomatic. Three patients complained of substernal pain and burning, and the other patient had back and chest pain. Three patients remained afebrile during their clinical course. Three had intermittent temperatures of 38.0 C, and 2 patients had temperatures as high as 40.0"C. Five of the 8 patients had a leukocytosis ranging from 11,000 to 17,000 per by John L. Cameron
2 405 Cameron et al: Intrathoracic Esophageal Disruptions Table 1. Data from Patients with Contained Esophageal Disruptions Patient No., Age (yr), Sex Race Cause Temperature hite lood Count Location in Esophagus ( C) (per mm3) (Third) Size (4 Pleural Effusion 1. 35, F 2. 57, M 3. 61, F 4. 53, F 5. 53, M 6. 46, M 7. 64, M 8. 64, M Vomiting Dilatation Vomiting ,000 13,000 11,300 13,000 13,400 Middle Upper Middle 2 x 2 2 x 6 2 x 5 4 x 4 4 x 9 2 x 5 3 x 4 3 x 2 No Right A C D Fig 1. (A) Gastrografin (meglucamine diatrizoate) swallow in a 64-year-old man following an episode of violent vomiting. An esophageal perforation with a contained mediastinal cavity measuring 3 by 4 cm is seen. A Gastrografin air-fluid level is visible in the cavity. () Five days after the first Gastrografin swallow, the cavity remains approximately the same size. (C) Thirteen days later, the cavity has contracted to 1 by 2 cm in size. (D) Twenty-seven days after the first swallow the cavity is almost gone, and the leak is almost sealed. Oral intake was resumed at this time. cubic millimeter. The remaining 3 patients had normal white blood counts. A pleural effusion was demonstrated radiographically in 7 of the 8 patients. In 3 patients it was bilateral and in 4, unilateral, usually on the left. In all instances the effusions were small. Gastrografin (meglucamine diatrizoate) swallows demonstrated the disruption to be in the lower third of the esophagus in 5 patients, in the middle third in 2 patients, and in the upper third in 1 patient. The esophageal disruption in each instance was contained in the mediastinum or between the mediastinum and the visceral lung pleura. In no instance did it communicate with the free pleural space. Size of the cavity ranged from 2 by 2 cm to 4 by 9 cm. In each patient the cavity appeared to be well drained back into the esophagus (Figs 1, 2).
3 406 The Annals of Thoracic Surgery Vol 27 No 5 May 1979 A C D Fig 2. (A) Gastrografin (meglucamine diatrizoate) swallow in a 53-year-old man 7 days following esophageal operation. An esophageal disruption with a 4 by 9 cm cavity contained between the mediastinum and lung pleura is seen. () Five days later, the cavity has already begun to contract. (C) Thirteen days later, the cavity size is approximately 2 by 2 cm. (D) Twentyseven days after the first swallow, only a small remnant of the cavity remains. Oral intake was resumed. This patient is the only one who had nasogastric suction during the period of nonoperative management. Method Following detection of the esophageal disruption, the decision was made in each instance to manage the patient nonoperatively (Table 2), with the provision that if the clinical status deteriorated, immediate thoracotomy and mediastinal drainage would be carried out. All patients were maintained on intravenous fluids. Five of the 8 patients were hyperalimented intravenously with hypertonic glucose and amino acid solutions. Nasogastric suction was employed in only 1 patient. All 8 patients received intravenous administration of antibiotics. The combination of gentamicin, clindamycin, and penicillin was used in 5 patients. One patient received cephalosporin and gentamicin; 1 patient, only cephalosporin; and the remaining patient, penicillin and Chloromycetin (chloramphenicol). Table 2. Treatment and Clinical Course Intravenous Days until Days to Patient Hyperali- Nasogastric Delay in Oral Intake Dis- No. Antibiotics mentation Suction Diagnosis Resumed charge 1 Yes No No 9 days Yes No No 3 days Yes Yes No 9 days Yes No No 8 hours Yes Yes Yes 7 days Yes Yes No 7 days Yes Yes No 2 days Yes Yes No 7 days 10 21
4 407 Cameron et al: Intrathoracic Esophageal Disruptions All patients slowly but steadily improved clinically. Fever persisted from 3 to 15 days (average, 7 days) in the 5 patients who were febrile. Leukocytosis persisted from 3 to 8 days (average, 5 days) in the 5 patients with elevated white blood counts. The size of the mediastinal cavity was followed closely with Gastrografin swallows performed initially every 3 to 5 days (see Figs 1,2). After it became clear that the patient was doing well, contrast studies were performed once a week. Oral intake was initiated when a Gastrografin study demonstrated that the mediastinal cavity had contracted and the esophageal disruption had sealed, or that the cavity had decreased sufficiently to ensure eventual closure. This took from 7 to 38 days (average, 18 days). Length of hospitalization after the esophageal disruption to the time of discharge ranged from 20 to 52 days (average, 28 days). In all 8 patients the mediastinal cavity eventually disappeared completely, and the esophageal leak sealed completely. No patient required any surgical procedure, minor or major. Comment Most intrathoracic esophageal disruptions are treated surgically. hen first seen, the patient often has severe chest and abdominal pain and shows signs of cardiovascular collapse. hen widespread mediastinal or pleural contamination occurs, mediastinal or pleural space infection or a combination of these results and sepsis ensues. The accepted management of such patients currently includes thoracotomy, opening the mediastinum widely, and pleural space drainage. If the perforation is recent and the esophageal margins will hold sutures, esophageal closure is carried out. In 1978, Symbas and colleagues [8] advocated reinforcing the esophageal repair with a fundoplication. If the perforation is old and the esophageal margins will not hold sutures, external drainage to establish an esophagocutaneous fistula is indicated. Results of this regimen vary. hen the disruption follows forceful vomiting, mortality ranges from 30 to 40% [l, 4, 5, 71. If the patient is operated on within the first 24 hours following perforation, mortality is in the range of 10%. hen the patient is not diagnosed early and is operated on 24 hours or more after the injury, mortality increases to 50% or greater. Patients with endoscopic perforations tend to do better because the injury is generally diagnosed earlier [5, 91. Patients with intrathoracic esophageal disruptions following esophageal operation do poorly, and mortality is in the range of 40% [91. Thus, even though surgical intervention is the accepted treatment, it is by no means universally successful, and ample room exists for other approaches. Occasionally a patient with an intrathoracic esophageal disruption is seen in whom an attempt at nonoperative management seems appropriate. Criteria for considering such an approach are as follows: (1) The esophageal disruption should be well contained within the mediastinum or between the mediastinum and visceral lung pleura. (2) The cavity should be well drained back into the esophagus. (3) Minimal symptoms should be present. (4) There should be minimal evidence of clinical sepsis. If these criteria are met, a conservative approach is reasonable, as indicated by our experience with 8 patients. Obviously, there is a great deal of room for clinical judgment concerning the presence or absence of sepsis: in this series, leukocytoses as high as 17,000 per cubic millimeter and fevers as high as 40 C were seen. Antibiotic therapy and intravenous hyperalimentation are the main thrusts of nonoperative management. Gentamicin, clindamycin, and penicillin can eliminate all of the aerobes and anaerobes that are encountered in the oral cavity and gastrointestinal tract, and this combination of antibiotic therapy is the regimen of choice. Intravenous hyperalimentation is important in placing the patient in positive nitrogen balance so that infection can be more readily controlled and wound healing encouraged. One patient in this series remained on intravenous fluids for 38 days before resuming oral intake; success without hyperalimentation would have been unlikely. Nasogastric suction was used in only 1 patient. hen gastric emptying is normal and an ileus is not present, a nasogastric tube is not necessary and can actually induce gastroesophageal reflux. In 5 of the 8 patients in this series, the selection of nonoperative management was rela-
5 408 The Annals of Thoracic Surgery Vol 27 No 5 May 1979 tively easy. The esophageal disruptions were not detected until 6 to 9 days after they had occurred or after esophageal operation, and the patients had already demonstrated that they were tolerating the injury well. In the remaining 3 patients, however, the disruptions were diagnosed 8 hours, 2 days, and 3 days after they had occurred and the decision as to the method of management was more difficult. However, because all 3 patients met the four criteria already listed, nonoperative management was selected. As more experience is gained with nonoperative treatment, we believe more patients with esophageal disruptions detected early will be started on the regimen if the four criteria are fulfilled. The proportion of patients with esophageal perforations suitable for nonoperative management is difficult to estimate. During the past ten years, 9 patients with oerhaave s syndrome were seen, and 2 were treated nonoperatively. Esophageal perforations resulted from esophageal dilatation in approximately 5 patients, l of whom was treated nonoperatively. Approximately 10 patients leaked following esophageal operation, and 5 were treated nonoperatively. (ecause of the small numbers of patients involved, these proportions may not be entirely accurate.) The frequency with which this method of management has been used has increased at this institution in recent years. Eight patients were managed nonoperatively during a nine-year period, 7 of them during the past five years and 4 during the past two years. In no other patients was this treatment regimen started and then later abandoned for thoracotomy because of failure. In recent years others have advocated managing esophageal disruptions without thoracotomy. A recent retrospective review compared the results of management of 18 patients with esophageal perforations secondary to a variety of insults treated by thoracotomy with 11 patients managed without major thoracotomy [5]. Mortality was 38% in the group managed surgically, and only 9% in the conservatively managed patients. Most of these patients did not have contained esophageal disruptions, and pleural drainage was used. In another series of 21 patients with intrathoracic esophageal perforations secondary to endoscopy, 18 were managed with antibiotics and without operation [61. Pleural drainage was employed if a hydrothorax was present. Mortality in this series was only 6%. Isolated case reports of survival following nonoperative management of intrathoracic esophageal disruptions, and advocating this approach, have also appeared recently [2, 31. Apparently, because of the less than satisfactory results of routine thoracotomy for esophageal disruptions, surgeons have cautiously explored other treatment regimens. hen the disruption is not contained and when there is free pleural or mediastinal contamination or both, it is still not clear to us which approach is preferable. Possibly the length of time that has lapsed before diagnosing the perforation will be the deciding factor. However, when the disruption is clearly contained and is well drained back into the esophagus, and when symptoms and signs of infection are minimal, nonoperative management with intravenous antibiotics and hyperalimentation is the treatment of choice. References 1. Abbott OA, Mansour KA, Logan D, et al: Atraumatic, so-called spontaneous rupture of the esophagus. J Thorac Cardiovasc Surg 59:67, rown RH, Cohne PS: Nonsurgical management of spontaneous esophageal perforation. JAMA 240:140, Larrieu AJ, Kieffer R: oerhaave syndrome: report of a case treated non-operatively. Ann Surg 181:452, Lawson RAM, utchart EG, Soriano A, et al: Spontaneous ruptures of the esophagus. J R Coll Surg Edinb 19:363, Lyons S, Seremetis MG, deguzman VC, et al: Ruptures and perforations of the esophagus: the case for conservative supportive management. Ann Thorac Surg 25:346, Mengoli LR, Klassen KP: Conservative management of esophageal perforation. Arch Surg 91238, Sawyers JL, Lance CE, Foster JH, et al: Esophageal perforation: an increasing challenge. Ann Thorac Surg 19:233, Symbas PN, Hatcher CR, Harlaftis N: Spontaneous rupture of the esophagus. Ann Surg 187:634, Triggiani E, elsey R: Oesophageal trauma: incidence, diagnosis, and management. Thorax 32: 241, 1977
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