COLLECTIVE REVIEW. Esophageal Perforations. Floyd D. Loop, M.D., and Laurence K. Groves, M.D.

Transcription

1 COLLECTIVE REVIEW Esophageal Perforations Floyd D. Loop, M.D., and Laurence K. Groves, M.D. P erforation of the esophagus constitutes a true emergency that demands immediate diagnosis and superior surgical judgment. Although esophageal disruptions have been described and reported for many hundreds of years, the dismal death rate remained unchanged until the 1940s. The advent of antibiotics marked a great advance in treatment of esophageal perforations; however, appropriate surgical intervention is the approach that has significantly improved the outcome of this previously fatal condition. Despite spectacular achievements in thoracic surgery during the past 25 years, the death rate associated with esophageal perforation is still between 15 and 30% [SO, 72, 791. This review includes discussion of the mechanism of injury, concepts in management, and reasons for the continuing high mortality. CAUSES OF ESOPHAGEAL PERFORATION The four most important causes of esophageal perforation are (1) iatrogenic injury from diagnostic procedures and operations; (2) spontaneous or postemetic rupture; (3) foreign bodies; and (4) external trauma. PA THOPHYSIOLOGY Instrumentation or penetrating wounds cause virtually all upper esophageal perforations. The laceration of the esophagus carries through the thin buccopharyngeal fascia, involving the retroesophageal or retrovisceral space. This plane extends from the base of the skull to the tracheal bifurcation; across this space the prevertebral fascia loosely attaches itself to the esophagus by sagittal septa. These septa prevent From the Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio VOL. 10, NO. 6, DECEMBER,

2 LOOP AND GROVES infection from spreading laterally in the neck but do not inhibit descent of the suppurative process into the mediastinum [ll. Rarely, perforations of the anterior esophageal wall, lateral pharyngeal space, or piriform fossa affect the mediastinum via the pretracheal space [63]. When integrity of the thoracic esophagus is lost, mediastinal contamination occurs directly and thus more rapidly than in upper esophageal perforations. In either case, saliva and gastric contents create a fulminating chemical and bacterial effect in the mediastinal tissue, the principal feature of which is hemorrhagic necrosis. The thin mediastinal pleura quickly ruptures from continued soilage, allowing negative intrathoracic pressure to draw gastric fluid through the perforation [6]. The subsequent pleural space contamination produces more fluid loss that soon leads to hypovolemia and shock. Fluid aspirated from the thorax is highly contaminated by food and assumes a brownish color as blood is acted on by the gastric juice [4]. Pleural fluid may accumulate as rapidly as 1,000 ml. per hour [61], compressing the lung, shifting the mediastinum, and further embarrassing the cardiorespiratory mechanism [24]. The increased pressure in one or both thoracic cavities eventually retards venous return. Ware and Strieder [74] describe the natural history of the condition as follows:... devastating necrotizing chemical insult with rapidly superimposed aerobic and anaerobic infection quickly jeopardizes the patient s life and he succumbs to gangrenous mediastinitis, pleuritis, pyopneumothorax and empyema usually in a matter of several hours to one to two days. IATROGENIC PERFORATION Accidental perforation from instrumentation most frequently takes place through the posterior wall of the cervical esophagus, or to the left side when the endoscopist is right-handed Palmer and Wirts [55] surveyed records of 40,000 esophagoscopies and found that the risk of perforation was 0.25%, with a mortality of 0.59%. Other authors [21, 43, 781 place the average incidence related to all forms of endoscopy between 0.4% and 1.0%. The incidence is declining, although the number of cases is increasing because more endoscopies are performed each year. The normal anatomy of the esophagus shows three levels of narrowing. The esophageal introitus is the narrowest region, and the cricopharyngeal muscle contributes to this decrease in lumen diameter. Instrumental injury most commonly occurs at this point as the esophageal wall is compressed against the sixth or seventh cervical vertebra. Chevalier Jackson called this normally constricted area Bab-el Man- 572 THE ANNALS OF THORACIC SURGERY

3 COLLECTIVE REVIEW: Esophageal Perforations deb or the gate of tears [Zl]. Hyperextension of the head, kyphosis, or, in the elderly patient, hypertrophic vertebral spurs exaggerate the pressure of the instrument against the cervical vertebra [63]. Once the cricopharyngeal level has been passed and no distal obstruction exists, it is unlikely that perforation will occur. The area of the aortic arch and left main bronchus constitutes the second level of narrowing. Perforations here are unusual but may occur from foreign bodies. The third level, at the gastroesophageal junction, is infrequently lacerated in the absence of neoplasm or a stricture. Other factors adding risk to esophagoscopy include poorly administered anesthesia, an inexperienced endoscopist, presence of pharyngeal diverticulum, an inflated endotracheal cuff, and biopsy beyond the area of direct vision. Perhaps mucosal atrophy plays a part in elderly patients [35, 641, since the Mayo Clinic reports a higher frequency of cervical perforation in women more than 50 years of age [78]. Dilation for benign or malignant stricture is the second most common cause of iatrogenic perforation. The category includes corrosive agents, the danger after their ingestion lying in diagnostic instrumentation or dilatation procedures. Although a rapid increase in dilator size or the use of an unsatisfactory guide often underlies this tragedy, several factors are important in preventing instrumental perforation after an esophageal burn. When the progress of reepithelialization is being viewed, the esophagoscope should never be advanced beyond the first ulcer. The ulcerative process does not heal in less than two weeks, and dilation should not be undertaken until one sees epithelialized mucosa. One month after steroid treatment the thin esophageal wall is more vulnerable to rupture than in the initial period after injury [14]. Special mention should be made of hydrostatic dilation of the terminal esophagus for achalasia. Such a procedure is truly effective only if bloodless myotomy is performed, and clearly there is a potential hazard to this technique. The passing of various tubes, palliative prostheses, and balloons have all been incriminated in esophageal injury. Most notorious are the gastric-cooling balloon and the Sengstaken-Blakemore tube. Esophageal disruption occurs when the device is kept inflated too long or when an uncontrollable patient extracts it while it is still in use. Plastic tubes for palliation of malignant obstruction are often hazardous to insert, and Wychulis, Fontana, and Payne [78] warn that the upper end of a Celestin tube forms sharp edges when grasped for removal. Paraesophageal operations such as vagotomy, hiatal hernia repair [44], and radical pneumonectomy [79] may be responsible for esophageal disruptions. Postlethwait and his colleagues [59] reported 24 esophageal perforations in 4,414 vagotomies, an incidence of 0.54%. The injuries VOL. 10, NO. 6, DECEMBER,

4 LOOP AND GROVES were responsible for 3 deaths. Takaro and his associates [67] analyzed reports of 24 esophagopleural fistulas after pneumonectomy; most of the patients had associated tuberculosis, which was on the right side in all but 3. More than half the fistulas occurred three months after the primary surgical procedure, and their causes therefore were more akin to granulomatous disease and infection than to a truly iatrogenic origin. The authors suggested preoperative use of esophagograms to detect unusual deflection or unsuspected diverticula. SPONTANEOUS RUPTURE This type of esophageal perforation is reported with increasing frequency and now rivals the incidence of instrumental injury. Spontaneous ruptures carry a more fatal prognosis than perforations secondary to instrumentation. Preexisting esophageal disease and misdiagnosis resulting in delayed treatment are the most important reasons for the mortality, which approaches 30% [79]. The adjective spontaneous should not imply the absence of precipitating factors or a previously normal esophagus; rather, the term means rupture not resulting from more obvious forms of direct trauma, foreign bodies, or instruments [2]. The term postemetic perforation has been suggested as more descriptive, although many reports include spontaneous perforation with no vomiting; e.g., after physical straining, lifting, blunt trauma, childbirth, or seizures [691. The famous Dutch physician Herman Boerhaave diagnosed a spontaneous esophageal rupture in 1724 [lo, 401. The victim, Baron von Wassenaer, Grand Admiral of the Fleet of Holland, felt slightly nauseated one night after having overeaten, and he took some light emetics. After vomiting, he experienced chest pain, and later Boerhaave found the baron sitting hunched over in bed in agonizing distress. The correct diagnosis was made, although no substantial treatment could be offered, and the patient died. Boerhaave s 70-page report+ describes subcutaneous emphysema and mentions that at autopsy the pleural fluid had the smell of roast duck, which the baron had eaten the day before. The tear was in the transverse direction, a rare alignment for postemetic ruptures. The rent almost always occurs in the lower third of the esophagus on the left posterolateral wall. A few ruptures have been reported on the right side of the midesophagus. The tear is usually linear and in a longitudinal axis, averaging 2.5 cm. in length [52]. The thoracic aorta and retropericardial fat support the esophagus on three sides, leaving the least supported lower left side to expand under the parietal pleura [2, 41. The liver and gastric fundus stabilize the short segment of abdominal esophagus. These anatomical facts correlate with Mosher s [49] reasons The interested reader may find an abstract of Boerhaave s original article in McKenzie s Diseases of the Nose and Throat t461 or the same abridged version reprinted in Barrett THE ANNALS OF THORACIC SURGERY

5 COLLECTIVE REVIEW: Esophageal Perforations for the constant site of rupture: (1) the musculature at the lower end of the esophagus is thin and terminates in a conical fashion; (2) segmental defects are found in the circular muscle at the distal end; and (3) the wall is further weakened by the entrance of vessels and nerves in this region. Experiments 113, 38, 42,461 using intact cadavers and gastroesophageal preparations have been designed to measure the force required to rupture the esophagus. In the intact cadaver, no rupture can occur unless the upper esophagus is tied off. The rent occurs in the same region found clinically, low on the left wall inferior to the pulmonary vein. The bursting pressure ranges from 3.5 to 6 pounds per square inch and creates a longitudinal defect. Mucosa bulges through the weakened area and offers a greater resistance than the muscular layer. The theories concerning inherent smooth-muscle weakness appear valid since no experimental ruptures were produced in the upper esophagus. Intact cadaver esophagi ruptured under less pressure than did the gastroesophageal preparations for two probable reasons: first, the esophagus in the cadaver remains well supported except for the lower left side; and second, a pressure gradient exists across the esophageal wall because of the lower intrathoracic pressure. Deterioration of the esophageal wall, which begins soon after death, accounts for some of the variation in pressure; within one hour the resistance may decline as much as 50% [19]. Also, experimentally the adult esophagus ruptures under less pressure than does that of the child. Up to four times more pressure is required to perforate the esophagus of children less than 12 years old [38]. Wangensteen s group [l 11 showed that sensitivity of the esophageal mucosa to gastric juice further weakens the wall and allows perforations to occur with less pressure. However, this does not prove that all spontaneous ruptures are due to esophagitis. In fact, 80% of the spontaneous or postemetic ruptures take place in normal esophagi; only 10% have a history compatible with esophagitis or ulcer To complicate matters, esophagitis is hard to recognize at postmortem examination since an inflammatory reaction occurs around the disruption. As expected, a rapid increase in pressure causes disruption sooner and at a much lower pressure than does gradual distention. Applying this experimental work to clinical conditions, the necessary obstructive factor could be spasm of the cricopharyngeal pinchcock, alcohol intoxication, or central nervous system disease producing muscular incoordination, and stenosis from tumor or esophagitis. The necessary coexistence of obstruction plus a sudden rise in intraluminal pressure explains why the condition is rarely seen despite the common occurrence of vomiting More than 80% of spontaneous esophageal perforations occur in VOL. 10, NO. 6, DECEMBER,

6 LOOP AND GROVES men, most commonly between the fifth and sixth decades of life [Z]. Typically, the adult history includes food or alcohol overindulgence and vomiting, although the review by Ware and colleagues [73] did not mention overindulgence in 85 patients with spontaneous perforation. They noted in the history the importance of persistent retching which leads one to suspect that spontaneous rupture can occur with an empty stomach. Several spontaneous perforations have been reported in newborn infants [29, 761. The absence of vomiting is notable in regard to perforations associated with distal esophageal obstruction. More forceful swallowing possibly leads to a sharp increase in intraluminal pressure, resulting in perforation of the lateral wall above the obstruction [18]. Esophagomalacia secondary to central nervous system disease contributes to a type of spontaneous rupture. Described by Rokitansky [60] in 1842, it originally was associated with intracranial tumors. Hypothalamic disease or interference with hypothalamic pathways is known to produce esophageal muscular incoordination, and intracranial abscesses, head injury, and aneurysms have all been implicated in the erosive process. Most reports describe a rupture in the lower third of the esophagus, the majority on the left side. This fact raises the probability of a mechanical tear rather than an erosion, although the esophageal wall frequently shows a definite alteration predisposing it to rupture. Gastric dilatation with or without bleeding might provide a reason for vomiting which, when coupled with muscular incoordination, leads to the rupture [41]. FOREIGN BODIES Diagnosis and extraction of foreign objects present unique problems. In children younger than 4 years of age pennies, buttons, and safety pins are the most frequent offenders in 90% of reported cases [30]. In that age group coins can become impacted just below the cricopharyngeal muscle, whereas in older children coins usually pass through that critical area. In the child younger than 4 years of age the foreign body may migrate laterally or ventrally through the wall, leading to respiratory distress or vessel erosion [47]. Plain roentgenograms of the neck should be taken in hyperextension, since in the normal position the clavicular shadow hides the esophageal inlet. This maneuver raises the larynx and inlet and makes them visible in the lateral projection. If the suspected object is not radiopaque, a thin barium solution may be administered orally and the fluoroscope used; also, small pieces of cotton soaked with thin barium solution may catch on the foreign body, whereas barium alone might pass through [ZO]. 576 THE ANNALS OF THORACIC SURGERY

7 COLLECTIVE REVIEW: Esophageal Perforations In adults, bones and food are most frequently responsible for esophageal injury. Upper dentures may inhibit the tactile sensation of the object before swallowing, thus disguising its size. However, any organic obstruction that reduces lumen size can stop the progress of poorly masticated food. Since the first symptoms of esophageal carcinoma may be obstruction from a foreign body, a barium study should be performed in adults to detect the reason for impaction [201. Esophagoscopy under general anesthesia is usually required for extraction, especially in the pediatric-age group. One dangerous manipulation known to produce lacerations is pushing the foreign body ahead of the esophagoscope. Bigler [S] and Symbas [66] reported success in passing a Foley urethral catheter beneath the foreign body, inflating the bag, and removing the object with gentle traction. This technique should not be used for sharp objects or when there has been more than a 24-hour delay. When the impacted material cannot be extracted, direct surgical intervention is indicated. This same approach applies to cases of free perforation or when the patient has mediastinal suppuration. Regardless of all caution employed, perforation is always possible; when it is suspected, the presence or absence of a leak should immediately be confirmed using radiopaque contrast fluid and roentgenography. EXTERNAL TRAUMA Most perforations from knife or gunshot wounds involve the cervical esophagus Subcutaneous emphysema in a patient with a neck wound indicates damage of the larynx, trachea, esophagus, or apical pleura [ZZ]. Since the morbidity and mortality rise with expectant treatment, cervical injuries penetrating the platysma muscle should be explored [23, 361. If associated injury seems minor and the patient s general condition appears stable, esophagoscopy, bronchoscopy, and oral contrast medium studies can be performed preoperatively to confirm or exclude occult injury. Esophageal injury must always be suspected. Lacerations often are small and easily missed. At operation, the accessible defect is repaired and the wound drained. The surgeon seldom encounters thoracic esophageal penetration as an isolated visceral injury. Involvement of the heart or great vessels frequently accompanies the esophageal wound [65]. Closure of the rent and wide drainage of the mediastinum are the basic surgical principles employed in treatment. Rupture of the esophagus from blunt abdominal or thoracic trauma mimics the spontaneous rupture. A sudden elevation in the intraesophageal pressure against a closed cricopharyngeal pinchcock is VOL. 10, NO. 6, DECEMBER,

8 LOOP AND GROVES probably a contributing factor. Injury to the esophagus should be suspected after blunt abdominal trauma when dyspnea and cyanosis are prominent despite minimal chest findings. Crushing chest injury need not be severe to produce esophageal disruption; in fact, ribs may not even be fractured [77]. DIAGNOSIS OF ESOPHAGEAL PERFORATION Although instrumental perforation usually takes place just below the cricopharyngeal muscle, the posterior location of the injury makes recognition difficult and the endoscopist may be unaware of his error C571. When the anatomy becomes confusing or the surgeon suddenly loses his way during the procedure, there is a good chance the esophagus has been lacerated. Suspected injury is best confirmed by immediate contrast swallow. One loses valuable time waiting for symptoms to develop. If the diagnosis is not suspected, dysphagia, pain on flexion of the neck, and cervical tenderness are the likely first clues. As the retroesophageal space becomes contaminated, high fever ensues within a few hours after the accident. Long delays in diagnosis lead to mediastinal infection, and symptoms and signs become similar to those seen in esophageal perforations located intrathoracically. Depending on the size and timing of the rent, subcutaneous air may be palpable in the neck or seen as a widened retrovisceral space on lateral roentgenograms. Evidence of extravasation of contrast material gives the definitive answer to the problem. Mackler s triad of vomiting, pain in the lower thorax, and subcutaneous emphysema is pathognomonic of spontaneous rupture of the esophagus [42]. However, at least one-third of spontaneous perforations are clinically atypical. Vomiting is sometimes conspicuously absent before the onset of pain. The typical history of overeating and alcoholic debauch are inconstant features. Pain is the striking and consistent symptom, epigastric or substernal early in the course and later extending laterally to the lower thorax and assuming a pleuritic character. Patients have complained of a searing or bursting sensation at the time of perforation. Vomiting, if present, subsides as the pain increases. The patient appears pale, sweating, occasionally cyanotic, and frequently dyspneic, and unless he is in profound shock, he is febrile. Hematemesis is seldom significant-a means of differentiating perforation from the Mallory-Weiss syndrome. The upper abdominal muscles may be rigid; however, the lower abdomen is relatively soft. Mediastinal air soon tracks upward, and subcutaneous emphysema was palpable in approximately 60% of the cases reviewed in the literature [56]. This may not be an early finding; Samson [61] pointed out that a nasal twang due to 578 THE ANNALS OF THORACIC SURGERY

9 COLLECTIVE REVIEW: Esopliageal Perforations air in the deeper tissues precedes neck crepitation by several hours. The symptoms and signs may be accentuated by deep breathing, swallowing, or changes in position [39]. The thoracic pain worsens despite all supportive treatment, and hypotension inevitably follows the presenting picture. The single most valuable diagnostic procedure is the upright chest roentgenogram [25]. The majority of patients have pleural effusion or hydropneumothorax, and 7% show evidence of fluid bilaterally [52]. Roentgenograms must be searched for evidence of air in the fascia1 planes of the mediastinum, particularly in the retrocardiac area. Later the mediastinum widens and air can be seen in the soft tissues of the neck. The presence of subdiaphragmatic air is extremely rare [69]. If the roentgenogram is underexposed or taken too early, mediastinal emphysema may be missed. Controversy exists over the type of contrast material to be employed in making the esophagograms. One group [50, 571 warns that barium acts as a foreign body in an infected area when it is extravasated into the pleural cavity. Others [2,26] believe that the contrast produced by barium is far superior to that of iodinated contrast media, and they point out that barium can be removed by irrigation during operative treatment of the defect. Lack of extravasation of the radiopaque medium does not necessarily exclude the presence of a perforation. Passage of the material may have been too rapid for the small size of the rent, or its location may have been viewed in a projection parallel to the body of the esophagus; thus the leak would be overlooked. When the esophagogram is normal and doubt concerning the diagnosis persists, Carter and Hinshaw [15] recommend esophagoscopy as a diagnostic procedure. The diagnosis of ruptured esophagus should be considered in any situation involving abdominal pain, particularly when vomiting is prominent in the patient s history [69]. Rigidity of the upper abdominal muscles often leads to a mistaken diagnosis of perforated intraabdominal viscus. Usually there is no history of ulcer in the patient with a spontaneous esophageal rupture, and the excruciating upper abdominal pain subsides after a few hours as the severity of the chest discomfort increases. Rarely is air noted under the diaphragm with esophageal perforation. Upper abdominal pain, vomiting, alcoholism, pleural effusion, and shock all may be associated with acute pancreatitis. The serum amylase content and roentgenograms of the chest demonstrating mediastinal or subcutaneous emphysema are the best aids in distinguishing pancreatitis from esophageal disruptions. Electrocardiograms and chest findings help exclude myocardial in- VOL. 10, NO. 6, DECEMBER,

10 LOOP AND GROVES farction. Pain from a dissecting aneurysm peaks during the initial dissection and subsides thereafter. Spontaneous pneumothorax does not produce the severe pain or shock that occurs with perforated esophagus, and pleural effusion develops as a late result. Mesenteric thrombosis may occur in elderly patients with a recent myocardial infarction or arrhythmia; however, the abdominal pain does not change in location and often is unrelenting despite narcotics. Other conditions to consider include pulmonary embolism, intraabdominal abscess, strangulated diaphragmatic hernia, and acute cholecystitis. The diagnosis in a clinical picture involving abdominal pain is made much easier if one thinks immediately of the possibility of a ruptured esophagus. When the patient relates the usual history, exhibits the diagnostic triad, and lacks free air under the diaphragm, most other differential conditions can be eliminated [Z]. TREATMENT Several factors have strengthened the foundation on which the success of surgical treatment now rests. Surgeons have acquired increasing experience with instrumentation and in the recognition of accidental perforations. Most physicians are now acquainted with spontaneous rupture, thereby mitigating errors in diagnosis and delay in treatment. Antibiotics improve the desperate picture of mediastinitis and reduce the late complications after surgical drainage. The site of injury necessarily divides surgical treatment into two groups: perforations affecting the upper esophagus and those occurring in the lower thoracic esophagus. The area of perforation greatly influences the mortality, mainly because a leak from the thoracic esophagus rapidly leads to suppurative mediastinitis with its sequelae. Any delay in operative intervention after the direct injury is tolerated poorly. The patient s age, the size of the rent, and the presence of underlying esophageal disease also affect the outcome of surgical treatment Surgical drainage was the first procedure to influence the outcome of upper esophageal perforations favorably. Jemerin s classic study [3 11 substantiated this change, which took place after Most of the patients in his series had cervical perforations caused by instrumentation. Before that date only 50% of his total number of patients underwent operative drainage, and 77% of them died. In the decade after 1936, 90% of patients underwent drainage, lowering the mortality to 17%. Even with the additi0.n of antibiotics, the problem of lower esophageal perforation was far from solved. To recall Samson s warning [611: These patients are sick unto death but fatal outcome cannot be escaped unless the rent is closed. The greatest offender was the unsuspected 580 THE ANNALS OF THORACIC SURGERY

11 COLLECTIVE REVIEW: Esophageal Perforations spontaneous rupture. Derbes and Mitchell [19] reported 71 such patients in whom no surgical treatment was undertaken-35% were dead within 24 hours, and all had died by the end of one week. Drainage procedures plus enterostomy for feeding were only temporizing measures in the lower perforations, and in the relatively few patients who survived, morbidity was high and convalescence prolonged. Many times, staged reconstruction was required to eliminate empyema cavities, fistulas, and strictures. Collis and his associates [ 161 accurately diagnosed a spontaneous rupture in 1944 and were the first to perform a thoracotomy for closure of the rent; unfortunately, the patient died. Barrett s excellent review of spontaneous perforation two years later [4] predicted the success of direct surgical repair, provided that the diagnosis could be made early. In 1947 Barrett [5] and Olsen and Clagett [53] reported cases in which repair through open thoracotomy was successful. Samson [611, Weisel [75], and Overstreet and Ochsner [54] were other early advocates of direct esophageal repair with drainage of the pleural cavity. Although delay from misdiagnosis is mainly responsible for the desperate preoperative condition of these patients, even after early diagnosis it is not always easy to convince the physician in charge that operation is necessary. This is especially true in regard to upper esophageal perforations, in which signs and symptoms are minimal. Immediate treatment regardless of the perforation site consists of administering antibiotics in therapeutic amounts, stopping all oral intake, restoring fluid balance, and, if possible, passing a Levin tube into the stomach. Perforations of the cervical esophagus with no distal obstruction require drainage of the retrovisceral space in most instances. Pearse s modification of cervical mediastinotomy [58] is as timely today as when it was published in Prolonged hospitalization after expectant treatment of upper esophageal perforation has been greatly modified by this simple technique. Pearse showed that death results from descending mediastinitis, not from the perforation per se or from localized abscess in the neck. Draining the pathway into the mediastinum eliminates the infection. An oblique incision is placed along the anterior border of the sternomastoid muscle. The carotid sheath is retracted posteriorly while the thyroid lobe is displaced anteriorly. The middle thyroid vein and inferior thyroid artery may require ligation. Soft drains are placed in the region of the abscess and in the mediastinal plane between the esophagus and the vertebral column. Suturing the laceration is not mandatory, since fistulas close promptly provided that no distal obstruction exists [12, 26, 321. Drains are left in place for four or five days, and the nasogastric tube is used for feeding purposes. VOL. 10, NO. 6, DECEMDER, 1970 $31

12 LOOP AND GROVES Lower esophageal rupture with no associated esophageal disease requires thoracotomy with layered closure of the defect. Shock is no contraindication to operative treatment, and a dramatic improvement in the overall picture frequently is noted as soon as the thorax is opened and the lung expands. Few emergencies could better fit the axiom: The patient is too ill not to operate. Most surgeons prefer a standard posterolateral incision in the seventh intercostal space. The extrapleural approach and posteroinferior mediastinotomy are outmoded [12]. The widely opened mediastinal pleura affords access to the rent, which is repaired in two layers with interrupted nonabsorbable sutures. Anterior and posterior chest tubes drain the pleural space, and they may be lightly sutured in place along lines of dependent drainage. Fluid in the opposite hemithorax requires insertion of a chest tube either preceding or at the conclusion of the operation. A nasogastric tube or gastrostomy keeps the esophagus at rest for approximately one week. Despite a layered closure and tube decompression, breakdown of the repair may occur because of edema or necrosis at the suture line. When the underlying process is esophagitis, this alone may be responsible for poor healing. Inadequate drainage results in empyema, atelectasis, and continued mediastinitis. Early in the postoperative course suture-line dehiscence produces increased drainage through the chest tube. Late disruptions create roentgenographic evidence of an air-fluid level and initiate a febrile course. Postoperative breakdown of the repair does not obligate the surgeon to reoperate for a second closure, provided that the leak is well drained. These fistulas close when the patient s nutrition can be maintained and no obstruction exists below the leak [56]. Tuttle and Barrett [72] disclosed poor results with jejunostomy and gastrostomy, and instead proposed feeding a full diet by mouth when the disruption is draining satisfactorily. A good nutritive state can be produced in from 7 to 14 days if 50% of the food passes into the stomach. The importance of multiple-tube waterseal drainage of the pleural space cannot be overemphasized. An adequately expanded lung will adhere to the parietal pleura within a few days, and empyema is thus avoided. The standard operative techniques must be modified when lower obstruction underlies the perforation. The esophagus is no exception to the basic surgical tenet that closure of a perforation proximal to an obstruction is doomed to failure. Closure of a rupture lying above a partially obstructing neoplasm or stricture rarely ends successfully. Attempts to dilate the distal pathological segment seem hazardous. An acute perforation situated near a carcinoma is best managed by a one-stage resection when the tumor can be safely removed. One operation avoids prolonged hospitalization and the less desirable staged 582 THE ANNALS OF THORACIC SURGERY

13 COLLECTIVE REVIEW: Esophageal Perforations procedures that accomplish nothing since the carcinoma usually is so advanced that resection is contraindicated by the time the mediastinitis has cleared. Between 1952 and 1957 several surgeons [9,45,62] reported favorable results after primary esophagogastrectomy in the presence of esophageal perforation. Recently Johnson and co-workers [34] showed that the obstructive process may be managed successfully by primary resection with gastroesophageal anastomosis, especially if one operates within 6 to 8 hours after the perforation. A delay in initiating surgical treatment also influences the decision for definitive resection. Fixation, digestion, and edema around the perforation site lead to an unsafe closure, and for these reasons Hendren and Henderson [28] have employed resection in the presence of established mediastinitis. In their 5 cases no postoperative infections occurred even though 3 patients were operated on the day after perforation. Thal s fundic patch operation [70] can be applied to perforations combined with stricture when no malignancy exists. The procedure was designed to widen a narrow lumen and provide a valve mechanism at the cardioesophageal junction. Late diagnoses are made less often today than formerly, although recent operation and administration of steroids and narcotics occasionally cloud the picture [79]. Perforation of the thoracic esophagus seen after 24 to 36 hours represents an unpromising situation. In these critical cases of mediastinitis, Johnson and Schwegman s method of esophageal exclusion [33, 371 may be lifesaving; however, it does entail secondary reconstruction of the esophagus. A cervical esophagostomy is created and the lower esophagus is divided in the abdomen. The proximal and distal ends of the esophagus are closed and the pleural cavity is drained. A gastrostomy is used for feeding. Later, the blind esophageal segment can be removed and the colon transplanted to restore continuity. Scattered through the literature are reports of nonoperative management of esophageal perforation [3, 17,48,68]. Some authors take the middle-of-the-road position, preferring the medical approach for small instrumental perforations and surgical intervention for spontaneous ruptures, external penetration, and large tears [27, 431. Unquestionably, minute cervical perforations-for example, from a pin or fishbonecan be managed by halting oral intake and administering high doses of antibiotics. Although instrumental lacerations of the upper esophagus have also been treated by the wait and see method, from 20 to 25% will ultimately need cervical drainage [7, 641. A more perilous approach calls for combining antibiotics with drainage in the treatment of thoracic esophageal perforation [48]. The size of the rent becomes the criterion, but even with contrast studies the VOL. 10, NO. 6, DECEMBER,

14 LOOP AND GROVES true size of the perforation is hard to estimate. One tragic fact related to the so-called conservative management is that some of the patients who died had benign disease [go]. The least publicized aspect is the prolonged disability and hospitalization which so often accompany this choice of treatment [26]. There are three circumstances in which observation and medical management should play no part: (1) after delayed diagnosis, (2) in the gravely ill patient, and (3) after rupture of the thoracic esophagus. Barrett s statement [6] aptly summarizes the current attitude toward conservative management:... to treat a perforation conservatively may succeed; but it is likely to fail in that the patient who survives the emergency can develop a mediastinal abscess or pleural complications and these result in prolonged illness and pathologic sequelae which can be virtually untreatable. SUMMARY Esophageal perforation, no matter how small, must be considered potentially fatal. Early recognition greatly influences the outcome and therefore is the most important single factor in management. Established treatment initially consists of eliminating oral intake, passing a nasogastric tube, providing fluid balance, and administering antibiotics in high doses. If there are compelling reasons, small upper esophageal perforations may be suitable for trial with medical management; however, this method involves risk, as evidenced by abscess formation in fully 20% of the patients so treated. Cervical mediastinotomy and drainage constitute the safest treatment, as morbidity is reduced and the hospital stay shortened. Perforation of the thoracic esophagus contaminates the mediastinal tissue and produces a fulminant infection that rapidly involves the pleural space. In addition to supportive measures, thoracotomy for repair of the defect becomes lifesaving. Underlying obstructive esophageal disease complicates the standard treatment. As with any hollow viscus, closure and drainage proximal to the obstruction give rise to a persistent fistula. To avoid this consequence, more radical operation is occasionally necessary and includes primary esophagogastrectomy or, in desperate circumstances, esophageal exclusion with secondary reconstruction. REFERENCES 1. Adkins, P. C. The diagnosis and management of esophageal perforation. Amer. Surg. 21:759, Anderson, R. L. Spontaneous rupture of the esophagus. Amer. J. Surg. 93:282, Aniansson, G., and Hallen, L. Perforation of the esophagus. Actu Otolaryng. (Stockholm) 59:554, THE ANNALS OF THORACIC SURGERY

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