Esophageal perforation and mediastinitis from fish bone ingestion. (Case Report).

Abstract: Esophageal perforation is a serious condition with a high mortality rate. Successful therapy depends on the size of the rupture, the time elapsed between rupture and diagnosis, and the underlying health of the patient. Common causes of esophageal perforation include medical instrumentation, foreign-body ingestion, and trauma. A case of esophageal perforation due to fish bone ingestion in a 70-year-old diabetic male is described here, with a review of the pertinent literature. The patient presented with odynophagia after a meal that included fish. Initial evaluation was nondiagnostic and the patient was discharged home. The patient returned 12 days later with fever, generalized weakness, and persistent dysphagia. Esophageal biopsy of a necrotic ulcer revealed foreign material with acute inflammatory changes. Computed tomography scan demonstrated a pneumomediastinum. The patient became hemodynamically unstable and died on the third hospital day.

Key Words: esophageal perforation, mediastinitis

**********

Key Points

* The clinical presentation of esophageal repture depends on the size and location of the injury and the length of time since the injury.

* Common causes of esophageal perforation include medical instrumentation, foreign-body ingestion, and trauma.

* Successful treatment of esophageal perforation depends upon the size of the rupture, time elapsed between rupture and diagnosis, and underlying health of the patient.

The most common cause of esophageal perforation is iatrogenic. Typically, perforation occurs during endoscopy, with or without dilation. Spontaneous perforations and trauma are responsible for up to 20% of perforations. (1) Although dysphagia is the main symptom when the esophagus is injured, dyspnea, epigastric pain, and signs of sepsis are also common. Location and size of the perforation, delayed diagnosis, and delay in initiating treatment are the main factors contributing to poor survival rates. We describe a patient with an esophageal perforation from a fish bone ingestion that resulted in mediastinitis.

Discussion

The esophagus is a muscular tube that lacks a serosal layer, making it more vulnerable to rupture or perforation. Once a perforation occurs, saliva, retained gastric contents, bile, and acid enter the mediastinum, resulting in mediastinitis. Since the mid-esophagus lies adjacent to the right pleura and the distal esophagus is next to the left pleura, perforations at these locations lead to collections at the respective pleural cavities. Large volumes of pleural fluid--often infectious and with a low pH-- can accumulate, contributing to cardiopulmonary difficulties.(2) These fluid collections can result in mediastinitis, pericarditis, or cardiac tamponade.(3) Within 12 hours of perforation, a polymicrobial infection is common; Staphylococcus, Pseudornonas, Streptococcus, and Bacteroides organisms are common pathogens.(4) Due to negative intrathoracic pressure, thoracic esophageal perforations are more likely to disseminate fluid and bacteria throughout the mediastinum.

The clinical presentation of esophageal rupture is dependent upon the size and location of the injury and the time course since the injury. Patients typically present with pain in locations throughout the chest, epigastrium, and upper abdomen. Signs and symptoms of esophageal rupture and perforation include an acutely ill-appearing patient with fever, subcutaneous or mediastinal emphysema, tachycardia, tachypnea, vomiting, and dysphagia. When the heart beats against air-filled tissues, mediastinal crunch (Hamman's sign) can be heard. (5)

Medical instrumentation in the esophagus is the most common cause of esophageal perforation. (1) The incidence of perforation from simple endoscopies is 0.03% while that for pneumatic dilation for achalasia ranges from 1 to 1 0%.6 The usual location of perforation from endoscopy is at the cricopharyngeus muscle but, when esophageal dilation is added to the procedure, the location is usually proximal to or at the stricture. (7,8)

Perforation of the esophagus can also occur secondary to foreign body ingestion. (9) The perforation most often occurs at areas of acute angulation or physiologic narrowing. The level of the cricopharyngeal muscle is again the most frequent location. The perforation identified by endoscopy on our patient was about 9 cm from the incisors. With gradual erosion of the impacted foreign body through the esophageal wall, perforation may occur within 2 weeks after ingestion. Our patient presented with mediastinitis 12 days after his initial ingestion of a fish bone, with subsequent rupture of the esophageal wall.

Trauma accounts for 8 to 15.3% of cases of esophageal perforation and rupture. (10) Penetrating injuries to the esophagus due to knife and gunshot wounds are more common than blunt trauma from high-speed motor vehicle accidents, where injury from the steering wheel can cause a rapid rise in intraesophageal pressure. Other causes of esophageal perforation include invasion of the esophagus by contiguous primary or metastatic carcinoma, particularly esophageal and lung cancers; caustic injury from ingestion of substances such as lye; medication-induced injury; infection, primarily herpes and fungal; and peptic ulcerative esophagitis. (11,12)

The diagnosis of spontaneous rupture or perforation of the esophagus most often relies on radiographic findings, but the clinician must first consider the diagnosis. Cervical perforations have lower mortality rates than thoracic perforations. (1) Thoracic perforations produce direct contamination of the mediastinum and pleural cavity. Once suspected, a posteroanterior and lateral upright chest x-ray should be obtained to identify any cervical or mediastinal emphysema, pneumopericardium, or pleural effusion. If the standing x-ray is negative and the clinical presentation continues to suggest perforation, an esophagram and/or chest CT scan should then be considered. (13)

Contrast films obtained with meglumine diatrizoate (Gastrograffin) are used to confirm the presence of an esophageal perforation. If a meglumine diatrizoate study is negative, a barium study may be required, since small tears may be missed. (14) If a thoracoesophageal fistula or free perforation into the lung is suspected, barium should not be used due to the possible risk of barium-induced mediastinal inflammation. A direct laryngoscopy was performed at the time of our patient's initial presentation and was negative. A meglumine diatrizoate study was then performed, which showed a filling defect but no foreign body. Contrast esophagrams have a reported false-negative rate that can exceed 10%. (l5)

CT scan can be useful in cases where esophagrams cannot be performed or are negative and when a high level of clinical suspicion remains. CT findings of esophageal rupture and mediastinitis can include air in the soft tissues of the mediastinum, abscess formation, and pleural effusions. A CT scan is useful in localizing fluid collections and can assist in their drainage. (16) In our patient, the CT scan showed free air in the mediastinum and pleural fluid collections (Fig. 3).

Although conservative management of perforations such as endoscopic closure can be successful, it is only appropriate in contained esophageal perforations in a stable patient without evidence of sepsis. (7,17) Overall, the mortality rate from esophageal perforation is 22%. (10) This rate is markedly increased in patients who have treatment delayed by more than 24 hours and in those with underlying esophageal disease, such as strictures and achalasia. The outcome is also dependent upon the location and etiology of the perforation. Prolonged prediagnostic course, evidence of underlying sepsis, and hemodynamic collapse were all predictors of the poor outcome in our patient.

The majority of esophageal perforations are not contained and require operative attention. Indications for surgery include Boerhaave syndrome (esophageal rupture from violent retching), clinically unstable patients with sepsis, contamination of the mediastinum or pleural space, perforation with retained foreign bodies, and failed medical therapy. (18) Primary repair of the laceration is reinforced by a flap of well-vascularized tissue. (19) When there is a long delay after the perforation, or the degree of mediastinitis is extensive with evidence of sepsis, an esophagostomy or a gastrostomy may be considered. An esophageal T-tube can also be placed to drain secretions and to allow healing of the injured tissue. (20) The sudden hemodynamic deterioration from overwhelming sepsis in our patient prevented surgical intervention.

Conclusion

Etiology, time delay between rupture and diagnosis, and location of an esophageal perforation affect management and results. The majority of esophageal perforations require urgent surgical treatment. The overall mortality rate for patients with esophageal rupture is 22%, but the survival rate nears 95% when the primary repair is completed within 24 hours of rupture. (10) Our case aptly demonstrates the clinical, radiologic, and therapeutic challenges of esophageal perforation and mediastinitis. High clinical suspicion of esophageal perforation is mandatory for timely diagnosis and treatment.

Accepted December 17, 2001.

References

(1.) Jones WG II, Ginsberg RJ. Esophageal perforation: A continuing challenge. Ann Thorac Surg 1992;53:534-543.

(2.) Attar S, Hankins JR, Suter CM, Coughlin TR, Sequeira A, McLaughlin JS. Esophageal perforation: A therapeutic challenge. Ann Thorac Surg 1990;50:45-51.

(3.) Sharland MG, McCaughan BC. Perforation of the esophagus by a fish bone leading to cardiac tamponade. Ann Thorac Surg 1993;56:969-971.

(4.) Brook I, Frazier EH. Microbiology of mediastinitis. Arch Intern Med 1996; 156:333-336.

(5.) Williamson WA, Ellis FH. Esophageal perforation, in Taylor MB, Gollan JL, Steer ML, Wolfe MM (eds): Gastrointestinal Emergencies. Baltimore, Williams & Wilkins, 1997, ed 2, p 31.

(6.) Miller RE, Bossart PW, Tiszenkel HI. Surgical management of complications of upper gastrointestinal endoscopy and esophageal dilation Including laser therapy. Am Surg 1987;53:667-671.

(7.) Wewalka FW, Clodi PH, Haidinger D. Endoscopic clipping of esophageal perforation after pneumatic dilation for achalasia. Endoscopy 1995;27:608-611.

(8.) Ballesta-Lopez C, Vallet-Fernandez J, Catarci M, Bastida-Vila X, Nieto-Martinez B. Iatrogenic perforations of the esophagus. Int Surg 1993;78:28-31.

(9.) Bufkin BL, Miller JI Jr, Mansour KA. Esophageal perforation: Emphasis on management. Ann Thorac Surg 1996;61:1447-1452.

(10.) Duranceau A. Perforation of the esophagus, in Sabiston DC Jr, Lyerly HK (eds): Textbook of Surgery: The Biological Basis of Modern Surgical Practice. Philadelphia, W.B. Saunders Co., 1997, ed 15, p 267.

(11.) Shaffer HA Jr, Valenzuela G, Mittal RK. Esophageal perforation: A reassessment of the criteria for choosing medical or surgical therapy. Arch Intern Med 1992;152:757-761.

(12.) Bladergroen MR, Lowe JE, Postlethwait RW. Diagnosis and recommended management of esophageal perforation and rupture. Ann Thorac Surg 1986;42:235-239.

(13.) Dodds WJ, Stewart ET, Vlymen WJ, Appropriate contrast media for evaluation of esophageal disruption. Radiology 1982;144:439- 441.

(14.) Phillips LG Jr, Cunningham J. Esophageal perforation. Radiol Clin North Am 1984;22:607-613.

(15.) Sarr MG, Pemberton JH, Payne WS. Management of instrumental perforations of the esophagus. J Thorac Cardiovasc Surg 1982;84:21 1-218.

(16.) White CS, Templeton PA, Attar S. Esophageal perforation: CT findings. AJR Am J Roentgenol 1993;160:767-770.

(17.) Nozoe T, Kitamura M, Adachi Y, Funahashi S, Yoh R, Iso Y, et al. Successful conservative treatment for esophageal perforation by a fish bone associated with mediastinitis. Hepatogastroenterology 1998;45:2190-2192.

(18.) Reeder LB, DeFilippi VJ, Ferguson MK. Current results of therapy for esophageal perforation. Am J Surg 1995;169:615-617.

(19.) White RK, Morris DM. Diagnosis and management of esophageal perforations. Am Surg 1992;58:112-119.

(20.) Mansour KA, Wenger RK. T-tube management of late esophageal perforations. Surg Gynecol Obstet 1992;175:571-572.

RELATED ARTICLE: Case Report

A 70-year-old Hispanic man with diabetes mellitus Type 1 and a history of four-vessel coronary artery bypass surgery in 1996 presented to the emergency room with generalized weakness. The patient had been found on the kitchen floor, incontinent of urine. Twelve days before admission, the patient had been seen in the emergency department with dysphagia and odynophagia after swallowing what he thought was a fish bone. At that time, the patient had laryngoscopy and esophagram, both of which were negative (Fig. 1), and was discharged home with a prescription for metoclopramide. Two days before the second presentation, the patient developed a fever with nonproductive cough and hoarseness. The dysphagia and odynophagia had persisted since the initial evaluation.

At admission, oral temperature was 103.3[degrees]F, pulse was 120 beats/mm, and blood pressure was 142/86 mm Hg. Physical examination showed decreased breath sounds in all lung fields, regular heart rate with no murmurs, no S3 or S4 heart sounds, no abdominal tenderness, normal active bowel sounds, no extremity edema, and no subcutaneous emphysema. Laboratory values included: sodium, 127 mmol/L; potassium, 4 mmol/L; chloride, 88 mmol/L; bicarbonate, 25 mmol/L; blood urea nitrogen, 35 mmol/L; creatinine, 1.0 mmol/L; glucose, 542 mg/dl; white blood cells, 11,900/[mm.sup.3]; hematocrit, 50.8%; platelet count, l86,000/[micro]l; lactate, 2.9 mmol/L; amylase, 51 U/L; lipase, 394 U/L; alkaline phosphatase, 76 U/L; aspartate aminotransferase, 37 U/L; alanine aminotransferase, 27 U/L; troponin <0.5 [micro]g/L. Arterial blood gas values showed a pH of 7.42; carbon dioxide level was 42 mm Hg; oxygen level was 71 mm Hg; and oxygen saturation was 95% on 2 L oxygen delivered by nasal cannula. Anteroposterior chest x-ray (F ig. 2) revealed bibasilar atelectasis and normal mediastinum. Electrocardiogram showed sinus rhythm with an old inferior-wall myocardial infarction and premature ventricular contractions.

The patient was admitted for fluid resuscitation, correction of electrolytes, and investigation of dysphagia and high fever. Several hours after admission, he developed atrial fibrillation, with heart rate of 160 to 180 beats/min. He was given metoprolol and diltiazem therapy with some effect, and treatment with a diltiazem drip was started. Treatment with amoxicillin-sulbactam and metronidazole was initiated. The patient remained tachycardic and became hypotensive. He was transferred to the cardiac critical care unit, where he was intubated for airway protection. Cardioversion was attempted but was unsuccessful. Amiodarone therapy was started, with improvement in heart rate control. While intubated, the patient underwent endoscopy, which revealed an esophageal ulcer with necrotic debris as well as gastritis and three duodenal ulcers with adherent clots, but no active bleeding.

Computed tomography (CT) of the chest (Fig. 3) demonstrated a pneumomediastinum. Tissue from the esophageal biopsy showed normal esophageal tissue with associated foreign body and bacterial colonization with acute inflammatory reaction (Fig. 4). Blood cultures grew Streptococcus viridans. The patient's blood pressure continued to decline, and he required multiple Vasopressors. He was considered not to be a surgical candidate due to his unstable condition. The patient died on the third hospital day. The family declined an autopsy.

From the Internal Medicine Residency Program, University of Connecticut School of Medicine, and Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT.

Reprint requests to Manny C. Katsetos, MD, Hartford Hospital, 80 Seymour Street, P.O. Box 5037, Hartford, CT 06102-5037. Email: [e-mail]

Copyright [c] 2003 by The Southern Medical Association 0038-4348/03/9605-0516