6. Macrae F, Tan K, Williams B. Towards safer colonoscopy: a report on the complications of 5000 diagnostic or therapeutic colonoscopies. Gut 1983;24:376-83. 7. Dubas F, Rohner A. Iatrogenic colorectal perforation: incidence, mechanism and prevention. Helv Chir/Acta 1985;52:681-6. 8. Bartizal J, Boyl DR, Folk FA, Smith D, Lescher TC, Freeark RJ. A critical review of management of 392 colonic and rectal injuries. Dis Colon Rectum 1974;17:313-8.
Esophageal hematoma and tear from a taco shell impaction To the Editor: Esophageal injury secondary to the ingestion of food is infrequent. Reported here is the occurrence of an esophageal hematoma and tear related to the consumption of tacos. A 55-year-old man, without previous gastrointestinal history, presented with progressive dysphagia and odynophagia. Five days earlier, the patient noted an acute onset of painful swallowing and a foreign body sensation while eating a hard shell taco, but was able to finish his meal. The odynophagia continued over the ensuing 5 days and the patient began to experience worsening dysphagia, initially to solids, progressing to liquids, and ultimately to his own secretions. Upper gastrointestinal endoscopy revealed a portion of a taco shell lodged from 17 to 19 cm from the incisors. The taco fragment was easily broken by the endoscope and readily advanced into the stomach. Examination of the esophagus revealed a submucosal prominence across from a linear tear in the area where the fragment had been lodged (Fig. 1). There also was surrounding esophagitis. Although a diagnosis of hematoma was entertained, the appearance alone of this submucosal process could not exclude the possibility of an underlying malignancy. Biopsies and brushings of the area revealed inflammatory cells only, without underlying tumor. The patient experienced almost immediate improvement, and his symptoms resolved within several weeks. A subsequent endoscopy revealed a normal esophagus, with complete resolution of the injuries. The consumption of tacos and corn tortilla products is very popular. However, only five previous cases of taco or corn chip esophageal tears were found through MEDLINE. 1- 3 As in this case, the previously described patients all experienced a sudden onset of symptoms while eating, and had worsening symptoms until the diagnosis was made. Esophageal hematomas are also infrequently reported. Although there is one report of pill-induced esophageal hematoma,4 no reports have related this injury to the ingestion of food, as illustrated by our patient. In a review of esophageal hematomas by Shay et al. 5 26 cases were identified. Most appeared to originate from Mallory-Weiss tears. Spontaneous hematomas were described in those with impaired hemostasis. 5 •6 Esophageal injury secondary to taco shells and corn tortilla products undoubtedly occurs more frequently than has been reported, perhaps owing to the usually benign clinical course. Linas M. Klygis, MD Department of Medicine Section of Gastroenterology Northwestern University Medical School Chicago, Illinois
100
Figure 1. An esophageal hematoma (t.) is present across from an esophageal fear (.&.) in the area where the taco shell fragment had been lodged for 5 days.
REFERENCES 1. Hunter TB, Protell RL, Horsley WW. Food laceration of the
esophagus: the taco tear. AJR 1983;140:503-4. 2. Meslin H, Kobernick M. Corn chip laceration of the esophagus and evaluation of suspected esophageal perforation. Ann Emer Med 1983;12:455-7. 3. Longstreth GF. Esophageal tear caused by a tortilla chip. N Engl J Med 1990;322:1399-1400. 4. Piccione PR, Winkler WP, Baer JW, Kotler DP. Pill-induced intramural esophageal hematoma. JAMA 1987;257:929. 5. Shay SS, Berendson RA, Johnson LF. Esophageal hematoma. Four new cases, a review, and proposed etiology. Dig Dis Sci 1981;26:1019-24. 6. Atefi D, Horney JT, Eaton SB, Shulman M, Whaley W, Galambos JT. Spontaneous intramural hematoma of esophagus. Gastrointest Endosc 1978;24:172-4.
Endoscopic removal of an impacted colonic foreign body (fish bone) complicated by a pelvic abscess To the Editor: Less than 1% of gastrointestinal foreign bodies perforate the bowel and the most common site of perforation is the ileocecal valve. 1,2 We report the case of a 70-year-old woman, who was admitted to the hospital with a 2-day history of lower abdominal crampy pain, diarrhea, fever, and chills. She denied any nausea, vomiting, or gastrointestinal bleeding. Her past medical history was remarkable for diverticular disease of the colon, hysterectomy, and appendectomy. Her physical examination revealed a well-developed, wellnourished, obese lady in no acute distress with a temperature of 100.8°F, a blood pressure of 120/70 and a pulse of 80. Cardiopulmonary examination was unremarkable. Abdominal examination revealed active bowel sounds, and a soft, depressible, non-distended abdomen, but with evidence of tenderness and rebound in the suprapubic area and left lower quadrant. There was no organomegaly, mass, or evidence of ascites. Rectal examination was unremarkable. Laboratory tests revealed a white blood cell count of GASTROINTESTINAL ENDOSCOPY
Figure 1. CT scan of the pelvis showing a soft tissue density in the pelvic floor compatible with an abscess. The colonic foreign body (fish bone) (arrow) was not described in the original x-ray report.
14,600 with 84% polymorphonuclear leukocytes. The rest of the laboratory tests, including urinalysis, electrolytes, and liver function tests, were all normal. X-Ray examination of the abdomen revealed a non-specific gas pattern without free air or masses. Computerized tomography of the abdomen and pelvis revealed evidence of a soft tissue density which distorted the fatty soft tissue in the pelvic floor compatible with diverticulitis or peri-diverticular collection (Fig. 1). The patient was treated for diverticulitis with intravenous fluids, cefoxitin (l g intravenously every 6 hours), and tobramycin (60 mg intravenously every 8 hours). Within 48 hours the patient's symptoms improved, the white blood cell count had decreased to 7900 and a repeat CT scan 1 week later revealed improvement in the appearance of the pelvis collection. The patient was discharged to her home receiving an oral cephalosporin. One week later, the patient's signs and symptoms had markedly improved. Colonoscopic examination was performed and revealed evidence of a foreign body at approximately 40.0 cm from the anal verge, which seemed to be impacted in both walls of the intestine (Fig. 2). Using the biopsy forceps, the tip of the impacted foreign body was liberated from the wall and then using the snare this foreign body was grasped and removed to the outside. It proved to be a fish bone measuring 5.2 cm in length. A repeat examination failed to reveal any laceration or trauma. At that point in time the patient was readmitted to the hospital, restarted on intravenous antibiotics and a repeat CT scan 4 days later revealed good resolution of the previously described inflammatory process. Retrospectively, the impacted foreign body was demonstrated on CT scans (Fig. 1). The patient remained asymptomatic and was discharged 2 weeks later. Successful colonoscopic extraction of foreign body from above the rectum has been reported by several authors. 3 - 6 The endoscopic technique of colonic foreign body extraction is safe, less costly, and should be considered as the first step in the management of these patients. Risk factors associated with an increased probability of perforation include inflammatory bowel disease, diverticulosis, colonic tumors, blind intestinal segments, and herVOLUME 38, NO.1, 1992
Figure 2. Colonoscopic examination showing the presence of an impacted fish bone in the sigmoid colon. Note the presence of a superficial, circular ulcer where one of the tips of the foreign body had perforated.
nias/ Our patient had a history of diverticular disease which we believe was a risk factor for the perforation. Clinically, perforation of the rectosigmoid colon may present in two different fashions. It is well known that perforation below the peritoneal reflection usually manifests insidiously with signs and symptoms of pelvic sepsis. Signs and symptoms usually occur several days after the injury. On the other hand, intraperitoneal rectosigmoid colon perforation presents with dramatic signs of acute peritonitis,7 Our patient presented differently. Although the site of perforation was at approximately 40.0 cm from the anal verge, her signs and symptoms were those of pelvic infection. Maleki and Evans8 reported their experience with 12 cases of foreign body perforation, all of which required exploratory surgery. Fish bones were identified in two cases and perforation was in the small bowel. The case herein reported demonstrates that an impacted foreign body in the left colon complicating a pelvic abscess may mimic acute diverticulitis and that such a foreign body may be removed successfully with a colonoscope without the need for surgical intervention. Juan J. Alberti-Flor, Moises E. Hernandez, Jose P. Ferrer, Adolfo Maldonado, Rogelio Saldivar,
MD MD MD MD MD
Department of Medicine Division of Gastroenterology and Radiology North Gables Hospital Coral Gables, Florida
REFERENCES 1. Hacker F, Cattau EL. Management of gastrointestinal foreign
bodies. Am Fam Phys 1986;34:101-8. 2. McManous JE. Perforation of the intestine by ingested foreign body. Am J Surg 1941;53:393. 3. Rocklin M, Apelgren K. Colonoscopic extraction of foreign bodies from above the rectum. Am Surg 1989;55:119-23. 101
4. Oehler JR, Dent TL, Ibrahim M, et al. Endoscopic identification and removal of an unusual symptomatic colonic foreign body. Dig Dis Sci 1979;24:263-9. 5. Wolf L, Geraci K. Colonoscopic removal of balloons from the bowel. Gastrointest Endosc 1977;24:4l. 6. Sorenson RM, Bond JH. Colonoscopic removal of foreign body from the cecum. Gastrointest Endosc 1975;21:134-5. 7. Kingsley AN, Abcarian H. Colorectal foreign bodies. Dis Colon Rectum 1985;28:941-4. 8. Maleki M, Evans W. Foreign-body perforation of the intestinal tract. Arch Surg 1970;101:475-7.
Post-sclerotherapy intramural esophageal hematoma: endoscopic and radiologic findings To the Editor: Endoscopic injection sclerotherapy is commonly used in the acute and chronic management of bleeding esophageal varices due to alcoholic cirrhosis. Many complications are described, including esophageal ulceration, chest pain, fever, and even perforation.! Esophageal hematoma has only been rarely described as a complication of this therapy.z-s We recently evaluated a patient with the typical endoscopic and radiologic findings of post-sclerotherapy intramural esophageal hematoma. A 59-year-old man with biopsy-proven alcoholic cirrhosis (Child's A) presented with actively bleeding esophageal varices. After the acute episode was successfully controlled with endoscopic sclerotherapy, he was begun on an eradication program of weekly injections. Only small varices remained after three sessions, so he was placed on a schedule of monthly follow-up. At the second monthly session, grade II varices were again noted at the gastroesophageal junction, thus two 2-ml intravariceal injections of 3% sodium tetradecyl sulfate in a 50% solution of D50 were performed without apparent incident. Several hours later, the patient presented for evaluation of severe odynophagia, near-total dysphagia, and blood-tinged sputum. There was no history of fever, retching, sneezing, or cough. Laboratory evaluation showed a platelet count of 50,000 prothrombin time of 10.5 seconds (normal up to 11.5), partial thromboplastin time of 25.7 seconds (normal up to 37), and a hematocrit of 45.5, all consistent with his baseline values. Chest x-ray showed no effusion or infiltrate. A contrast study of the esophagus revealed a large filling defect extending the length of the esophagus (Fig. 1). Endoscopy demonstrated a well-demarcated hematoma of the left and posterior esophageal walls extending from the upper esophageal sphincter to the gastroesophageal junction. When the patient developed fever to 103.5°F, broad-spectrum antibiotics were begun. A CT scan showed the hematoma, but no evidence of perforation. The patient was begun on intravenous hyperalimentation and kept fasting with gradual resolution of fever and symptoms over 9 days. Follow-up endoscopy at 8 days (Fig. 2) showed mucosal bridging, ulceration, and a smaller residual hematoma. Endoscopy at 6 weeks showed healing of the esophagus. The patient has subsequently done well. Intramural esophageal hematoma is an unusual compli102
Figure 1. Gastroviste esophagram showing a large intraluminal filling defect (arrows) running the length of the esophagus.
cation of disorders of coagulation, but may occur in otherwise normal patients associated with the Mallory-Weiss syndrome. 6 It has rarely been described after endoscopic sclerotherapy, with only four English language cases reported. z-s Although all reported patients had cirrhosis with coagulopathy, close analysis of injection techniques, sclerosant solutions, and clinical/laboratory data reveal no other identifiable risk factors for this complication. The diagnosis should be suspected in the early post-sclerotherapy patient with the triad of severe dysphagia, odynophagia, and bloodtinged sputum; it is confirmed by characteristic endoscopic and radiologic findings. Fortunately, as in our patient, conservative therapy is GASTROINTESTINAL ENDOSCOPY