the organism could have colonized the patient's oro­pharynx or our water solutions prior to endoscopy.

Several points regarding sclerotherapy techniquemight be considered based on our experience. First,there is evidence that solutions such as tetradecylsul­fate are less ulcerogenic than sodium morrhuate.15

•16

Second, use of sterile water supplies, disinfected en­doscopes' and prophylactic antibiotics in patients whoare severely immunocompromised or who have val­vular heart disease seem prudent precautions to con­sider. Third, sterile disposible injectors may be pref­erable to reusable injectors in order to minimize therisk of using a contaminated or inadequately sterilizeddevice. Finally, ensuring superficial nonintramural in­jection of sclerosants is likely to minimize the risk oftransmural necrosis of the esophagus.

We have employed sclerotherapy in 40 patients overthe past 2 years, and this case represented the firstdeath attributable to sclerotherapy. Autopsy con­firmed a large penetrating esophageal ulcer. S. mar­cescens was possibly introduced into the esophagealvarices at the time of sclerotherapy, thus generating amycotic ulcer.

REFERENCES1. Allison JG. The role of injection sclerotherapy in the emergency

and elective management of bleeding esophageal varices. J AMA1983;249:1484-7.

2. MacDougall BRD, Westaby D, Theodossi A, Dawson JL, Wil­liams R. Increased long-term survival in variceal hemorrhage

Solitary brain abscess followingendoscopic injection sclerosis ofesophageal varices

Fred L. Cohen, MDRoger S. Koerner, MDSheldon J. Taub, MD

Previous reports on endoscopic injection sclerosisfor the treatment of bleeding esophageal varices doc­ument an incidence of bacteremia of 2% to 50%.1Diagnostic upper gastrointestinal endoscopy itself orin combination with biopsy has an associated inci­dence of bacteremia of 3% to 8%.2-4 No major clinicalcomplications have been reported as a result of thisbacteremia.1

This report describes the development of a brainabscess 3 weeks following endoscopic injection scle­rosis of a bleeding esophageal varix and 1 week aftera follow-up endoscopy for melena. It represents a

From the Palm Beach Gardens Medical Center, Palm Beach Gardens,Florida. Reprint requests: Fred L. Cohen, MD, P.O. Box 12246, LakePark, Florida 33403.

VOLUME 31, NO.5, 1985

using injection sclerotherapy. Lancet 1982;1:124-7.3. Chung R, Lewis JW. Cost of treatment of bleeding esophageal

varices. Arch Surg 1983;118:482-5.4. Monroe P, Morrow CF, Millen JE, Fairman RP, Glauser FL.

Acute respiratory failure after sodium morrhuate esophagealsclerotherapy. Gastroenterology 1983;85:693-9.

5. Ayres SJ, Goff JS, Warren GH, Schaefer JW. Esophagealulceration and bleeding after flexible fiberoptic esophageal veinsclerosis. Gastroenterology 1982;83:131-6.

6. Barsoum MS, Mooro HA, Bolous FI, Ramzy AF, Rizk-AlahMA, Mahmoud Fl. The complications of injection sclerotherapyof bleeding esophageal varices. Br J Surg 1982;69:79-81.

7. Carr Locke DL, Sidky K. Broncho-oesophageal fistula-latecomplication of endoscopic variceal sclerotherapy. Gut1982;23:1005-7.

8. Cohen LR, Korsten MA, Scherle J, Velez ME, Fisse RD, AronsEJ. Bacteremia after endoscopic injection sclerosis. Gastroin­test Endosc 1983;29:198-200.

9. Ayres SJ, Goff JS, Warren GH. Endoscopic sclerotherapy forbleeding varices-effects and complications. Ann Intern Med1983;98:900-3.

10. Rose JDR. Injection sclerotherapy: intravariceal or paravari­ceal? (letter). Gastroenterology 1983;84:1073.

11. Grube JL, Kozarek RA, Sanowski RA, Legrand J, Kovac A.Venography during endoscopic injection sclerotherapy ofesoph­ageal varices. Gastrointest Endosc 1984;30:6-8.

12. Galambos JT. Endoscopic sclerotherapy (editorial). Ann InternMed 1983;98:1009-11.

13. Yu VL. Serratia marcescens-historical perspective and clinicalreview. N Engl J Med 1979;300:887-93.

14. Thomas FE, Jackson RT, Melly A, Alford RH. Sequentialhospital-wide outbreaks of resistant Serratia and Klebsiellainfections. Arch Intern Med 1977;137:581-4.

15. Jensen DM. Sclerosants for injection sclerosis of esophagealvarices. Gastrointest Endosc 1983;29:315-7.

16. Gibbert V, Feinstat T, Burns M, Trudeau W. A comparison ofthe sclerosing agents tetradecylsulfate and sodium morrhuatein endoscopic injection sclerosis of esophageal varices. Gas­trointest Endosc 1982;28:147.

significant central nervous system complication re­lated to these endoscopic procedures and, to ourknowledge, has not been reported previously.

CASE REPORT

A 76-year-old, insulin-dependent diabetic woman pre­sented 22 days following elective endoscopic sclerotherapyfor previously bleeding esophageal varices with a 3-dayhistory of headache, neck pain, and a progressive speech andlanguage disturbance. There was no history or clinical evi­dence of ear or mastoid disease, pulmonary infection, orheart disease. She had a history of alcoholism and Laennec'scirrhosis and had undergone numerous previous endoscopiesand injection scleroses from 1982 through August 1984, 6months prior to the current illness. The most recent scle­rotherapy was a planned follow-up injection and not specif­ically carried out in relation to active bleeding. All injectionprocedures had been performed utilizing standard currentantiseptic cleansing techniques with green soap and Cidexbetween procedures. The endoscopies were performed in theleft lateral decubitus position with the Olympus XQ panen­doscope. The sclerosing agent was a combination of sodiumtetradecyl sulfate and saline. Topical anesthesia was used

331

Figure 1. CT scan with contrast done at the time of admission,showing a ring-enhancing mass lesion in the left posteriortemporal lobe.

with intravenous diazepam for sedation. A diagnostic endos­copy without sclerosis was performed (14 days after theinjection sclerosis and 5 days prior to the development ofneurologic symptoms) because of melena with the finding ofan esophageal ulcer secondary to the sclerosis.

Temperature on admission was 101°F. The neck wasmildly stiff, and although quite alert, she was moderatelydysphasic with a mild right hemiparesis and bilateral Babin­ski signs. There was no papilledema. The cardiopulmonaryexamination was normal. Sinus and chest x-rays were nor­mal. An echocardiogram showed only a calcified papillarymuscle and concentric left ventricular hypertrophy. A CTscan with contrast enhancement (Fig. 1) showed a ring­enhancing lesion in the left posterior temporal lobe. She wasstarted on high doses of intravenous penicillin, choloram­phenicol, and dexamethasone and underwent an emergencyleft temporal burr hole. Seven milliliters of pus was aspiratedand cultured microaerophilic streptococcus, a commonmouth and upper respiratory tract organism. Based on itssensitivity to penicillin, chloramphenicol was discontinued,dexamethasone was tapered, and her neurologic status, clin­ical condition, and subsequent CT scans improved.

DISCUSSION

Endoscopic injection sclerosis has enjoyed an in­creasing popularity over the past 5 years based at leastin part on its reportedly low morbidity and mortalityrelative to other available treatment modalities. Com­plications have been similar in most series and haveincluded transient fever, bacteremia, superficial

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esophageal ulceration, esophageal stricture, bleedingof varices, pleural effusion, retrosternal pain, andesophageal perforation.1, 5-12 The complication rate ap­pears to be directly related to the severity of theunderlying liver disease. Fever is common, usually lowgrade, and may persist for about 36 hours. There isgeneral agreement that the fever and bacteremia arenot directly related and that the fever may result frompyrogens in the sclerosant.5

, 13 A recent investigation1

disclosed a 50% incidence of bacteremia followinginjection sclerosis with no bacteremia in a controlgroup without sclerosis. The most common organismwas a streptococcus which was felt to be a contaminantfrom the oropharynx. Consideration for routine anti­biotic prophylaxis was advanced, but no conclusionwas drawn.1

In our patient, there is virtually no doubt that theabscess was directly related to the procedures. Onemight legitimately speculate as to whether it is morelikely to have been from the endoscopic sclerotherapyof 3 weeks prior to presentation or the diagnosticendoscopy of less than 1 week prior to presentation.This question is not directly answerable because ofthe number of factors that govern the production of aclinical syndrome of brain abscess including host­organism interaction, the size and number of lesions(if multiple), the specific brain site involved, andthe neighboring anatomical disturbances involvingventricles, venous sinuses, and cisterns.14 Availableevidence would appear to incriminate the injectionsclerosis based on (1) the much higher incidence ofbacteremia from sclerosis than from diagnostic endos­copy and (2) the fact that the microaerophilic strep­tococcus is a relatively slow-growing organism in vitroand is unlikely to have formed a discreet, well-circum­scribed "mature" abscess in 5 days.

The mortality of brain abscess varies directly withthe patient's level of consciousness at the time ofdiagnosis. In patients presenting in coma, the mortal­ity approaches 90%.14 The overall mortality figures of40% for the period from 1950 through 1975 have beencredited to the modern antibiotic era.14 The decreaseto current mortality rates of 10% to 20%15,16 has beenattributed to modern diagnostic techniques, especiallyCT scanning, leading to earlier surgical intervention.Morbidity figures are more difficult to obtain but maybe as high as 30%. A high incidence of seizures isreported to occur following successful treatment ofbrain abscess.14

Brain abscess remains an extremely serious andpotentially lethal disease. The occurence of this com­plication would appear to underscore the concernsregarding the necessity or desirability of antibioticprophylaxis in high risk cases4 and the need for aprospective randomized controlled study of routineantibiotic prophylaxis in this increasingly utilized pro­cedure.

GASTROINTESTINAL ENDOSCOPY

REFERENCES1. Cohen LB, Korsten MA, Scherl EJ, Velez ME, Fisse RD, Arons

EJ. Bacteremia after endoscopic injection sclerosis. Gastroin­test Endosc 1983;29:198.

2. Mellow MH, Lewis RJ. Endoscopy-related bacteremia: inci­dence of positive blood cultures after endoscopy of the uppergastrointestinal tract. Arch Intern Med 1976;136:667.

3. Baltch AL, Buhac I, Agrawal A, O'Connor P, Bram M, MalatinoE. Bacteremia after upper gastrointestinal endoscopy. ArchIntern Med 1977;137:594.

4. Shull HJ, Greene BM, Allen SD, Dunn GD, Schenker S. Bac­teremia with upper gastrointestinal endoscopy. Ann Intern Med1975;83:212.

5. Lewis J, Chung RS, Allison J. Sclerotherapy of esophagealvarices. Arch Surg 1980;115:476.

6. Terblanche J, Northover JMA, Bornman P, et al. A prospectiveevaluation of injection sclerotherapy in the treatment of acutebleeding from esophageal varices. Surgery 1979;85:239.

7. Macdougall BRD, Theodossi A, Westaby D, Dawson JL, Wil­liams JL. Increased long-term survival in variceal haemorrhageusing injection sclerotherapy; results of a controlled trial. Lan­cet 1982;1:124.

8. Palani CK, Abuabara S, Kraft AR, Jonasson O. Endoscopicsclerotherapy in acute variceal hemorrhage. Am J Surg1981;141:164.

Intraduodenal diverticula of the commonbile duct

Robert C. Shamberger, MDMichael R. Treat, MD

Leslie W. Ottinger, MD

Biliary cysts and diverticula compose only a smallportion of biliary tract anomalies but are particularlyimportant because of the frequent clinical symptomsand functional abnormalities which they produce. Apatient recently presented with an episode of retro­sternal pain and during his evaluation was found tohave cholelithiasis and a mass in the second portionof the duodenum eventually shown to be a diverticu­lum from the common bile duct.

CASE REPORT

The patient is a 55-year-old man who initially presentedwith an acute episode of retrosternal pain. The pain wasbilateral and constricting in nature and varied in severityover 1 hour. He denied nausea and vomiting. There was noprevious history of cardiac or biliary disease.

On the admission physical examination, his heart andabdomen were normal. The admission EKG demonstratedonly mild elevation of the ST segment. He was admitted to

From the Surgical Service of the Massachusetts General Hospitaland the Department of Surgery, Harvard Medical School, Boston,Massachusetts. Reprint requests: Robert C. Shamberger, MD, De­partment of Surgery, Children's Hospital Medical Center, 300 Long­wood Avenue, Boston, Massachusetts 02115.Dr. Shamberger's present address is Department of Surgery Chil-dren's Hospital Medical Center, Boston, Massachusetts. 'Dr. Treat's present address is Department of Surgery ColumbiaPresbyterian Hospital, New York, New York. '

VOLUME 31, NO.5, 1985

9. Clark AW, Westaby D, Silk DBA, et al. Prospective controlledtrial of injection sclerotherapy in patients with cirrhosis andrecent variceal hemorrhage. Lancet 1980;2:552.

10. Johnston GW, Rodgers HW. A review of 15 years' experiencein the use of sclerotherapy in the control of acute hemorrhagefrom oesophageal varices. Br J Surg 1973;60:797.

11. Fleig WE, Stange EF, Ruettenauer K, Ditschuneit H. Emer­gency endoscopic sclerotherapy for bleeding esophageal varices:a prospective study in patients not responding to balloon tam­ponade. Gastrointest Endosc 1983;29:8.

12. Fleischer DE, Roth BE, Larson DE, Green ML. Therapeuticendoscopy for control of upper gastrointestinal bleeding. Gas­trointest Endosc 1983;29:245.

13. Brayko CM, Kozarek RA, Sanowski RA, Testa AW. Bacteremiaduring esophageal variceal sclerotherapy: its cause and preven­tion. Gastrointest Endosc 1985;31:10.

14. Goodman SJ, Stern WE. Cranial and intracranial bacterialinfections. In: Youmans JR, ed. Neurological surgery, 2nd ed.Philadelphia: WB Saunders, 1982:3323-57.

15. Gruszkiewicz MD, Doron Y, Peyser E, Borovich B, SchachterMD, Front D. Brain abscess and its surgical management. SurgNeuroI1982;18:7.

16. Alderson D, Strong AJ, Ingham HR, Selkon JB. Fifteen-yearreview of the mortality of brain abscess. Neurosurgery 1981;8:1.

the coronary care unit for observation. There was no eleva­tion of the cardiac isoenzymes of CPK and LDH, and atreadmill exercise test was negative. The LDH was 316 lUIliter (normal range, 80 to 200) and the SGOT was 248 lUIliter (7 to 28), which rapidly returned to normal. A normalalkaline phosphatase, 117 IUIliter (70 to 230), amylase, 49111100 ml, and lipase, 0.811/100 ml (0.3 to 1.0), were reported.

An abdominal sonogram identified an echogenic focus inthe right upper abdomen. An upper gastrointestinal series

Figure 1. Polypoid mass is demonstrated on the medialaspect of the second portion of the duodenum by bariumduodenography.

333