Nd:YAG laser for diminutive polyps To the Editor: We have used the Nd:YAG laser with an attached flat fulgurating tip for the coagulation of polyps 5 mm in size or less. The contact tip allows for minimal depth of penetration in contrast to the Nd:YAG laser used with the open fiber. As with the heat probe and bipolar probe, no ground plate is necessary. The potential for serosal injury should be less than with the commonly used monopolar forceps. We have treated over 25 polyps without complication utilizing this method. When a polyp is encountered, a cold forceps biopsy is taken. The Nd:YAG laser fiber tip is introduced through the biopsy channel of the instrument and the contact tip is placed directly on the lesion. Several 10-watt laser pulses are applied. Laser application continues until visible coagulation (whitening) of the lesion is observed. An average of three to four pulses per lesion is used. To date this method has been both safe and effective. In addition, given the small size of the laser fiber with contact tip, we have been able to use this even in endoscopes with relatively small channel sizes. Elliott N. Fraiberg, MD Margie Wiedemann, RN, CGC Kathy Dean, RN Endoscopy Unit St. Joseph Mercy Hospital Pontiac, Michigan
Removal of colonic medium size sessile polyps without diathermy
to tent the polyp toward the lumen while the assistant continues to close the loop to produce the desired guillotine effect. After transection has been accomplished, the base of the polyp is observed for 1 to 2 min to verify that there is no residual bleeding. If bleeding occurs either electrocoagulation with the ball-point electrode or an infusion of dilute epinephrine can be used to stop it. Bleeding stopped spontaneously without need for further intervention in all 25 cases. Recovery of the resected polyp was postponed until the operator was satisfied that there was no residual bleeding; then the resected polyp was recovered by aspiration. Although the experience with this method is still limited, there is ground for its use as a routine technique. The risk of hemorrhage appears to be low and the risk of perforation negligible while the advantages include economy, quickness, and simplification of the polypectomy procedure. J. C. Meeroff, MD Riviera Beach VA
ope, Florida
REFERENCES 1. Cohen LB, Waye JD. Treatment of colonic polyps. Practical consideration. Clin Gastroenterol 1986;15:359-76. 2. Tedesco FJ. Colonoscopic polypectomy. In: Silvia SE, ed. Therapeutic gastrointestinal endoscopy. New York: Igaku-Shoin, 1984:Chapter 12, 269-88. 3. Waye JD, Bishop D. Endoscopic polypectomy snares. A comparative evaluation. Endosc Rev 1984;1:6-12.
Bacteremia following sclerotherapy in portal hypertension To the Editor:
To the Editor: Sessile polyps of approximately 0.5 to 1.0 em in diameter are among the most common polyps identified at colonoscopy. These medium size polyps are too large to be destroyed using the hot biopsy forceps technique. Irrespective of their configuration which can be spherical or irregularly shaped with small or large areas of attachment to the intestinal wall, l these polyps are usually taken out using the snarecauthery technique. The only precondition to attempt this procedure is that the base of the polyp is not too wide and allows the formation of a pseudostalk. Transection of these polyps using "mixed" electrical current produces very little hemorrhage if any. Nevertheless, there is an increased risk of burning the wall of the colon or causing transmural perforation from excessive electrical energy.2 An innovative method for the removal of such polyps consists in transecting the polyp at the level of the pseudostalk by strangulation using the polypectomy snare but without applying any electrical current. To this date we have used the technique in 25 patients with normal coagulation laboratory values and no history of bleeding disorders. In all cases transection was obtained in a matter of seconds while bleeding from the base of the polyp was negligible. The technique requires a snare with sufficient "guillotine force," that is, a large wire loop, that can be retracted into the sheath at least 1 cm. 3 The snare is placed around the polyp and slowly closed in order to form a pseudostalk. Once the loop is tightened around the pseudostalk, the snare is pulled 136
There are a number of reports in the literature on the incidence of bacteremia following sclerotherapy in cirrhotic patients. 1- 5 We would like to report our experience in cirrhotic and noncirrhotic portal hypertension. We compared the incidence of bacteremia following sclerotherapy in 25 patients, each of cirrhotic and noncirrhotic portal hypertension (20 had extrahepatic portal venous obstruction and 5 had noncirrhotic portal fibrosis/idiopathic portal hypertension). Sclerotherapy was performed after cleaning the fibroptic flexible endoscope and the needle with 2% glutaraldehyde and clean water. Blood cultures were taken at 5 and 30 min after sclerotherapy. If the patient developed fever or had bacteremia in the earlier samples, a repeat sample was taken at 24 hours. We found bacteremia in 4 (16%) of the 25 patients with cirrhosis (pneumococcus in 2 patients at 5 min only, Streptococcus faecalis and Klebsiella pneumoniae in 1 patient at 5 and 30 min, Staphylococcus epidermidis in 1 patient at 5 and 30 min). None grew these organisms at 24 hours after sclerotherapy. In contrast, none of the 25 patients with noncirrhotic portal hypertension developed bacteremia. This incidence of 16% bacteremia following sclerotherapy in cirrhotics is in accordance with the incidence reported in the literature. 1- 5 This is higher when compared with the incidence of 3 to 4% reported in patients without any liver disease or portal hypertension after routine endoscopy. Failure to detect bacteremia in noncirrhotic patients with portal hypertension following sclerotherapy may suggest a good GASTROINTESTINAL ENDOSCOPY
local inflammatory response of an uncompromised host and a competent hepatic reticuloendothelial system to limit bacterial invasions. 6 Thus, portal hypertension per se does not lead to bacteremia following sclerotherapy. Although the number of patients in the study are small, we concluded that only patients with cirrhosis and valvular heart disease should be given prophylactic antibiotics before sclerotherapy. Y. K. Chawla, MD Bipin Sethi, MD A. Ayyagiri, MD J. B. Dilawari, FRCP Department of Hepatology Postgraduate Institutes of Medical Education and Research Chandigarh, India
REFERENCES 1. Cohen LB, Korsten MA, Scherl EJ, et al. Bacteremia after endoscopic injection sclerosis. Gastrointest Endosc 1983; 29:198-200.
2. Camara DS, Gruber M, Barde CJ, et al. Transient bacteremia following injection sclerotherapy of esophageal varices. Arch Intern Med 1983;143:1350-2. 3. Gerhartz HH, Sauerbruch T, Weinzieri M, et al. Nosocomial septicemia in patients undergoing sclerotherapy for variceal hemorrhage. Endoscopy 1984;16:129-30. 4. Sauerbruch T, Holl J, Ruckdeschel G, Forst! J, Weinzierl M. Bacteriaemia associated with endoscopic sclerotherapy of oesophageal varices. Endoscopy 1985;17:170-2. 5. Brayko CM, Kozarek RA, Sanowski RA, Testa AW. Bacteremia during esophageal variceal sclerotherapy: its cause and prevention. Gastrointest Endosc 1985;31:10-2. 6. Botoman VA, Surawicz CM. Bacteremia with gastrointestinal endoscopic procedures. Gastrointest Endosc 1986;32:342-6.
Abstracts ENDOSCOPY AROUND THE WORLD
Editor for Abstracts, James S. Barthel, MD Panel of Reviewers Jamie S. Barkin Stanley B. Benjamin Lawrence J. Brandt Edward L. Cattau Sarkis J. Chobanian Peter B. Cotton Kenneth A. Forde Lionello Gandolfi David Y. Graham Richard H. Hunt Dennis M. Jensen Seibi Kobayashi
Richard A. Kozarek Glen A. Lehman Charles J. Lightdale Finlay Macrae Zdenek Maratka Mark H. Mellow Patrice A. Michaletz Paul Rozen Melvin Schapiro Walter L. Trudeau C. N. J. Tytgat Richard A. Wright
Prediction of the first variceal hemorrhage in patients with cirrhosis of the liver: a prospective multicenter study THE NORTH ITALIAN ENDOSCOPY CLUB FOR THE STUDY AND TREATMENT OF ESOPHAGEAL VARICES
N Engl J Med 319:983-989, 1988 VOLUME 35, NO.2, 1989
In an attempt to identify endoscopic and clinical characteristics which might be used to predict the occurrence of a first variceal hemorrhage, the authors conducted a prospective multicenter study of 321 cirrhotic patients with esophageal varices and no prior history of upper gastrointestinal bleeding. The endoscopic appearance of the varices was classified according to the guidelines suggested by the Japanese Research Society for portal hypertension and numerically ranked using the variceal scoring system devised by Beppu et al. (Gastrointest Endosc 27:213-218, 1981). Eight variables were studied: size, color, location of the varices, presence and grade of red wale marks and cherry red spots, the presence of hematocystic spots, esophagitis, and diffuse redness. Clinical and laboratory features were also evaluated. Among the 321 patients, 85 had upper gastrointestinal bleeding during a median follow-up period of 23 months. Of these 85 patients, 57 were diagnosed as having variceal bleeding because an actively bleeding varix or a varix with an adherent clot was seen. In the remaining 28 patients, the source of bleeding was presumed to be variceal. In this study, the criteria devised by Beppu et al. were confirmed to be useful in predicting the first variceal hemorrhage; however, the risk of bleeding was substantially less than what would have been expected from Beppu's data. Therefore, the variceal scoring system, while generally valid, was not found useful in predicting the bleeding tendency in individual patients. In an attempt to define the risk of the initial variceal hemorrhage for a given patient, the authors then applied univariate analysis to their clinical and endoscopic criteria. Among the nine clinical criteria, five were found useful, and among the eight endoscopic criteria, six were found useful. Three criteria (Child's class, variceal size, and grade of red wale marks) were used to perform a multivariate regression analysis and arrive at a prognostic index. This index was then applied to a different population of 75 cirrhotics serving as controls in a separate study of variceal hemorrhage. However, little information was given about this validation. Features such as patient characteristics and length of follow-up were omitted. Cirrhotics with variceal hemorrhage have an exceedingly poor prognosis. The first episode of variceal bleeding is fatal in 30 to 50% of cases and 50 to 80% of survivors rebleed within 2 years. Although portasystemic shunts, variceal sclerosis, and beta blockers may help prevent rebleeding, no therapy has had a dramatic effect on patient survival. One way to reduce mortality is to treat prophylactically those patients at high risk for variceal hemorrhage. Unfortunately, such treatment has not been demonstrated to be effective, although beta blockers have shown some promise in this regard. In part, this apparent lack of efficacy may be explained by our inability to identify a subgroup of patients at highest risk for variceal hemorrhage; i.e., a type II error in which the beneficial effect 137