Endoscopic Electrocoagulation in the Management of Upper Gastrointestinal Tract Bleeding

Endoscopic Electrocoagulation in the Management of Upper Gastrointestinal Tract Bleeding

Symposium on Surgical Endoscopy of the Gastrointestinal Tract Endoscopic Electrocoagulation in the Management of Upper Gastrointestinal Tract Bleedin...

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Symposium on Surgical Endoscopy of the Gastrointestinal Tract

Endoscopic Electrocoagulation in the Management of Upper Gastrointestinal Tract Bleeding

john P. Papp, M.D.*

Radio frequency electrical current has been used by surgeons to produce heating, coagulation, and hemostasis for more than 50 years. However, it was only in 1965 that Siegel and Dunn described the mechanism of blood vessel closure by high frequency electrocoagulation (coaptation). 28 The physical features of coaptation were described by Siegel and Hatke in 1967. 29 Shortly thereafter, fiberoptic endoscopes were developed and lengthened, allowing the endoscopist to view with one instrument the esophagus, stomach, and duodenum. Concomitantly, electrodes were developed to pass through the biopsy channel of the new fiberoptic endoscopes. These developments provided the endoscopist the ability to perform electrocoagulation in the upper gastrointestinal tract. The decade of the 1970s saw an unprecedented awakening in endoscopic research in the laboratory and in the clinical application of new therapeutic modalities. Three methods of electrocoagulation have been studied, (1) monopolar electrocoagulation, (2) fulguration, and (3) bipolar electrocoagulation. These methods to produce coaptation are influenced by (1) the length of the coagulation, (2) the setting of the power source, (3) the pressure of contact, (4) the milieu of activation of the electrode, and (5) the amount of impedance. It is important to understand the difference between these modalities. The word "coagulation" can mean either fulguration or desiccation. Fulguration is defined as applying sparks to tissues to produce necrosis without a cutting effect. Electrosurgical desiccation is defined as necrosing tissue by directly applying the electrosurgical electrode to the tissue so that no sparking and no cutting occur. An electrosurgical electrode can fulgurate if it is sparked above tissue and it can desiccate if pressed firmly against moist tissue. Electrosurgical principles in gastrointestinal endoscopy have recently been reviewed by me. 22 The main difference between monopolar electro*Associate Clinical Professor of Medicine, Michigan State University College of Human Medicine; Director, Endoscopy Unit, Blodgett Memorial Medical Center, Grand Rapids, Michigan

Surgical Clinics of North America-Yo!. 62, No. 5, October 1982

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JOHN P. PAPP

coagulation and bipolar electrocoagulation is that monopolar electrocoagulation produces a greater depth of desiccation. Experimental evaluation of monopolar electrocoagulation was first reported by Blackwood and Silvis using the Bovie electrosurgical unit and subsequently the Cameron-Miller electrosurgical unit. 2• 3 My colleagues and I also evaluated the effects of monopolar electrocoagulation on dog esophageal, gastric, and duodenal mucosa using varying times and settings on the Cameron-Miller coagulation unit (ModelB0--7051). 24• 25 The safest settings were 5 to 5.5 for one or two second applications. No area was repeatedly coagulated. The depth of injury did not correlate with the visual size of the ulcer produced. More than three seconds of electrocoagulation at a setting of 5 or higher in the esophagus resulted in transmural necrosis. In contrast, Mann and Mann found no transmural injury to the esophagus at setting 5 for .one, three, and five second applications. 14 Computer-assisted electrocoagulation in canine gastric bleeding ulcers was disappointingly not helpful. Excessively deep injury of the gastric wall was reported by Piercey et al. 26 Dennis et al. studied the safety and efficacy of using electrofulguration to control bleeding from standard canine experimental ulcers. 4 They found electrofulguration to be effective, but tissue injury was unpredictable and deep. Bipolar electrocoagulation in dogs has less depth of injury when compared with monopolar electrocoagulation. 16• 27 Further development has not seemed practical because precise placement of the two electrode tips is required to produce hemostasis. A probe made by ACMI (Stamford, Connecticut) has recently been designed to take advantage of minimal tissue injury produced during coagulation by the bipolar modality. The probe is called the BICAP (bipolar circumactive probe). There are six equally spaced longitudinal microelectrodes along the sides and over the tip. The power unit incorporates a water pump allowing a powerful water jet to be delivered out of the tip of the probe to clear the targeted area. Since the electrodes cover the tip as well as the sides, a lesion may be approached directly, tangentially, or obliquely. Auth et al. reported effective hemostasis in canine ulcers with minimal injury at a setting of 7 for one second. 1 Because of the lower power output, a visible vessel may theoretically be directly electrocoagulated without fear of disruptiQn and subsequent increased bleeding. A cooperative study is currently being conducted in Europe and the United States to determine the clinical effectiveness of the probe in patients with actively bleeding lesions of the upper gastrointestinal tract. Successful electrocoagulation can be performed only if the endoscopist can see the area of bleeding. Therefore, the stomach must be cleared of blood and clots. Prior to endoscopy, an Edlich gastric lavage tube is passed into the stomach. Two or more liters of saline are used to lavage the stomach. Thereafter the patient is sedated as necessary with intravenous diazepam. If no lesion is seen in the esophagus, the endoscope is passed along the lesser curvature of the stomach into the duodenum. If no duodenal site for bleeding is found, the endoscope is withdrawn into the stomach for delineation of the cause of bleeding. Electrocoagulation should not be attempted if torrential bleeding is present. Electrocoagulation should not be used on esophageal varices. If an arterial vessel is seen to be actively

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Figure 1. The monopolar electrode is placed near the arterial vessel and moved circumferentially, applying electrocoagulation until the bleeding stops.

bleeding, or if a non-bleeding vessel is seen, one of three techniques of applying electrocoagulation may be used. The techniques of Gaisford8 and Fruhmorgen et al. 7 are almost the same. However, Gaisford uses saline· and Fruhmorgen distilled water. Fruhmorgen' s technique is called the electro-hydro-thermo-electrode technique. Matek et al. 15 modified Fruhmorgen's electrode by adding a spring mechanism, which allows the contact pressure of the electrode to remain almost constant. My technique differs from those of the physicians just mentioned. Once the actively bleeding vessel is seen, the Cameron-Miller monopolar electrocoagulation electrode is placed within 2 to 3 mm of the vessel and moved around the vessel in a circular manner so that electrocoagulation is applied for 2 to 2¥2 seconds until the bleeding stops (Fig. 1). Four to six applications may be necessary at a setting of 5 on the Cameron-Miller electrocoagulation unit. The amount of joules used varies with the size of the vessel, the amount of impedance, how often the electrode is cleaned, and whether the electrode is activated while going through blood to touch the area around the vessel or whether it is activated when on tissue. The smaller the vessel, the less the amount of joules required. Vessels between 1 and 2 mm may require from 104 to 134 joules of energy per application. 23 It is important to remember that electrocoagulation produces high amounts of energy, which, when applied to a vessel directly, will result in destruction of the vessel and further bleeding. This is in contrast to the multipolar probe (BICAP), which uses only 14 joules per application. The principle in my method is that electrocoagulation causes coaptation of the arterial vessel in the muscular and submucosal layers of the bowel wall. Therefore, more energy penetration is required than with the multipolar probe .

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CLINICAL EXPERIENCE Since 1971, 610 patients with acute bleeding in the upper gastrointestinal tract have had endoscopy by me within six hours of their admission to Blodgett Memorial Medical Center to evaluate the cause of bleeding. Of these patients, 329 had ulcer disease, as follows: 188 duodenal, 120 gastric, 19 marginal, and 2 esophageal. Thirty-five patients (18.6 per cent) and 31 patients (25. 8 per cent) had actively bleeding arterial vessels in their duodenal and gastric ulcers, respectively. These data are very similar to those in the national American Society for Gastrointestinal Endoscopy (ASGE) study, in which 29.8 per cent and 22.5 per cent of duodenal and gastric ulcers, respectively, were actively bleeding. Ninety-five patients over a nine-year period have been treated in a consecutive but uncontrolled series with monopolar electrocoagulation. All patients with active bleeding seen by me were included in the series. Some of this experience has been previously reported. 18-21 No patient was excluded because of age, medical illness, or unsuccessful electrocoagulation. Except for eight patients with arteriovenous malformations that were not actively bleeding and one patient with intermittent bleeding from a gastric varix, all others had lesions with arterial pumping vessels, as follows: 31 gastric ulcers, 6 marginal ulcers, 35 duodenal ulcers, 12 Mallory-Weiss tears, and 2 esophageal ulcers. When a clot of blood has swirling blood beneath it, the coagulation probe is placed into the clot and coagulated so that the clot becomes attached to the probe and can be effectively removed from the area requiring treatment. In this series, I used the Olympus GIF-D3 and GIF-1T endoscopes with the Cameron-Miller flexible suction coagulator electrode and coagulation unit. All patients underwent gastric lavage via an Edlich tube with iced saline. Of the 86 patients with active bleeding, eight had unsuccessful attempts at electrocoagulation (2 Mallory-Weiss and 6 duodenal ulcers) because of torrential hemorrhage obscuring vision or because of inability to place the probe near the bleeding vessel owing to anatomic location. Surgical treatment in the eight patients confirmed the endoscopic diagnosis. Of the remaining 78 patients, 10 rebled (5 duodenal and 5 gastric ulcers). Four had successful reelectrocoagulation. Five patients had surgery. One patient continued to bleed despite surgery and died. One patient had a cardiac arrest prior to surgery and died. Excluding those patients with active bleeding that have had surgery or died, 72 patients have been followed for an average of 4.2 years. Only two patients have had recurrent bleeding after leaving the hospital (three and five years). Both were found to have developed duodenal ulcers while on aspirin treatment for arthritis. Both patients had a visible vessel, which was electrocoagulated with no further bleeding. The average age of patients with gastric ulcers was 64 and that of patients with duodenal ulcers was 70. About one half of these patients had serious medical problems during their hospitalization that required admission to an intensive care unit. Nine of the 86 patients have died, but none of the deaths were the result of successfully electrocoagulated vessels causing bleeding. Five died from other medical problems, and one patient

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continued to bleed despite surgery, resulting in a mortality of 7.1 per cent. Three patients died several months after hospitalization from carcinomatosis. The mortality of 7.1 per cent compares favorably with other reports, in which 20 to 50 per cent mortality occurred in patients over the age of 60 with upper gastrointestinal tract hemorrhage. 10 It is important to point out that in my series all the patients would have been referred to surgery for treatment had not electrocoagulation been performed. No morbidity or mortality occurred as a result of electrocoagulation. In addition, in retrospective analysis, the cost and length of hospitalization were found to be reduced in those patients treated by electrocoagulation. 24 The published experience in the United States of Gaisford, 8 Sugawa, 30 Volpicelli, 32 and me totals 178 patients treated by electrocoagulation in an uncontrolled series. A combined success of 88 per cent on the first attempt to stop bleeding was reported. In a European survey, a 70 per cent success rate was reported in 314 patients with actively bleeding lesions, but 5 perforations were reported. Wara et al. reported an 81 per cent success rate using monopolar electrocoagulation and simultaneous irrigation. 33 Koch et al. early in the development of electrocoagulation as a therapeutic modality reported 1 death and 3 perforations in 15 patients. 12 The patient with the bleeding gastric varix was the first patient in my series and has been described previously. 17 The eight patients with either gastric or duodenal arteriovenous malformation had an average age of 76 and an average blood replacement of 14 units prior to successful management by electrocoagulation. Some lesions could be treated at one sitting, and others required two to four sittings. The electrode was always initially placed along the margins of the malformations and moved circumferentially. At subsequent sittings, the electrode is placed more centrally. Similar success with monopolar electrocoagulation of gastric arteriovenous malformations has been reported by other authors. 34· 35 The electrode is never initially placed centrally on the lesions, for massive bleeding may occur.

THE VISIBLE VESSEL It has been reported that bleeding in nonsurgically treated patients with ulcer disease may range from 25 to 75 per cent. 5 • 13 Foster et al. reported that gastric and duodenal ulcers bearing the stigmata of recent hemorrhage (fresh bleeding, fresh or altered blood clot or black slough adherent to the lesion, or a vessel protruding from the base or margin of an ulcer) had an incidence of recurrent bleeding of 30 to 56 per cent and required emergency surgery in 45 and 63 per cent of their series, respectively. 6 Jones et al. in a series of 229 cases of further hemorrhage after admission to a hospital reported a mortality of 28.8 per cent. 11 In an attempt to determine the significance of the visible vessel in an ulcer in patients having had an acute hemorrhage in the upper gastrointestinal tract, I reviewed six years of experience (1972-1977) and found that four of every five visible vessels had recurrent bleeding. Therefore, a prospective randomized study was begun in 1977 to evaluate how often the visible vessel treated medically will r~bleed and whether prompt electro-

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coagulation would reduce the incidence of recurrent bleeding. Cost and length of hospitalization were also compared. Between 1977 and 1979, 181 patients with acute upper gastrointestinal tract bleeding not due to varices or active arterial bleeding had endoscopic evaluation. Ulcer disease was found in 103 patients. The criteria for acute bleeding included a history .of hematemesis, melena, or hematochezia of less than 24 hours documented by a bloody nasogastric aspirate or a stool specimen positive for gross or occult blood. Fifty-three patients were seen initially in the emergency room. The remainder were already hospitalized, either on the general floors or in various intensive care units. Endoscopy of the upper gastrointestinal tract was performed on all patients within six hours of admission with the Olympus GIF -1 T endoscope. Prior to endoscopy, an Edlich gastric lavage tube was passed and the stomach was lavaged with iced saline. Intravenous diazepam was given as necessary for sedation. Contraindications to entry into the study included pregnancy, cirrhosis with or without varices, coagulopathy, perforated viscus, acute myocardial infarction, and more than one lesion that could cause upper gastrointestinal tract bleeding. Patients were eligible for entry into the study if there were no contraindications and if a visible vessel was seen, was not bleeding and did not have a clot. The vessel had to be protruding from the ulcer bed and characterized as circular in shape, having both width and height. All vessels were measured by the ACMI marker (7036B). Approval for this study was obtained from the Blodgett Hospital Human Research Committee. Opaque sealed envelopes were used, assigning patients either to immediate electrocoagulation with concomitant cimetidine and magnesium hydroxide treatment or to medication (cimetidine plus magnesium hydroxide) alone. The cimetidine was given intravenously (300 mg) every 6 hours, and the magnesium hydroxide, 45 ml four times a day, was given for 48 hours. If the patient remained stable, food was then given and advanced as tolerated. Mter endoscopy, the patients were managed by their own physicians in an intensive care unit. Recurrent bleeding was defined as the onset of hematemesis after endoscopy, a drop in systolic pressure greater than 25 mm Hg, and increased rectal bleeding. Endoscopy was repeated on all patients suspected of recurrent bleeding to confirm the occurrence of bleeding and the site. Meticulous care was used in placing the electrode near the visible vessel, usually a distance of 3 mm from the vessel. The probe was moved around the vessel in a circular manner while the foot pedal was activated on the Cameron-Miller coagulator unit. Each application was coagulated for two to three seconds at a setting of 5. Firm but giving pressure was applied. No area received more than one application. The vessel is never directly electrocoagulated, for destruction of the vessel results in active bleeding. Of the 103 patients with ulcer disease eligible for this study between 1977 and 1979, 32 were found to have a visible vessel. Sixteen patients were randomized to a control group. Seven had gastric ulcers and nine had duodenal ulcers. Patients in the gastric ulcer control group had an average age of 61. The ulcers ranged in size from 0.5 to 2 em and vessels from 1 to 3 mm in diameter. All vessels were central in the gastric ulcers. Six of the

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ENDOSCOPIC ELECTROCOAGULATION IN GASTROINTESTINAL BLEEDING

seven control patients rebled in 8 hours to 20 days (8 hours, 8 hours, 12 hours, 26 hours, 38 hours, and 20 days). Three were referred to surgery after documentation of rebleeding and three had electrocoagulation with cessation of bleeding. One patient with a 1 mm vessel did not rebleed. No deaths occurred. Nine control patients with an average age of 62 had duodenal ulcers ranging in size from 1 to 3 em with vessels 1 to 3 mm in diameter. Four were central and five near the rim of the ulcer. Seven vessels rebled from 4 hours to 5 days in seven patients (4 hours, 5 hours, 7 hours, 12 hours, 24 hours, 36 hours, 5 days). Two patients with 1 mm vessels near the rim did not have recurrent bleeding. Because of recurrent bleeding, six patients had a vagotomy and pyloroplasty with oversewing of the vessel. One patient continued to bleed despite surgery and died five days postoperatively. One patient was treated with electrocoagulation with cessation of bleeding. Sixteen patients were randomized to treatment with electrocoagulation as soon as the visible vessel was identified. Ten patients with an average age of 58 had gastric ulcers ranging in size from 0.5 to 3 em with vessel diameters ranging in size from 1 to 3 mm. Nine vessels were central and one near a rim. One patient with a 2 mm central vessel had recurrent bleeding after three days requiring surgery. The ulcer was high in the fundus and technically difficult to electrocoagulate. None of the remaining nine treated gastric ulcer vessels rebled. Six treated patients with an average age of 53 had duodenal ulcers ranging in size from 1 to 2 em. The vessels were 1 to 3 mm in diameter. Three vessels were central and three near the rim. After electrocoagulation, none of the vessels rebled in the patients with duodenal ulcers. No patients died or experienced morbidity from electrocoagulation (Table 1). All of the patients in the group receiving electrocoagulation, except the one patient who had recurrent bleeding, had follow-up endoscopy after eight weeks. All were found to have complete healing of their ulcer disease. They were on varying programs of antacids and cimetidine. These patients

Table I.

Randomized Trial of Electrocoagulation of Visible· Vessels

RECURRENT

Control Gastric ulcer Duodenal ulcer Coagulated Gastric ulcer Duodenal ulcer

AVERAGE

NO. OF

HEM OR-

SURG-

COAGU-

PTS.

RHAGE

ERY

LATION

16

13/16

7

6n

3/6

3/6

on

9

7/9

6/7

117

119

16

1116

10

1110

1/1

0/10

0/10

6

0/6

0/6

0/6

0/6

DEATH

HOSPITAL

TOTAL

DAYS

COST

LAB.

18.5*

$5709*

$2445*

8.3

$3157

$ 712

*Average hospitalization and costs of nine patients who underwent surgery.

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JOHN P. PAPP

have been followed for an average of 26 months without recurrence of ulcer symptoms or bleeding. In the control group, the three patients who did not have rebleeding had an average hemoglobin level of 8. 9 gm per 100 mi. They received 3 units of blood each. The 13 control patients who rebled had an average hemoglobin level of 9.1 gm per 100 ml just before surgery and 8. 8 gm per 100 ml just prior to electrocoagulation. They received an average of 6 units of blood prior to surgery or electrocoagulation. In the group treated immediately by electrocoagulation, hemoglobin values averaged 9 gm per 100 ml just before endoscopy. They received 3 units of blood each during their hospitalization.

COST AND LENGTH OF HOSPITALIZATION In the randomized control group of 16 patients in this study, 3 patients did not have recurrent bleeding. They were hospitalized an average of 8.3 days. Their total hospital costs averaged $2323, and laboratory costs averaged $721. There were 13 patients with recurrent bleeding in the control group. Four were treated by electrocoagulation. They were hospitalized an average of 13.2 days and had average total and laboratory costs of $4342 and $842, r~spectively. The remaining nine control patients had surgery. They were hospitalized for an average of 18.5 days and sustained an average cost of $5709 and an average laboratory cost of $2445. Those patients who received immediate electrocoagulation were hospitalized an average of 8.3 days. Their average total and laboratory costs were $3157 and $712, respectively. The foregoing costs represent 1977-1979 costs at Blodgett Memorial Medical Center and have not been adjusted to reflect inflation. No physicians' fees are included in the data.

DISCUSSION This study shows that 13 of 16 control patients (81 per cent) with a visible vessel rebled at times varying from 4 hours to 20 days, whereas only 1 (6 per cent) of.16 patients rebled after treatment with electrocoagulation. This study emphasizes that patients with a visible vessel are at a high risk of recurrent bleeding and that -electrocoagulation is effective in preventing rebleeding safely and without morbidity or mortality. These prospective data support Griffiths' retrospective data, which reported recurrent bleeding in 24 of 28 patients with a visible vessel, 9 and Vall on et al., who could not prevent rebleeding from the visible vessel with the argon-ion laser. 31 In the group treated by electrocoagulation compared with the control group treated by either surgery or electrocoagulation after recurrent bleeding, the hospital stay was reduced by an average of 7.6 days, the total cost averaged $1868 less; and the laboratory cost averaged $801 less. Electrocoagulation in patients who experienced rebleeding resulted in a shorter hospital stay by .an average of 5.3 days. Total cost averaged $1367 less and

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laboratory cost averaged $1603 less. Patients with a visible vessel were hospitalized a mean of 23 days in Griffiths' study, 9 suggesting a benefit of electrocoagulation in reducing hospitalization by 56 per cent in those immediately electrocoagulated after rebleeding when compared with patients requiring surgery. This study demonstrates that patients with a visible vessel after bleeding will have rebleeding in the majority of instances (81 per cent) and that monopolar electrocoagulation is 94 per cent effective in the prevention of rebleeding. Monopolar electrocoagulation of the visible vessel is valuable as the primary therapeutic modality to prevent further bleeding.

CONCLUSION The combined European and American success rate with monopolar electrocoagulation in producing hemostasis in several uncontrolled series of patients with arterial bleeding has been between 70 and 88 per cent. The patient with a visible ulcer vessel will rebleed in four out of five cases in a controlled series. Monopolar electrocoagulation prevents rebleeding in 94 per cent of the treated group of patients. Cost and length of hospitalization were reduced in the uncontrolled and controlled series herein reported. Monopolar electrocoagulation should be part of the endoscopist's armamentarium when the treatment of the patient with upper. gastrointestinal tract hemorrhage is undertaken.

R-EFERENCES 1. Auth, D. C., Gilbert, D. A., Apie, E. A., et al.: The multipolar probe-a new endoscopic technique to control gastrointestinal bleeding. Gastrointest. Endosc., 26:63, 1980 (abstr.). 2. Blackwood, W. D., and Silvis, S. E.: Gastroscopic electrosurgery. Gastroenterology, 61:305, 1971. 3. Blackwood, W. D., and Silvis, S. E.: Standardization of electrosurgicallesions. Gastrointest. Endosc., 21:22, 1974. 4. Dennis, M. B., Peoples, J., Hulett, R., et al.: Evaluation of electrofulguration in control of bleeding experimental gastric ulcers: Dig. Pis. Sci., 24:845, 1979. 5. Donaldson, R. M., Jr., Hardy, J., and Papper, S.: Five-year follow-up study of patients with bleeding duodenal ulcer with and without surgery. N. Engl. J. Med., 259:201, 1958. . 6. Foster, D. N., Miloszewski, K. J. A., andLosowsky, M.S.: Stigmataofrecenthemorrhage in diagnosis and prognosis of upper gastrointestinal bleeding. Br. Med. J., 1:1173, 1978. 7. Fruhmorgen, W. M., Kaduk, B., Reidenbach, H. D., et al.: Modified electrocoagulation and its possibilities in the control of gastrointestinal bleeding. Endoscopy, 4:253, 1979. 8. Gaisford, W. D.: Endoscopic electrohemostasis of active upper gastrointestinal bleeding. Am. J. Surg., 137:47, 1979. 9. Griffiths, W. J., Neumann, D. A., and Welsh, J. D.: The visible vessel as an indicator of uncontrolled or recurrent gastrointestinal hemorrhage. N. Engl. J. Med., 300:1411, 1979. 10. Himal, H. S., Watson, W., Jones, C. W., et al.: The management of upper gastrointestinal hemorrhage. Ann. Surg., 179:489, 1972. 11. Jones, P. F., Johnston, S. J., McEwan, A. B., et al.: Further hemorrhage after admission to hospital for gastrointestinal hemorrhage. Br. J. Med.,3:660, 1973. 12. Koch, H., Pesch, H. J., Bauerle, H., et aL: Experimentelle Untersuchungen und klinische

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16. 17. 18. 19. 20. 21. 22. 23.

24. 25. 26.

27.

28. 29. 30. 31. 32.

33. 34.

35.

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Erfahrungen zur Electrokoagulation blutende Lasionen im oberen Gastrointestinaltrakt. Fortschr. Endoskop., 10:67, 1972. Malt, R. A.: Control of massive upper gastrointestinal hemorrhage. N. Engl. J. Med., 286:1043, 1972. Mann, S. K., Mann, N. S.: Effect of monopolar electrocoagulation on esophagus, stomach, and duodenum in dogs. Am. J. Gastroenterol., 71:568, 1979. Matek, W., Fruhmorgen, P., Kaduk, B., eta!.: The healing process of experimentally produced bleeding lesions after hemostatic electrocoagulation with simultaneous instillation of water. Endoscopy, 12:231, 1980. Moore, J.P., Silvis, S. E., and Venues, J. A.: Evaluation of bipolar electrocoagulation in canine stomachs. Gastrointest. Enclose., 24:148, 1978. Papp, J. P.: Endoscopic electrocoagulation in upper gastrointestinal hemorrhage: A preliminary report. J.A.M.A., 230:1172, 1974. Papp, J. P. : Endoscopic electrocoagulation of upper gastrointestinal hemorrhage. J. A.M. A., 236:2076, 1976. Papp, J. P.: Endoscopic electrocoagulation of actively bleeding arterial upper gastrointestinal lesions. Am. J. Gastroenterol., 71:516, 1979. Papp, J. P.: Electrocoagulation of actively bleeding Mallory-Weiss tears. Gastrointest. Enclose., 26:128, 1980. Papp, J. P.: Electrocoagulation in upper gastrointestinal bleeding. Dig. Dis. Sci., 26:41s, 1981. Papp, J. P.: Endoscopic Control of Gastrointestinal Hemorrhage. Boca Raton, Florida, CRC Press, 1981. Papp, J. P., Auth, D. C., and Silverstein, F. E.: Analog computer evaluation of monopolar electrocoagulation in patients having had UGI bleeding. Gastrointest. Enclose., 26:73, 1980 (abstr.). Papp, J. P., Fox, J. M., and Nalbandian, R. M.: Experimental electrocoagulation of dog esophageal and duodenal mucosa. Gastrointest. Enclose., 23:27, 1976. Papp, J.P., Fox, J. M., and Wilks, H. S.: Experimental electrocoagulation of dog gastric mucosa. Gastrointest. Enclose., 22:27, 1975. Piercey, J. R. A., Auth, D. C., Silverstein, F. E., et a!.: Electrosurgical treatment of experimental bleeding canine gastric ulcers; development and testing of a computer control and better electrode. Gastroenterology, 74:527, 1978. Protell, R. L., Gilbert, D. A., Jensen, D. M., eta!.: Computer assisted electrocoagulation: Bipolar vs monopolar in the treatment of experimental gastric ulcer bleeding. Gastroenterology, 76:1221, 1979 (abstr.). Siegel, B., and Dunn, M. R. : The mechanism of blood vessel closure by high frequency electrocoagulation. Surg. Gynecol. Obstet., 121:823, 1965. Siegel, B., and Hatke, F. L.: Physical factors in electrocoagulation of blood vessels. Arch. Surg., 95:54, 1967. Sugawa, C., Shier, M., Lucas, C. E., et al.: Electrocoagulation of bleeding in the upper part of the gastrointestinal tract. Arch. Surg., 110:975, 1975. Vallon, A. G., Cotton, P. B., Alurence, B. H., et al.: Randomised trial of endoscopic argon laser photocoagulation in bleeding peptic ulcers. Gut, 22:228, 1981. Volpicelli, N. A., McCarthy, J. D., Bartlett, J. D., et al.: Endoscopic electrocoagulation: An alternative to operative therapy in bleeding peptic ulcer disease. Arch. Surg., 113:483, 1978. Wara, P., Hojsgaard, A., and Amdrup, E.: Endoscopic electrocoagulation-an alternative to operative hemostasis in active gastroduodenal bleeding. Endoscopy, 12:237, 1980. Weaver, G. A., Wilk, H. E., and Olson, J. E.: Successful endoscopic electrocoagulation of gastric lesions of hereditary hemorrhagic telangiectasia responsible for repeated hemorrhage. Gastrointest. Enclose., 27:181, 1981. Weingart, J., Lux, G., Elster, K., et al.: Recurrent gastrointestinal bleeding in Osler's disease successfully treated by endoscopic electrocoagulation in the stomach. Endoscopy, 7:160, 1975.

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