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Perforated Duodenal Ulcer an Alternative Therapeutic Plan

Perforated Duodenal Ulcer an Alternative Therapeutic Plan

SPECIAL ARTICLE Perforated Duodenal Ulcer An Alternative Therapeutic Plan

Arthur J. Donovan, MD; Thomas V. Berne, MD; John A. Donovan, MD

n alternative plan for the treatment of a perforated duodenal ulcer is proposed. We will focus on the now-recognized role of in the genesis of the ma- jority of duodenal ulcers and on the high rate of success of therapy with a combina-

tion of antibiotics and a proton-pump inhibitor or histamine2 blocker in treatment of suchA ulcers. Knowledge that half the cases of perforated duodenal ulcer may have securely sealed spontaneously at the time of presentation is incorporated in the therapeutic plan. Patients with a perforated duodenal ulcer who have already been evaluated for H pylori and are not infected or, if infected, have received appropriate therapy should undergo an ulcer-definitive operation if they are suitable surgical candidates. Most authorities recommend surgical closure of the perforation and a parietal cell . The remaining patients should have a gastroduodenogram with water- soluble contrast medium. If the perforation is sealed, the patient can be treated nonsurgically. If the perforation is leaking, secure surgical closure of the perforation is necessary. Following recov- ery from the immediate consequences of the perforation, evaluation for H pylori should be con- ducted. If the patient is infected, combined medical therapy is recommended. If the patient is not infected, Zollinger-Ellison syndrome should be ruled out and medical therapy is recommended if the ulcer has not been treated previously. Elective ulcer-definitive surgery should be considered for the occasional uninfected patient who has already received appropriate medical therapy for the ulcer. Arch Surg. 1998;133:1166-1171 When a duodenal ulcer perforates into the tral role in the genesis of peptic ulcer.1 In , there are 3 components almost all instances, duodenal ulcer is a of the resulting clinical syndrome that curable infectious disease. One should as- should be considered in developing a ra- sume that a duodenal ulcer is associated tional plan of treatment. These are the ul- with infection with H pylori until it is oth- cer, the perforation, and the resulting peri- erwise proven. Almost all of the excep- tonitis. This article proposes a therapeutic tions will be in the group of cases associ- plan based on existing knowledge of these ated with the use of nonsteroidal anti- 3 areas. This plan would be an alternative inflammatory drugs (NSAIDs),1-3 and in to current surgical practice. This discussion cases with severe hypersecretion, such as will concern duodenal and juxtapyloric ul- the Zollinger-Ellison syndrome. cer and exclude other gastric ulcers. A high percentage of H pylori infec- tion has been reported in patients with per- THE ULCER forated duodenal ulcer. Ng et al4 reported that 51 (70%) of 73 cases of perforated duo- In recent years, it has been proven that denal ulcer were infected with H pylori.If Helicobacter pylori infection plays a cen- NSAID users were excluded, the number rose to 58 (80%). Sebastian et al5 reported From the Department of Surgery, University of Southern California, Los Angeles a positive radioactive carbon 13 urea breath (Drs A. J. Donovan and Berne); and the Division of , Southern test, a reliable indicator of H pylori infec- California Permanente Medical Group, Los Angeles (Dr J. A. Donovan). tion, in 24 of 29 cases of perforated peptic

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 ulcer. Tokunaga et al6 reported H pylori in 92% of cases of of the to some of the surrounding viscera, and perforated ulcer. The tissue density of infection was greater in these instances the contents of the stomach do not es- with perforation than with hemorrhage or obstruction. cape into the .” Wangensteen13 recognized the Appropriate antibiotic treatment results in eradica- process of self-sealing of a perforated ulcer and in 1935 tion of H pylori infection in more than 90% of cases.1,7 reported 7 cases treated nonsurgically. Reinfection with H pylori is rare. Current therapy of duo- Little further interest was expressed in nonsurgical denal ulcer associated with H pylori combines the use of treatment of perforated duodenal ulcer until the report of 14 antibiotics and proton-pump inhibitors or histamine2 (H2) Taylor in 1946. At the time of surgery, he had observed blockers. This combined medical therapy reduces the re- that cases of perforated duodenal ulcer were often al- lapse rate by at least 90% compared with that experi- ready sealed. The seal was usually by apposition of the per- enced with H2 blockers or proton-pump inhibitors alone; foration to the undersurface of the quadrate lobe of the ie, customary medical therapy.1,7,8 A consideration of tech- between the fossa and the falciform liga- niques for diagnosis of infection with H pylori and of de- ment. He selected 28 typical cases of perforated duodenal tails of combined medical therapy of duodenal ulcer as- ulcer with overt for nonsurgical treatment. In sociated with H pylori is beyond the scope of this essay. his opinion, effective gastric decompression and continu- These observations regarding H pylori render inap- ous drainage was of critical importance in this method of propriate former attempts to distinguish between an acute treatment. He believed that continuous drainage induced and chronic duodenal ulcer based on duration of symp- self-sealing. Among his 28 cases, 24 patients had an un- toms. Helicobacter pylori is the dominant clinical deter- eventful recovery, 3 patients died of causes other than the minant. With the exception of cases associated with consequences of the perforation, and 1 patient died con- NSAIDs, the ulcer will usually reflect infection with sequent to the perforation. H pylori, irrespective of the duration of symptoms. Seeley and Campbell15 reported a series of cases of young American military personnel treated nonsurgi- THE PERFORATION cally with excellent results. That article and others, in- cluding a recent randomized trial by Crofts et al,16 have The first and only mandatory obligation of the surgeon supported the efficacy of nonoperative treatment in se- is to eliminate peritoneal soilage through the perfora- lected cases. Nevertheless, the nonsurgical approach has tion. This can be achieved either by surgical closure or not been generally accepted by surgeons because of con- by self-sealing of the perforation. cern as to the presence and reliability of self-sealing, the excellent immediate results achieved with the Graham Surgical Closure closure, and the attractiveness of an immediate defini- tive therapy. The most accepted method of surgical closure of the per- In the mid 1950s, interest in nonsurgical treatment foration is the so-called Graham patch. In 1937, Graham9 of perforated duodenal ulcer was rekindled at the Uni- described the placement of through-and-through sutures versity of Southern California under the aegis of Clar- at the site of perforation that were tied over a free graft of ence J. Berne, MD, and Leonard Rosoff, Sr, MD. They ob- omentum. This technique has been modified and today sur- served that a surgeon could be unblinded as to presence geons generally close the perforation either with through- or absence of a spontaneous seal by performing a gas- and-through sutures (abutment) or with interrupted Lem- trodenogram with water-soluble contrast media.17 Ra- bert sutures (plication) and then place an omental pedicle diograms of a gastroduodenogram revealing a duodenal graft over the closure. We tack the graft over the closure ulcer that perforated and sealed spontaneously are shown rather than incorporate the omentum in the ends of the su- in Figure 1. tures that have been used to close the perforation. The lat- Criteria for spontaneous sealing are filling of the duo- ter step invites strangulation of the omentum. A more re- denum, demonstration of an ulcer, and lack of spillage cent development has been the introduction of laparoscopic of the media into the peritoneal cavity. Failure to dem- techniques for closure of the perforation.10 onstrate spillage, in the absence of filling of the duode- The modified Graham technique has been extraordi- num, cannot be accepted as evidence for self-sealing. Py- narily effective. Failure of the modified Graham closure is loric spasm may, on occasion, preclude duodenal filling generally limited to cases of perforation of the most se- and mask a freely leaking perforation.11 verely scarred and distorted duodenum or of a saddle ul- For almost a decade beginning in the late 1950s, pa- cer that has extended from the posterior wall of the duo- tients with a diagnosis of perforated ulcer admitted to the denum anterosuperiorly. Failure is defined as early Los Angeles County–University of Southern California postoperative reperforation, obstruction, and/or hemor- Medical Center were hemodynamically stabilized and rou- rhage. When such severe disease is encountered during sur- tinely underwent a gastroduodenogram. A satisfactory gas- gery, a more aggressive surgical procedure, such as pylo- troduodenogram was obtained in more than 90% of the roplasty or an antral resection, is strongly recommended.11 cases. Among 377 cases with a satisfactory gastroduo- . denogram, self-sealing was documented in 162 (43%).18 With rare exception, these patients who had self-sealing Self-Sealing ulcers also had overt peritonitis. They were not cases of forme fruste perforation, a condition described by Singer In 1843, Crisp12 noted that, in perforations of the stom- and Vaughn.19 The latter are cases with sudden abdomi- ach, “occasionally the aperture is filled up by adhesion nal pain and pneumoperitoneum, but without or with

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 No Spill Ulcer

Air

Figure 1. Left, Radiogram demonstrates free subdiaphragmatic air. Right, Radiogram from a gastroduodenogram in the same patient demonstrates a duodenal ulcer without extraluminal spillage of contrast media. The perforation of the ulcer has sealed spontaneously. Reprinted from Ann Surg 1979;189:627-636.

minimal sign of peritonitis. The perforation is sealed be- ment was 3%.11,20,22 These results in patients with nonsur- fore anything other than air has a chance to leak into the gical treatment are equal or better than the record in pa- peritoneal cavity. tients with surgical closure of the perforation. The 2 pa- A subsequent small study by Donovan et al20 and tient cohorts are not similar and should not be compared information provided by Li21 further support the fact that directly. about half of the cases of duodenal ulcer with perfora- Thus, based on our experience, it may be concluded tion will be self-sealed when the patient is admitted to that self-sealing will occur with high frequency in cases of the hospital. The initial clinical examination is unreli- perforated duodenal ulcer and that the presence of self- able in predicting which patients with perforation and sealing can be reliably established by a gastroduodeno- peritonitis will have a sealed perforation. Massive pneu- gram with water-soluble contrast media. Nonsurgical treat- moperitoneum is likely to be associated with a non- ment of the patient with self-sealing can be undertaken with sealed perforation. Surgeons do not generally believe that the assurance that the seal will be secure and that the in- their surgical experience supports such a high inci- cidence of septic intra-abdominal complications will be very dence of self-sealing. Undoubtedly, as Taylor14 sug- low. This option is particularly attractive in a case consid- gested, the self-seal is inadvertently broken in the pro- ered to be at high surgical risk because of age and/or asso- cess of surgical exposure. ciated disease.22 A surgical procedure performed to close When spillage of contrast media is demonstrated, the an already-sealed perforation is unnecessary. media may flood the peritoneal cavity, course along the undersurface of the liver, or be shunted into the right lower THE PERITONITIS quadrant. Localization of gastroduodenal contents in the latter area may mimic the signs of acute . Oc- Perforation of a duodenal ulcer allows egress of gastric casionally, the extraluminal contrast may be localized to and duodenal contents into the peritoneal cavity with a the area adjacent to the perforation—a collar-button leak.11 resulting initial chemical peritonitis. If there is continu- The process of self-sealing is a dynamic one. We believe ing leakage of gastroduodenal contents, bacterial con- that a collar-button leak represents a late stage in this pro- tamination of the peritoneal cavity can occur. The peri- cess. A second gastroduodenogram shortly after demon- toneum that is compromised by the chemical peritonitis stration of such a restricted spillage may reveal a com- is an inviting target for opportunistic bacterial contami- plete seal. We have not hesitated to treat a patient with a nation. The relatively small size of the perforation gen- collar-button leak nonsurgically. erally prevents the egress of large amounts of undi- The spontaneous seal of a perforated duodenal ulcer gested food. is remarkably secure. Among 152 cases of self-sealing docu- If the perforation is determined to be self-sealed as mented by gastroduodenogram treated nonsurgically and shown by gastroduodenogram, nonsurgical therapy can reported from the institutions with which we have been be pursued. Elements involved in the nonsurgical treat- associated, there were 2 instances of repeat leak. The rate ment of a patient with a self-sealed perforation include of intra-abdominal abscess following nonsurgical treat- gastric drainage, antibiotics, and early administration of

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 an H2 blocker or proton-pump inhibitor. Repeated clini- quent major morbidity from peptic ulceration. This was in cal examinations to assure early progressive resolution the form of reperforation, hemorrhage, obstruction, or in- of evidence of peritonitis are mandatory. If the physi- tractability.25 An acute ulcer, when defined as an ulcer with cian is unable to conduct such examinations, nonsurgi- a history of dyspepsia of less than 3 months’ duration, was cal treatment is contraindicated. considered less likely to have such adverse long-term ef- Following the initial correction of hypovolemia, fluid fects.14 However, Boey et al26 reported that as many as one requirements should barely exceed that needed for main- third of the cases of acute ulcer, as defined above, had ex- tenance. Fluid sequestration into the peritoneal cavity perienced major late morbidity due to peptic ulcer after sur- (third spacing) will cease. The signs of peritonitis, such gical closure of an ulcer that perforated. as muscle rigidity and tenderness, will begin to resolve. During the latter half of the 20th century, in- Indeed, if such beginning resolution is not apparent within creased awareness of the then high incidence of future 12 hours, the diagnosis of self-sealed perforated ulcer morbidity due to peptic ulcer in a patient in whom a duo- should be questioned. There is always the remote pos- denal ulcer had perforated led to increased interest in ul- sibility that a patient with a documented ulcer in the duo- cer-definitive surgery at the time of perforation of a chronic denum, diffuse peritonitis, and pneumoperitoneum, but ulcer. Experience accumulated that ulcer-definitive sur- without leakage on a gastroduodenogram, may have per- gery could be performed at the time of perforation with forated another lesion of the . a low morbidity and death rate. Jordan et al27 champi- The lack of early spontaneous resolution of peritoni- oned vagotomy and gastric resection. Others favored va- tis and of third spacing in a case that is being treated non- gotomy and pyloroplasty.11,28 More recently, most au- surgically should lead the surgeon to reconsider the diag- thorities have recommended surgical closure of the nosis of sealed perforated ulcer and to explore the abdomen. perforation and parietal cell vagotomy.29-31 The low in- Boey et al23 studied risk factors for death from perfo- cidence of adverse side effects of parietal cell vagotomy, rated duodenal ulcer and identified 3 factors: major medi- as well as a low early morbidity and death rate, sup- cal illness, preoperative shock, and long-standing perfo- ported the use of the operation in all cases of perforated ration (Ͼ24 hours). In the presence of all 3, the death rate ulcer, not only in those cases with a presumed chronic was 100%. In most instances, major medical illness oc- ulcer.29,31 Purulent peritonitis and severe associated dis- curs in old age, an independent risk factor that is associ- ease have been considered contraindications to an ulcer- ated with a higher death rate.17 Shock is initially a reflec- definitive operation, in contrast with secure closure of tion of hypovolemia due to sequestration of fluid consequent the perforation.20 to peritonitis and later may be a reflection of . The Most of the studies of perforation of duodenal ul- adverse effect of delay in diagnosis is to a major degree re- cer that have been the basis for the therapeutic recom- lated to the development of bacterial peritonitis, a hall- mendations discussed earlier antidate the widespread use mark of continuing leakage. A delay in diagnosis and treat- of proton-pump inhibitors and H2 blockers. These agents ment for longer than 12 hours has been reported to increase represent a major therapeutic advance. They are re- death rates.24 This is undoubtedly true if the perforation is ported to have reduced both the incidence of perforated open and leaking. We believe that whether the perfora- peptic ulcer32 and the incidence of relapse after surgical tion is leaking or sealed is more important as a factor in closure of a perforation.33 None of the studies address the death rates than an arbitrary number of hours following question of eradication of H pylori on the natural his- perforation before treatment is instituted. tory of the duodenal ulcer that perforates. Occasionally, the gastroduodenogram will demon- strate spill in a patient with a severe associated disease. AN ALTERNATIVE THERAPEUTIC PROGRAM The patient would benefit from a brief period of inten- sive preoperative therapy. An example would be a pa- Several facts included in the previous discussions sup- tient with florid congestive heart failure. In these pa- port an alternative to the currently accepted therapy of tients, we have placed drains to the site of perforation the perforated duodenal ulcer, that is, immediate sur- under local anesthesia. The procedure has been per- gical closure of the perforation with or without an formed at the bedside and by using a technique similar ulcer-definitive procedure. The following facts are to open diagnostic peritoneal lavage. These should be of included: the sump suction type. An external fistula is estab- • Most ulcers are associated with infection with lished. Surgery can be deferred briefly pending comple- H pylori, including ulcers that perforate. tion of essential medical therapy. Tension pneumoperi- • Almost all ulcers associated with H pylori can be toneum, if present, can have severe deleterious effects on healed with combined medical therapy; ie, antibiot- cardiorespiratory function during the period of preop- ics and proton-pump inhibitors or H2 blockers. The erative preparation. A needle paracentesis can provide dra- rate of relapse is very low. Reinfection is rare. matic relief. • The administration of H2 blockers and proton-pump inhibitors and elimination of NSAIDs are now EVOLUTION OF TREATMENT essential components of medical therapy. Such therapy has favorably affected the natural history of The dominant treatment of perforated duodenal ulcer in duodenal ulcers, including those that perforate. the first half of the 20th century was surgical closure.9 In • Approximately half of duodenal ulcers that perforate most perforated duodenal ulcers that were successfully sur- will have self-sealed when first seen by the physician. gically closed, the perforation was a harbinger of subse- • The perforation of a duodenal ulcer that has sealed

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 Perforated Duodenal Ulcer nonsurgical treatment should be initiated. After recov- ery from the consequences of the perforation, a decision Known Helicobacter pylori Negative No Prior Evaluation of H pylori can be made as to the advisability of an elective ulcer cura-

or or tive operation. When free leakage is seen from the duo- denum, the perforation should be securely closed by a Inadequate Diagnosis +/– Prior Treatment H pylori Treatment H pylori technique chosen by the surgeon. The surgeon’s judgment as to risk in the individual Suitable Surgical Candidate Poor Surgical Risk Gastroduodenogram case will determine whether an ulcer-definitive operation will also be perfomed at that time or subsequently. Tests Ulcer-Definitive Leaking Surgery Gastroduodenogram Sealed for H pylori with a rapid turnaround time that would be Nonoperative suitable for use in any severely ill patient have been devel- Sealed Leaking Secure Closure Therapy oped.34 If readily available, a determination might be made Nonoperative Secure ∗ ∗ Evaluation H pylori of H pylori infection at the time of perforation and cases Treatment Closure with negative results might be immediately identified. These H pylori Infection H pylori Negative cases could then be treated as described previously.

Treatment No Prior Prior H pylori Treatment Treatment INADEQUATE PRIOR EVALUATION AND/OR TREATMENT Consider Medical Ulcer- Treatment Definitive Three premises underlie suggestions for therapy in this Surgery group: (1) Most duodenal ulcers will be associated with Figure 2. An algorithm of suggested selective treatment of a duodenal ulcer H pylori. (2) Ulcer-definitive surgery should not be em- that has perforated. Asterisk indicates to consider elective ulcer-definitive ployed until an ulcer associated with H pylori has had the surgery. benefit of combined medical therapy. (3) Treatment at the spontaneously can be treated nonoperatively with time of perforation should be an assured closure of the per- low morbidity, including releakage and abdominal foration, pending determination of H pylori status. abscess. This group will include (1) patients who were asymp- • Death due to peritonitis reflects protracted leakage tomatic prior to perforation, (2) symptomatic patients and secondary bacterial contamination. without evaluation or with inadequate evaluation for • Major associated disease is a significant risk factor for H pylori, some of whom may have had prior medical death following perforation of a duodenal ulcer. therapy for the ulcer, and (3) occasional patients known Based on the above considerations, we suggest to be infected with H pylori who may not have received that patients with duodenal ulcer that perforate be appropriate combined medical therapy. In all of these divided into those with prior evaluation for H pylori cases, a gastroduodenogram should be obtained. Be- and appropriate therapy for duodenal ulcer and those cause a gastroduodenogram will be performed in all cases, without adequate prior evaluation and/or treatment poor-risk patients will be included automatically . for duodenal ulcer. If a duodenal ulcer is demonstrated and there is not spillage of contrast media, the patient should be treated PRIOR EVALUATION FOR H PYLORI nonoperatively. If there is a leaking perforation, the per- AND APPROPRIATE THERAPY foration should be securely closed by the most appro- priate technique as determined by the surgeon. The premise underlying the following suggestions is that When the patient has recovered from the conse- the perforation represents failure of nonsurgical therapy. quences of the perforation, evaluation for H pylori This group will include 2 cohorts with proven and pre- should be conducted. If infected, the patient should be viously treated duodenal ulcer: (1) cases evaluated and treated with combined medical therapy. Ulcer- found not to be infected with H pylori that have already definitive surgery should be considered in an infected received medical therapy and (2) cases infected with patient only if there is relapse after appropriate com- H pylori that have received appropriate combined medi- bined medical treatment. The number of uninfected cal therapy. patients will be in a distinct minority. Ulcers due to If a patient is a good operative risk, he or she NSAIDs, Zollinger-Ellison syndrome, and severe acute should be prepared for surgery with the intent of per- stress will comprise almost all of these uninfected forming an ulcer-definitive procedure of the surgeon’s cases. A trial of medical therapy would be appropriate choice. Most authorities would support a secure surgi- in an uninfected patient who had not received cal closure of the perforation and a parietal cell adequate prior medical therapy. An elective ulcer- vagotomy.29-31 Vagotomy and pyloroplasty or antrec- definitive operation should be strongly considered in tomy are acceptable alternatives. Purulent peritonitis an uninfected patient who has received reasonable would dictate only secure closure of the perforation. prior medical therapy. These recommendations assume that the Zollinger- These suggestions are outlined in the algorithm in Ellison syndrome has been excluded. Figure 2. A patient in this category who is a poor operative risk because of associated disease and/or age should have Corresponding author: Arthur J. Donovan, MD, 1201 a gastroduodenogram. If the perforation has self-sealed, Heatherside Rd, Pasadena, CA 91105.

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©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/29/2021 17. Berne CJ, Mikkelsen WP. Management of perforated peptic ulcer. Surgery. 1958; REFERENCES 44:591-603. 18. Rosoff LR Sr. Discussion of reference #20. Ann Surg. 1979;189:636. 1. Graham DY. Treatment of peptic ulcers caused by Helicobacter pylori [edito- 19. Singer HA, Vaughn RT. Treatment of forme fruste type of perforated peptic ul- rial]. N Engl J Med. 1993;328:349-350. cer. Surg Gynecol Obstet. 1930;50:10-16. 2. Gutthann SP, Garcia-Rodriguez LA, Raiford DS. Individual nonsteroidal anti- 20. Donovan AJ, Vinson TL, Maulsby GO, Gewin BA. Selective treatment of duode- inflammatory drugs and other risk factors for upper gastrointestinal bleeding and nal ulcer with perforation. Ann Surg. 1979;189:627-636. perforation. Epidemiology. 1997;8:18-24. 21. Li AKC. Response to letter to the editor re: reference #16. N Engl J Med. 1989; 3. Hirschowitz BI. Nonsteroidal anti-inflammatory drugs and the gastrointestinal 321:1051. tract. Gastroenterologist. 1994;2:207-223. 22. Berne TV, Donovan AJ. Nonoperative treatment of perforated duodenal ulcer. Arch 4. Ng EK, Chung SC, Sung JJ, et al. High prevalence of Helicobacter pylori infec- Surg. 1989;124:830-832. tion in duodenal ulcer perforations not caused by non-steroidal anti- 23. Boey J, Choi SKI, Poon A, et al. Risk stratification in perforated duodenal ulcers. inflammatory drugs. Br J Surg. 1996;83:1779-1781. Ann Surg. 1987;205:22-26. 5. Sebastian M, Chandran VP, Elashaal YI, Sim AI. Helicobacter pylori infection in 24. Svanes C, Lie RT, Svanes K, et al. Adverse effects of delayed treatment for per- perforated . Br J Surg. 1995;82:360-362. forated peptic ulcer. Ann Surg. 1994;220:168-175. 6. Tokunaga Y, Hara K, Ryo J, Kitaoka A, Tokuka A, Ohsumi K. Density of Helico- 25. Griffin GE, Organ CH Jr. The natural history of perforated duodenal ulcer treated bacter pylori infection in patients with peptic ulcer perforation. J Am Coll Surg. by suture plication. Ann Surg. 1976;183:382-385. 1998;186:659-663. 26. Boey J, Lee NW, Wong J, Ong GB. Perforations in acute duodenal ulcers. Surg 7. Holtman G, Tally NJ. Clinical approach to the Helicobacter-infected patient. In: Gynecol Obstet. 1982;155:193-196. Blaser MJ, Smith PD, Ravdin JI, et al, eds. Infections of the Gastrointestinal Tract. 27. Jordan GL, Angel RT, Debakey ME. Acute gastroduodenal perforation: compara- New York, NY: Raven Press; 1985:565-587. tive study of treatment with simple closure, subtotal and hemigas- 8. Bardhan KD, Wurzer H, Marcelino M, Jahsen J, Lotay N, Roberts PM. Ramtidine trectomy and vagotomy. Arch Surg. 1966;92:449-455. bismuth citrate with clarithromycin given twice daily effectively eradicates Heli- 28. Pierandozzi JS, Hinshaw DB, Stafford CE. Vagotomy and pyloroplasty for cobacter pylori and heals duodenal ulcers. Am J Gastroenterol. 1998;93:380-385. acute perforated duodenal ulcer: a report of 75 cases. Am J Surg. 1960; 9. Graham RR. The treatment of perforated duodenal ulcers. Surg Gynecol Obstet. 100:245. 1937;64:235-238. 29. Jordan PH Jr, Thornby J. Perforated pyloroduodenal ulcers: long term results 10. Lau WY, Leung KH, Kwong KH, et al. A randomized study comparing laparo- with omental patch closure and parietal cell vagotomy. Ann Surg. 1995;221:479- scopic versus open repair of perforated duodenal ulcer using suture or suture- 486. less technique. Ann Surg. 1996;224:131-138. 30. Sawyers JL, Herrington JL. Perforated duodenal ulcer managed by proximal gas- 11. Berne CJ, Rosoff LR Sr. Acute perforation of peptic ulcer. In: Nyhus LM, Wastell tric vagotomy and suture plication. Ann Surg. 1977;185:656-660. C, eds. Surgery of the Stomach and Duodenum. 3rd ed. Boston, Mass: Little Brown 31. Boey J, Branicki DM, Alagaratham TT, et al. Proximal gastric vagotomy: the pre- & Co Inc; 1977:441-457. ferred operation for perforated acute duodenal ulcer. Ann Surg. 1988;208: 12. Crisp E. Cases of perforation of the stomach with deductions therefrom relative 169-173. to the character and treatment of that lesion. Lancet. 1843;2:639. 32. Hermansson M, Stael von Holstein C, Ziling T. Peptic ulcer perforation before 13. Wangensteen OH. Nonoperative treatment of localized perforations of the duo- and after the introduction of H-2 receptor blockers and proton pump inhibitors. denum. Minn Med. 1935;18:477-480. Scand J Gastroenterol. 1977;32:523-529. 14. Taylor H. Peptic ulcer perforation treated without operation. Lancet. 1946;2:441-444. 33. Macintyre IM, Miller A. Impact of H-2 receptor antagonists on the outcome of 15. Seeley SF, Campbell D. Nonoperative treatment of perforated duodenal ulcer: a treatment of perforated duodenal ulcer. J R Coll Surg Edinb. 1990;35: further report. Surg Gynecol Obstet. 1956;102:435-446. 348-352. 16. Crofts TJ, Kenneth GM, Park MB, Steele RJC, Chung SSC, Li AKC. A randomized 34. Westblom TU, Laging LM, Midfiff BR, et al. Evaluation of QuickVue, a rapid en- trial of nonoperative treatment for perforated duodenal ulcer. N Engl J Med. 1989; zyme immunoassay test for detection of serum antibodies to Helicobacter py- 320:970-973. lori. Diagn Microbiol Infect Dis. 1993;16:317-320.

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ARCHIVES OF INTERNAL MEDICINE Is Routine Replacement of Peripheral Intravenous Catheters Necessary? Thomas Bregenzer, MD; Dieter Conen, MD; Pascal Sakmann, MD; Andreas F. Widmer, MD, MS Background: Guidelines developed by the Centers for Disease Control and Prevention, Atlanta, Ga, recommend that pe- ripheral intravenous catheters be changed every 3 days. However, routine replacement of central venous catheters is no longer supported in their latest update. Objective: To evaluate the risk to patients of having peripheral intravenous catheters left in place for as long as they are clinically indicated. Methods: This observational study in a university-affiliated, 700-bed hospital was designed to evaluate the day-specific risk (incidence density) for phlebitis, catheter infection, and obstruction with catheters remaining in place as long as clinically indicated. All consecutive patients who required peripheral intravenous catheterization for 24 hours or more were enrolled during a 10-week period. Outcome variables are phlebitis, catheter-related infections, and obstruction. Evaluated risk fac- tors include age, sex, underlying disease, anatomical insertion site, catheter diameter, first or subsequent catheter, duration of catheterization, type of admission, hospital location, type of infusate, and antibiotic therapy. Results: A total of 609 catheters that were in place for 1 to 28 days were evaluated. Phlebitis, catheter-related infection, and obstruction occurred in 19.7%, 6.9%, and 6.0% of catheters, respectively. We were unable to demonstrate an increased risk after 3 days of catheterization. The day-specific risk indicated a linear function of all outcome variables. Conclusions: The hazard for catheter-related complications—phlebitis, catheter-related infections, and mechanical complications— did not increase during prolonged catheterization. The recommendation for routine replacement of peripheral intravenous cath- eters should be reevaluated considering the additional cost and discomfort to the patient. (1998;158:151-156)

Reprints: Andreas F. Widmer, MD, MS, Division of Clinical Epidemiology, University Hospital Basel, CH-4031 Basel, Switzerland (e-mail: [email protected]).

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