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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Management of perforated duodenal ulcer

, M.D. Fracs.

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The first report of a series of patients presenting with perforation of a duodenal ulcer was made in 1817 by Travers. The earliest operative description was made by Mikulicz in 1884 but the first successful operation for a perforated duodenal ulcer was not until 1894.

Over the last two decades there have been a number of advances in the management of perforated duodenal ulcer that have suggested that the morbidity and mortality of the disease might be decreased. These include risk stratification to define patients suitable for various treatment protocols, an expanded role for non-operative treatment, a developing role for laparoscopic surgery and more precise identification of those patients suitable for immediate definitive ulcer management. Most recently the discovery of the role of Helicobacter pylori in the pathogenesis of duodenal ulcer threatens to change the entire management algorithm for perforated duodenal ulcer.

Pathogenesis and epidemiology

Perforation complicates duodenal ulcer about half as often as bleeding and most perforated ulcers are on the anterior surface of the duodenum. The patient population tends to be elderly (mean age 60–70), chronically, ill patients often (40–50%) taking ulcerogenic medication.

The incidence of perforated duodenal ulcer in the West is relatively stable, the age of presentation increasing, and the sex incidence becoming more even.

The continuing problem with perforated duodenal ulcer stands in contrast to the fall in admissions for uncomplicated duodenal ulcers noted since the 1970's and largely attributed to the introduction of H2 antagonists (Grade C). In the third world the clinical picture is different with a high male : female ratio (approximately 8 : 1), younger age, and a strong link with cigarette smoking. In addition in the third world there is a high incidence of patients who present late and this may partly account for the high mortality (20%) reported in some studies.

Helicobacter pylori is implicated in 70–92% of all perforated duodenal ulcers even if those secondary to Non-Steroidal Antiinflammatory Drugs are included. The second most common cause of perforated duodenal ulcer is the ingestion of Non-Steroidal Antiinflammatory drugs. The number of perforated duodenal ulcers related to Non-Steroidal Antiinflammatory drugs has increased greatly in developed countries such that 40–50% of perforated duodenal ulcers are caused by them. The least common cause is pathologic hypersecretory states, such as Zollinger-Ellison syndrome, although these should be considered in all cases of recurrent ulcer after adequate treatment.

In the modern treatment of perforated duodenal ulcer it must be born in mind that appropriate treatment of H. pylori infection results in eradication of the bacteria and healing of uncomplicated ulcers in more than 90% of cases. Therefore, in the majority of cases duodenal ulcer may be regarded as a curable infectious disease or related to the ingestion of an ulcerogenic drug (Grade A/B).

Formerly the distinction between acute and chronic ulcers was thought to be important but understanding of the role of H. pylori is likely to make this distinction irrelevant.


The most characteristic symptom is the suddenness of the onset of epigastric pain. The pain rapidly becomes generalised although occasionally it moves to the right lower quadrant. The patient is loathe to move. There may be a history of previous dyspepsia, previous or current treatment for a duodenal ulcer, or ingestion of ulcerogenic drugs. On examination the patient is in obvious pain. Hypotension is a late finding as is a high fever. The abdominal findings are characteristically described as of board-like rigidity. With time the patient may improve with dilution of the duodenal contents by exudate from the peritoneum but this is later replaced by the signs and symptoms of bacterial peritonitis.

Once an ulcer perforates the subsequent clinical picture is influenced by whether or not the ulcer self seals.

In approximately 40–50% of cases the ulcer self-seals with omentum or by fusion of the duodenum to the underside of the liver between the gallbladder and the falciform ligament. This is important when one considers whether or not laparotomy is indicated to deal with the perforation itself as will be seen below.

On an erect Chest X Ray free air can be seen in about 80% of cases. In doubtful cases a water-soluble gastroduodenogram will show the leak from the duodenum or its sealing. This can be a useful test when one is considering non-operative treatment or in the situation where the diagnosis is in doubt.

Risk Stratification

Mortality from perforated duodenal ulcer is dependant upon the presence or absence of several risk factors. Individual risk can also be assessed by use of APACHE II. Overall mortality is approximately 10% in most studies. In the developing world the high morbidity and mortality experienced by patients with perforated duodenal ulcer is probably due to delayed presentation. Those in whom the diagnosis is overlooked almost always die.

Risk factors affecting prognosis are delayed treatment (> 24 hours), preoperative shock (BP < 100 mmHg), and concurrent serious medical illness. When all three are present the mortality rises to 100% (Grade C).


Non-operative treatment

In 1935 Wangensteen noted that ulcers are able to self seal and reported on seven cases treated without surgery. In 1946 this observation was confirmed by Taylor and he treated 28 cases without surgery with good success. This was in the context of the high mortality and morbidity associated with surgical management at the time.

Subsequent work showed that a water-soluble contrast study could confidently demonstrate the presence of self-sealing in 40–50% of cases. In 1989 a trial from Hong Kong by Crofts et al. showed that non-operative treatment for perforated duodenal ulcer was accompanied by a low mortality rate and was not associated with a large number of complications when the gastroduodenogram documented a sealed perforation (Grade A).

In practical terms, when the diagnosis of a perforated duodenal ulcer is established the patient is aggressively resuscitated, nasogastric suction begun, and broad spectrum antibiotic cover instituted. If a tension pneumoperitoneum embarrasses respiration this can be aspirated to release the pneumoperitoneum. A gastroduodenogram is performed to confirm self-sealing.

The peritonitis should resolve in 4 to 6 hours and if there is continued major fluid loss after this time or if there are progressive signs of peritonitis or increasing pneumoperitoneum then surgical intervention is required.

In the study by Crofts they carefully selected patients under the age of 70 who were haemodynamically stable, had been perforated for less than 24 hours, and could be closely monitored. Using these criteria 70% of patients were selected to be randomized to be treated in this way. Despite this encouraging report, and a number of other non-randomised studies, non-operative treatment of perforated duodenal ulcer has not become popular. Non-operative management has not been widely adopted probably due to problems with repeated review by senior surgeons, problems with misdiagnosis, and the lack of opportunity to perform definitive ulcer surgery. Non-operative treatment has largely been restricted to those too unwell to undergo laparotomy. In this small subgroup of extremely sick patients it has been shown that they can be managed conservatively and any intraabdominal abscesses which arise can be treated by interventional radiology, albeit with a high mortality (Grade C).

When a policy of non-operative management is adopted it is important to perform follow-up endoscopy to monitor ulcer healing, treat for H. pylori, and to provide an accurate diagnosis (Grade C).

Surgical treatment

Laparoscopic Surgery

The traditional management of a perforated duodenal ulcer has been a Graham Omental Patch and a thorough abdominal lavage. More recently this has been shown to be able to performed using a laparoscope. The only proven advantage of the laparoscopic technique appears to be decreased postoperative pain. Operating times are longer compared to open techniques and hospital time appears to be similar to conventional treatment. This technique has not been subjected to any large prospective trials and at present must not be considered as standard management. Of note several groups have demonstrated the feasibility of laparoscopic definitive ulcer surgery (Grade A/C).

Immediate Definitive Surgery

Over the last one hundred years a number of attempts have been made to improve upon the results of simple closure and lavage. This has been in response to the large number of patients (25–85%) who continue to have symptoms attributable to their ulcer diathesis after surgery. The incidence of ulcer symptoms, in most studies, is related to whether the ulcer is acute or chronic (history greater than 3 months) as judged by preoperative history. Patients with chronic ulcer symptoms generally have a higher incidence of subsequent recurrent ulcers. Up to 71% come to require subsequent definitive surgery although in most studies the figure is considerably less than this (Grade C).

Since the 1940's the concept of immediate definitive ulcer surgery has been promulgated and debated amongst surgeons. There is good evidence that, in the emergency situation, highly selective vagotomy (proximal gastric, or parietal cell vagotomy) combined with simple omental patch closure of the perforation, in patients without the risk factors mentioned above, is just as effective as that performed in the elective setting (Grade C). This is associated with a less than 1% mortality rate and a 4–11% ulcer recurrence rate. The success of this operation is surgeon-dependent. Truncal vagotomy with drainage has its advocates as an expedient operation familiar to most surgeons.

Immediate definitive ulcer surgery has not gained widespread popularity due to an unfounded feeling that it is associated with a higher mortality than simple closure. It has been argued that a if blanket definitive surgical approach were adopted then 50–60% patients would be at risk of suffering from complications of surgery they did not require. In experienced hands, however, a highly selective vagotomy is associated with very low morbidity (Grade A).

Many agree that an appropriate approach is to select only those with a chronic history (> 3 months) and without preoperative risk factors for immediate definitive surgery. A major difficulty is defining preoperatively the patients who truly have a chronic ulcer history as many patients are too unwell to give a reliable history. In addition, many ulcers have a silent ulcer history with as many as 70% of perforations occurring as the first manifestation of the ulcer diathesis.

It must be recalled, however, that in the developed world the surgeon's major role in the management of perforated duodenal ulcer will continue to be the performance of lifesaving operations in elderly unfit patients.

Conservative Surgery

There has been a return to the use of simple omental patch closure since the late 1970's with the introduction of post-operative H2 antagonists and more recently Proton Pump Blockers. Over the last 10 years this trend has only grown stronger due to the discovery of the role of H. pylori in the pathogenesis of duodenal ulcer.

Given that H. pylori is able to be implicated in up to 90% of perforated duodenal ulcers it would seem logical to utilise patch closure and subsequent antibiotic treatment of the infectious agent saving definitive surgical ulcer management for those who fail this regimen. This has recently been tested in a randomiced controlled trial from Hong Kong where it was found that simple dosure of duoderal ulcer perforation with eradication of H. pylori resulted in ulcer healing in 78% of patients with only a 48% recurrence rate at one year (Grade A).

The counter argument is that perforated duodenal ulcer patients represent a subgroup of patients with a very vigorous ulcer diathesis and simple closure of the ulcer and treatment of the infecting organisms may not be adequate. Until further clinical trials are performed in relevant population groups we will not know the definitve answer.

It would seem reasonable, however, to err on the conservative side at this time. It is no light matter to perform a vagotomy on every patient with a perforated duodenal ulcer especially in the light of the probable role of H. pylori.

Therapy for H. pylori

There have been a number of regimens proposed for the eradication of H. pylori.

The most effective present first line regimen for eradicating H. pylori, with approximately 90% eradication rates, is a combination of Bismuth, Metronidazole and Amoxycillin or Tetracycline given for a period of 14 days with or without proton pumpblocker (Grade A/B).

It is important to check for eradication, as resistance is developing to the first line regimens, especially in the third world. Tests to confirm eradication include endoscopy and biopsy and non invasive tests such as serology or breath testing for urea. At present it would seem prudent to perform a post-operative endoscopy to confirm H. pylori eradication, confirm the diagnosis, and to check ulcer healing.

If H. pylori is eradicated the risk of reinfection is low, in the order of 1% per year, and the ulcer is likely to heal. If the ulcer heals there is no role for continuing with antisec-retory drugs. If the patient needs to continue Non Steroidal Antiinflammatories the most effective prophylactic drug is Misoprostol (Grade B).


The present management of perforated duodenal ulcer is in flux. The great debates of earlier in the century regarding simple patch closure versus immediate definitive surgery have been complicated by the arguments for and against laparotomy, the introduction of laparoscopy, and the discovery of the role of H. pylori.

Faced with a patient with a perforated duodenal ulcer the surgeon should bear in mind the role of non-operative treatment in the first instance. If this option is selected the patient will require close vigilance and a readiness to intervene at any moment that the patient shows signs of deterioration or failure to progress satisfactorily (Grade A).

If operative management is considered to be indicated, the evidence at present supports simple omental patch closure and lavage followed by antibiotic treatment for H. pylori (Grade A). If the patient remains with an ulcer after surgery and H. pylori eradication then a Highly Selective Vagotomy should be performed after exclusion of a pathological hypersecretory state (Grade C).

In the rare case of a patient who has been investigated and found to be negative for H. pylori , or who has been treated and then perforated, immediate definitive ulcer surgery should be performed in the absence of preoperative risk factors. If the surgeon is not experienced with Highly selective vagotomy then in the emergency situation a Truncal Vagotomy and Pyloroplasty is adequate treatment. If the patient perforates while taking ulcerogenic drugs a simple closure and lavage should suffice.

As the ulcer diathesis in many patients is silent, ulcer healing and H. pylori eradication should be confirmed by endoscopy.

Until a randomised prospective trial is performed the relative merits of the treatment strategies outlined above will continue to be controversial.


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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6926


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