Duodenal Bleeding-H.Pylori

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michelleDO

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64 yo F s/p truncal vagotomy with graham patch 2nd to bleeding duodenal ulcer. pmHx: DM2, CAD, CABG, Right BKA. currently hemodynamically stable.

Question: anyone knows if this patient still needs to be treated with triple therapy?
currently on protonix drip without any antibiotics. awaiting biopsy results. CDC recommends treating patients who has evidence of ulcer bleeding and I think if not mistaken those already diagnosed with H.Pylori.

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Last edited:
64 yo F s/p truncal vagotomy with graham patch 2nd to bleeding duodenal ulcer. pmHx: DM2, CAD, CABG, Right BKA. currently hemodynamically stable.

Question: anyone knows if this patient still needs to be treated with triple therapy?
currently on protonix drip without any antibiotics. awaiting biopsy results. CDC recommends treating patients who has evidence of ulcer bleeding and I think if not mistaken those already diagnosed with H.Pylori.

I don't know that you need to treat all GI bleeds empirically for H. pylori, but obviously you'd treat if they're found to have an active infection. There shouldn't be a big waiting period for your CLO or histology results.

The only group that absolutely needs antibiotics with an UGI bleed are cirrhotics....IMHO.

My question: Was there some sort of drainage procedure done as well along with the vagotomy? It seems odd to do a graham patch and vagotomy.....usually you need to couple vagotomy with either an antrectomy or pyloroplasty.....also graham patch does nothing for a bleeding ulcer, but is a good treatment for perforated duodenal ulcers.
 
Yes...Pyroloplasty was done. This patient was eventually treated with triple therapy prior to confirmed H.pylori result based on among other things low socioeconomic background (most prevalent) location of ulcer and bleeding.
 
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Yes...Pyroloplasty was done. This patient was eventually treated with triple therapy prior to confirmed H.pylori result based on among other things low socioeconomic background (most prevalent) location of ulcer and bleeding.

So where did they put the graham patch?

Did they check for h. pylori? Was it positive? If not, were the antibiotics stopped?

When you say they chose to treat h. pylori empirically based on ulcer location, do you mean in the duodenum vs. the stomach?

Did this patient have any other risk factors for PUD? Was the patient on NSAIDs?

Should we treat all bleeding duodenal ulcers with empiric antibiotics? Maybe just the ones with a low socioeconomic status?

Honestly, I don't know the answer to that. Surely some of these patients will be h. pylori negative and some positive. Do we think that 24 hours of oral antibiotics while we wait for the CLO or histology test will make a big difference? It's been well-proven that h. pylori eradication decreases rebleeding rates.......who knows.....I'll have to get on uptodate.com when I get to the hospital tomorrow.
 
So where did they put the graham patch?

Did they check for h. pylori? Was it positive? If not, were the antibiotics stopped?

When you say they chose to treat h. pylori empirically based on ulcer location, do you mean in the duodenum vs. the stomach?

Did this patient have any other risk factors for PUD? Was the patient on NSAIDs?

Should we treat all bleeding duodenal ulcers with empiric antibiotics? Maybe just the ones with a low socioeconomic status?

Honestly, I don't know the answer to that. Surely some of these patients will be h. pylori negative and some positive. Do we think that 24 hours of oral antibiotics while we wait for the CLO or histology test will make a big difference? It's been well-proven that h. pylori eradication decreases rebleeding rates.......who knows.....I'll have to get on uptodate.com when I get to the hospital tomorrow.

Here's what UTDOL has to say, for what it's worth:

Empiric treatment versus specific testing — In settings where the prevalence of H. pylori in DU is greater than 90 percent [9,10], empiric therapy for the infection is reasonable for uncomplicated cases [11]. However, the prevalence of H. pylori in DU appears to be considerably less than 90 percent, particularly in the United States. (See "Helicobacter pylori-negative peptic ulcer disease".) The prevalence of H. pylori is also lower in patients with complicated DUs (ie, those complicated by bleeding or perforation) compared with those with uncomplicated disease [12,13]. Patients with H. pylori negative ulcers appear to have a significantly worse outcome especially if treated empirically for infection [14]. Thus, documenting infection even in patients with DU (uncomplicated or complicated) is an appropriate caution prior to initiating antimicrobial therapy. (See "Indications and diagnostic tests for Helicobacter pylori infection".)










Medline ® Abstracts for References 9-14
of 'Management of duodenal ulcers in patients infected with Helicobacter pylori'


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9
TI Helicobacter pylori-negative duodenal ulcer.
AU Borody TJ; George LL; Brandl S; Andrews P; Ostapowicz N; Hyland L; Devine M
SO Am J Gastroenterol 1991 Sep;86(9):1154-7.

Most patients with chronic duodenal ulcer (DU) craters have gastritis associated with Helicobacter pylori (HP), now thought to be the major cause of DU. A smaller proportion of DU patients have no detectable HP. In this study, we examined the frequency and causes of HP-negative duodenal ulcers. In 302 consecutive patients with endoscopic diagnosis of duodenal ulcer, 284 (94%) were found to have associated HP gastritis, whereas 18 (6%) were HP-negative on histology, culture, and urease test. The largest subgroup of HP-negative patients (8/18) was made up of those who had been taking nonsteroidal antiinflammatory drugs (NSAIDs), followed closely (4/18) by patients with recent intake of antibiotics. Causes of DU in the remaining subgroups included two patients with duodenal Crohn's disease, two with Gastrospirillum hominis infection, one with penetrating carcinoma of the pancreas and one with no detectable cause. We conclude that, although the most common causal factor of duodenal ulcer is HP, some 6% of DU's will be HP-negative, signaling unusual etiology. It is now important to identify the cause of duodenal ulcer so as to initiate appropriate therapy.

AD Centre for Digestive Diseases, Sydney, Australia.
PMID 1882793

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10
Tytgat, G, Langenberg, W, Rauws, E, Rietra, P. Campylobacter-like organism (CLO) in the human stomach. Gastroenterology 1985; 88:1620.

no abstract available

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11
TI Clinical utility and cost effectiveness of Helicobacter pylori testing for patients with duodenal and gastric ulcers.
AU Greenberg PD; Koch J; Cello JP
SO Am J Gastroenterol 1996 Feb;91(2):228-32.

OBJECTIVE: current consensus guidelines recommend that all patients demonstrating either a gastric or duodenal ulcer be tested for Helicobacter pylori, the most common cause of ulcers. We determined the clinical utility and cost effectiveness of H. pylori testing in patients with duodenal and gastric ulcers. METHODS: A retrospective evaluation and cost-effectiveness analysis of 565 consecutive patients with endoscopically demonstrated gastric or duodenal ulcers over a 4-yr period in a large, urban general hospital. The main outcome variables are the percentage of patients who had a gastric biopsy, the prevalence of H. pylori, and the cost effectiveness of testing (antral biopsy, CLO test, serum antibody, and urea breath test) for H. pylori. RESULTS: Significantly more patients with endoscopically documented duodenal ulcers had an antral biopsy performed in 1993 and 1994 when compared with patients from 1991 and 1992 (p<0.00001). For patients with gastric ulcers, biopsies were performed at a similar rate throughout this study. Overall, patients with duodenal and gastric ulcers demonstrated H. pylori 75% and 69% of the time, respectively. The total charges for biopsy documentation and treatment of H. pylori in all duodenal ulcer patients in this cohort was estimated at $25,135. If a biopsy for H. pylori had been performed in all patients the actual charges would have been $77,443. Conversely, charges would have been only $8085 had all patients been empirically treated for H. pylori based on the high pretest probability of infection. CONCLUSIONS: Routine testing for H. pylori is very expensive, regardless ofthe diagnostic method used. Biopsy results do not provide clinically useful information in most patients with duodenal ulcers and may be misleading if falsely negative.

AD Division of Gastroenterology, Hepatology, and Clinical Nutrition, San Francisco General Hospital, California, USA.
PMID 8607485

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12
TI Acute perforated duodenal ulcer is not associated with Helicobacter pylori infection.
AU Reinbach DH; Cruickshank G; McColl KE
SO Gut 1993 Oct;34(10):1344-7.

Most patients with chronic duodenal ulcer disease have Helicobacter pylori infection and eradicating it considerably reduces the relapse rate. The prevalence of H pylori in 80 patients (mean age = 52 years, range 17-85) presenting with acute perforated duodenal ulcer was examined and compared with age and sex matched hospital control patients. H pylori state was assessed by serum anti-H pylori IgG (Helico-G kit, Porton) using a titre of 18 or less as negative with a specificity of 89% and sensitivity of 88%. Only 47% of the perforated duodenal ulcer patients were positive for H pylori and this was similar to the value of 50% in the controls. In 51 of the perforated duodenal ulcer patients 14C-urea breath tests were also performed 4-10 weeks after surgery and this confirmed that only 49% were positive for H pylori. None of these patients had received perioperative drugs that might have eradicated the infection. The H pylori positive and H pylori negative perforated duodenal ulcer patients were similar with respect to age (53, 51), smoking (84%, 83%), and consumption of more than 15 units of alcohol per week (42%, 38%). Duodenal ulcer disease had been diagnosed before acute perforation in only 24% of those with H pylori and also 24% of those without the infection. Regular non-steroidal anti-inflammatory drug (NSAID) use was common in both those with (44%) and without (45%) H pylori. In conclusion, the lack of association of acute perforated duodenal ulcer and H pylori infection suggests that perforated duodenal ulcer has a different pathogenesis from chronic duodenal ulcer disease, and that the first should not be regarded simply as a complication ofthe second.

AD University Department of Surgery, Western Infirmary, Glasgow.
PMID 8244099

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13
TI Helicobacter pylori and complicated ulcer disease.
AU Laine LA
SO Am J Med 1996 May 20;100(5A):52S-57S; discussion 57S-59S.

Approximately 20-25% of patients with peptic ulcer disease develop complications--bleeding, perforation, or obstruction. Although the majority of patients with complicated ulcers are infected with Helicobacter pylori, the prevalence of infection appears to be lower in these patients compared with patients with uncomplicated ulcers. Among patients who present with a bleeding ulcer, approximately one-third will develop recurrent bleeding in the following 1-2 years if left untreated after ulcer healing. A number of studies have shown that the recurrence of rebleeding is virtually abolished if patients receive H. pylori eradication therapy. In contrast, the rate of rebleeding in patients receiving maintenance antisecretory therapy is around 10%. Thus, H. pylori infection status must be determined in patients presenting with complicated ulcer disease and, if positive, eradication therapy initiated. Eradication should be documented at least 4 weeks after the end of therapy (by endoscopic biopsy or urea breath test) and maintenance antisecretory therapy discontinued if the infection is cured.

AD Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA.
PMID 8644783

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14
TI Helicobacter pylori-negative duodenal ulcers: prevalence, clinical characteristics, and prognosis--results from a randomized trial with 2-year follow-up.
AU Bytzer P; Teglbjaerg PS
SO Am J Gastroenterol 2001 May;96(5):1409-16.

OBJECTIVE: The proportion of Helicobacter pylori-negative duodenal ulcer disease appears to be increasing. Data on clinical outcome and prognosis in this subgroup are lacking. METHODS: Two hundred seventy-six duodenal ulcer patients randomized, irrespective of H. pylori status, to either eradication therapy or maintenance omeprazole (double-blind, double-dummy design) for 1 yr were studied. Patients were followed up for a total of 2 yr, with visits performed every 2 months the first year and every 6 months the following year. Endoscopies for assessment of ulcer relapse were done at 6 and 12 months or in the event of symptomatic relapse. H. pylori status was assessed by culture, immunohistochemistry, and urea breath test at entry, at 6, 12, and 24 months or at failure. The primary endpoint was discontinuation, irrespective of reason. Patients were considered H. pylori negative if all three tests were negative. Patients were considered H. pylori-positive if any of the three diagnostic tests were positive. Study staff were blinded to H. pylori results. RESULTS: Thirty-two (12%) patients were H. pylori negative at entry. There were no differences according to H. pylori status for a number of clinical and demographic characteristics. However, H. pylori-negative patients had a shorter history of ulcer symptoms and were more likely to be NSAID users (19% vs 1%, p<0.001). Only 28% of the H. pylori-negative patients completed the study, as compared with 40% of H. pylori-positive patients (p = 0.0005). The main reasons for the poorer prognosis in H. pylori-negative patients were relapse of ulcer/ulcer not healed (35% vs 26%) and relapse of severe dyspepsia symptoms without ulcer relapse (16% vs 7%). H. pylori-negative patients randomized to eradication therapy left the study early compared with H. pylori-negative patients randomized to long-term omeprazole therapy. Outcome in omeprazole-treated patients did not differ according to H. pylori status (p = 0.3). CONCLUSIONS: Clinical characteristics in H. pylori-negative and positive duodenal ulcer patients differ little. Clinical outcome over 2 yr is significantly poorer in H. pylori-negative patients, especially if treated empirically with eradication therapy. These results suggest that H. pylori infection should be assessed in all duodenal ulcer patients before treatment is decided.

AD Department of Medicine M, Glostrup University Hospital, Denmark.
PMID 11374675
 
I guess the idea of treating HP wihtout any confirmed diagnosis in patients after endoscopy/surgery with bleeding gastric or duodenal ulcers in the ICU setting is like treating all patients with sepsis in the ICU with steroids. Will help in only a handful but would be harmful to others. So just like doing the stimulation test checking adrenal insufficiency in septic patients, it would likely be more beneficial to test for Hp prior to adding antibiotics to PPI.

From Current Medical Diagnosis + Treatment 2010

The Long-term prevention of rebleeding - it is recommended that all patients with bleeding ulcers be tested for Hp infection and treated IF POSITIVE. 4-8 weeks later needs confirmation of eradication.

Post surgical (graham patch) patients with perforated ulcers treated for Hp had reduction in ulcer recurrence obviating the need for intraoperatie vagotomy.
 
by the way what were the complications with treating for Hp prior to confirmed diagnosis? - thanks;)
 
I guess the idea of treating HP wihtout any confirmed diagnosis in patients after endoscopy/surgery with bleeding gastric or duodenal ulcers in the ICU setting is like treating all patients with sepsis in the ICU with steroids. Will help in only a handful but would be harmful to others. So just like doing the stimulation test checking adrenal insufficiency in septic patients, it would likely be more beneficial to test for Hp prior to adding antibiotics to PPI.

That's what I was trying to get at. I'm not sure there's a very good role for empiric treatment unless you live in a 3rd world country where H. pylori is endemic.

Still, I'm not sure if a one-liner from "Current Medical Diagnosis and Treatment" should be enough for the case to be closed. Alot of those review books are too vague to be helpful in a specific clinical situation like this.

The best way to find out is to do the lit search and also look at expert guidelines (e.g. the American College of Gastroenterology).

Did you guys test for H. pylori? Was it positive?

Post surgical (graham patch) patients with perforated ulcers treated for Hp had reduction in ulcer recurrence obviating the need for intraoperatie vagotomy.

Was this ulcer perforated? I thought you said it was bleeding. Those are two totally different beasts, and I've never seen them happen simultaneously in the same patient, other than in a trauma situation.

If someone has an anterior duodenal perforation, and they've never been treated for PUD in the past, you can usually do just a graham patch. Vagotomy and graham patch would almost never go together, as it doesn't address the need for a drainage procedure.

If the patient was recurrent, i.e. had failed PPI, and had a perforated DU, then Vagotomy with pyloroplasty or antrectomy would be in order....but in those situations, your ulcer is excised, and there's nowhere to place the patch......I'm sorry if that came off as nitpicky, but in surgery there's a big difference in those two situations.

Did they really do a patch? Where did they put it?


Anyway, I hope you don't feel personally attacked, as your last post sounded sort of defensive. When it comes to critical care, and surgery in general, the devil is in the details. When you're trying to save a very sick patient with multiple simultaneous problems, you have to have a strong understanding of everything going on, and you have to make evidence based decision.
 
Hey thanks for the reply - no i never feel offended, I like discussions.

I agree with you with evidence based decision and always will strive for that.

the patient only had bleeding no perforation. Yes, a biopsy was done. Didn't check the result or get a chance to find out why the surgeon opted for that specific procedure for a bleeding ulcer instead of perforation (yes they did do a patch - and no not sure where the surgeon placed it). don't know if the patient had prior diagnosis of Hp or been treated in the past as i was the new SICU resident taking care for the patient only for a brief time before she was soon transferred to the regular floor and never followed up. trying to see if there is any literature out there that studies the clinical outcome of patients treated immediately with triple therapy post surgery. - thanks
 
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