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 Table of Contents  
Year : 2017  |  Volume : 2  |  Issue : 4  |  Page : 109-112

Hemorrhagic duodenal ulcer and subsequent acute appendicitis following lobectomy for lung cancer

1 Department of Surgery, Footscray Hospital, Victoria, Australia
2 Department of Surgery, The University of Melbourne, Victoria, Australia

Date of Submission17-Jun-2017
Date of Acceptance08-Oct-2017
Date of Web Publication28-Dec-2017

Correspondence Address:
Tyson A Moore
Department of Surgery, Western Health, Footscray Hospital, Victoria 3011
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ts.ts_15_17

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A 62-year-old Vietnamese male presented for an elective video-assisted thoracoscopic surgery lobectomy for treatment of a suspicious lung mass. Postoperatively, he developed a hemorrhagic duodenal ulcer requiring endoscopic hemostasis. Interestingly, he subsequently became septic secondary to perforated acute appendicitis necessitating laparoscopic appendectomy. Surgery can evoke a physiological stress response and may be a causative factor in the pathogenesis of stress ulcers in surgical patients. A recent article has found an association between the development of acute appendicitis in patients with a history of peptic ulcer disease. The pathological mechanism responsible for this association may be the result of an imbalance of the autonomic nervous system and neuromusculature spasms at the ceco-appendiceal junction.

Keywords: Appendicitis, duodenal ulcer, Helicobacter pylori, stress ulcer

How to cite this article:
Moore TA, Chan ST. Hemorrhagic duodenal ulcer and subsequent acute appendicitis following lobectomy for lung cancer. Transl Surg 2017;2:109-12

How to cite this URL:
Moore TA, Chan ST. Hemorrhagic duodenal ulcer and subsequent acute appendicitis following lobectomy for lung cancer. Transl Surg [serial online] 2017 [cited 2021 Jan 28];2:109-12. Available from: http://www.translsurg.com/text.asp?2017/2/4/109/221874

  Introduction Top

It is well known that surgical patients are at increased risk of developing stress ulcers.[1] Acute appendicitis is one of the most common surgical emergencies, with an estimated lifetime risk of 7%–16%.[2] A recent case–control study has demonstrated a link between patients who had a history of peptic ulcer disease and subsequently developed acute appendicitis.[2]

Our case report describes a patient who underwent lung lobectomy, subsequently suffered a hemorrhagic duodenal ulcer, and most interestingly then developed acute appendicitis. To the best of our knowledge, such a case has never before been published in the literature.

  Case Report Top

A 62-year-old Vietnamese male underwent migrant screening, where a chest X-ray showed a suspicious lung opacity. His only medical history was that of a 30-pack-year smoking history. A computed tomography (CT) scan of his chest demonstrated a spiculated mass within the right upper lobe measuring 13 mm × 17 mm × 16 mm with associated hilar lymphadenopathy. This mass was also intensely metabolically active on positron emission tomography scan. He underwent elective video-assisted thoracoscopic surgery (VATS) with right upper lobectomy. The final histopathology report showed moderately differentiated pulmonary adenocarcinoma, predominantly acinar histology with focal solid histology, and no vascular invasion or lymphatic involvement (T1b N0 MX).

On postoperative day two, he had multiple episodes of coffee-ground vomit and melena. He was not tachycardic but became hypotensive with a blood pressure of 75/45 mmHg. His hemoglobin dropped from 12.9 g/dL to 8.2 g/dL. An urgent upper gastrointestinal endoscopy was performed, which demonstrated a superficial duodenal ulcer with oozing hemorrhage (Forrest Class Ib) on the posterior wall of the first part of the duodenum [Figure 1]. Hemostasis was achieved with epinephrine and bipolar gold probe coagulation. Helicobacter pylori antibody-serum testing was positive and he was commenced on eradication therapy (amoxicillin + clarithromycin) and prescribed a proton pump inhibitor.
Figure 1: Upper gastrointestinal endoscopy. (a) Duodenal bulb with overlying clot and active ooze. (b) Epinephrine injection. (c) Post gold probe application

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On postoperative day five, he became tachycardic at 135 beats/min with a low-grade fever of 37.9°C. His white cell count had risen to 22.3 × 109/L and his C-reactive protein had almost doubled from 116 to 213 mg/L. Initially, it was thought that he was developing a chest infection as the intercostal catheter remained in situ from his VATS lobectomy. Microbiological examination of the pleural fluid was unremarkable and a chest X-ray showed no consolidation. The patient subsequently complained of generalized abdominal pain with maximal tenderness on palpation in the right iliac fossa. An abdominopelvic CT scan showed radiographic findings suggestive of acute appendicitis [Figure 2]. He proceeded to have an emergency laparoscopic appendectomy and histopathological findings were consistent with perforated acute appendicitis. His recovery was unremarkable and was discharged home on postoperative day seven.
Figure 2: Abdominopelvic computed tomography scan. (a) Coronal and (b) transverse sections demonstrating an enlarged appendix with appendiceal wall thickening consistent with acute appendicitis (arrows)

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  Discussion Top

In this case report, we described a Vietnamese male who developed a hemorrhagic duodenal ulcer following VATS lobectomy for pulmonary adenocarcinoma. It is well documented in the literature that postoperative patients are a high-risk group for the development of stress ulcers.[1] However, there is a lack of evidence regarding the benefits of stress ulcer prophylaxis (SUP) in noncritically ill and surgical patients.[3],[4] The American Society of Health-System Pharmacists has implemented strict indications for SUP including patients who have coagulopathy, have been mechanically ventilated for >48 h, and have had a gastrointestinal ulcer within the past year.[5] During his hospital stay, he did not receive SUP, but following his hemorrhagic duodenal ulcer, he was prescribed esomeprazole as an inpatient and on discharge. Based on the aforementioned guidelines, it would have been inappropriate to prescribe SUP to this patient.

Other potential underlying factors to explain the development of the hemorrhagic duodenal ulcer are his gender and ethnicity. A meta-analysis has shown that Helicobacter pylori infection is significantly linked with male gender.[6]Helicobacter pylori infection has also been shown to be associated with the presence of stress ulcers.[7],[8] Epidemiological data suggest that Asian nations have a higher prevalence of Helicobacter pylori infection in comparison to Western countries.[9] There have been many explanations for the existence of this enigma including bacterial factors, the host's genetic factors, and environmental factors.[10] As this patient had proven serological evidence of Helicobacter pylori infection, this may have rendered him more susceptible to stress ulcer formation postoperatively. It is also possible that he had a preexisting undiagnosed duodenal ulcer and the stress associated with VATS lobectomy was sufficient to trigger ulcerative hemorrhage. It must also be appreciated that this duodenal ulcer may have developed incidentally.

The most interesting component of this case report is that the patient developed acute appendicitis following his hemorrhagic duodenal ulcer. A case report describing two children was the first article to demonstrate patients presenting with the coexistence of perforated duodenal ulcer and acute appendicitis.[11] Furthermore, a recent case–control study [2] published in Nature Scientific Reports in 2015 revealed the first evidence of an association between patients with a history of peptic ulcer disease presenting with acute appendicitis. However, this association was only statistically significant in younger patients and not those in the >60-year-old age group,[2] and therefore cannot be applied to this patient as he was 62 years of age at the time. Potential reasons for the lack of association in the older age group include anatomical differences in the elderly appendix and poor colonic peristalsis.[2] Although the pathophysiology of acute appendicitis remains unclear, appendiceal luminal obstruction is considered the most common cause of the condition.[12],[13] Contrary to this assertion, two large retrospective review articles found that only a small fraction of appendicitis specimens histologically had mechanical obstruction.[14],[15] Histological analysis of the appendix of this patient did not reveal any obstruction of the appendiceal lumen.

Although the mechanism for the link between acute appendicitis and previous peptic ulcer disease remains uncertain, it may be the result of an imbalance of the autonomic nervous system and neuromusculature spasms at the ceco-appendiceal junction.[16] Indeed, studies have postulated that duodenal ulcers, pylorospasms, and appendicitis can occur concurrently due to similar nervous system connections between the pylorus, duodenum, and appendix.[17],[18] Furthermore, a porcine study has shown that antral ulcers disrupt the neuronal regulation of the pyloric sphincter muscles, leading to pylorospasms.[19] The histology of the appendix mimics that of the colon, and consists of the same mucosal and muscular layers.[20] The question remains as to whether there is a true sphincter at the appendiceal orifice that could result in uncontrolled spasms. This notion was suggested by Wangensteen et al.[21] but no evidence was found as to its existence. Taken together, it can be extrapolated that interruption of the aforementioned common nervous supply by a peptic ulcer may lead to uncontrolled spasms at the ceco-appendiceal junction. Although this has never been proven and is pure speculation based on these studies, it does raise some valid questions about the pathogenesis of acute appendicitis. Of course, as with his duodenal ulcer, the development of acute appendicitis in this patient may also be entirely incidental.

This case report is the first published article to demonstrate a patient who suffered a hemorrhagic duodenal ulcer post lung lobectomy and subsequently developed acute appendicitis. A recent case–control study has suggested that an imbalance of the autonomic nervous system and neuromusculature spasms at the ceco-appendiceal junction may explain the link between acute appendicitis and a previous diagnosis of peptic ulcer disease. However, further research is required to fully elucidate the pathophysiological mechanisms underlying this association and also to determine if the same relationship exists in elderly populations. Clinicians should be mindful to suspect acute appendicitis in patients with a history of peptic ulcer disease presenting with abdominal pain so that early intervention will lead to optimal patient outcomes and avoid complications.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Hata M, Shiono M, Sekino H, Furukawa H, Sezai A, Iida M, Yoshitake I, Hattori T, Wakui S, Soeda M, Taoka M, Negishi N, Sezai Y. Prospective randomized trial for optimal prophylactic treatment of the upper gastrointestinal complications after open heart surgery. Circ J 2005;69 (3):331-4.  Back to cited text no. 1
Ming-Chieh Tsai, Li-Ting Kao, Herng-Ching Lin, Shiu-Dong Chung, Cha-Ze Lee. Acute appendicitis is associated with peptic ulcers: A population-based study. Sci Rep 2015;5:18044.  Back to cited text no. 2
Bez C, Perrottet N, Zingg T, Leung Ki EL, Demartines N, Pannatier A. Stress ulcer prophylaxis in non-critically ill patients: A prospective evaluation of current practice in a general surgery department. J Eval Clin Pract 2013;19 (2):374-8.  Back to cited text no. 3
Hong MT, Monye LC, Seifert CF. Acid suppressive therapy for stress ulcer prophylaxis in noncritically ill patients. Ann Pharmacother 2015;49 (9):1004-8.  Back to cited text no. 4
ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis. ASHP Commission on Therapeutics and approved by the ASHP Board of Directors on November 14, 1998. Am J Health Syst Pharm 1999;56 (4):347-79.  Back to cited text no. 5
de Martel C, Parsonnet J. Helicobacter pylori infection and gender: A meta-analysis of population-based prevalence surveys. Dig Dis Sci 2006;51 (12):2292-301.  Back to cited text no. 6
van der Voort PH, van der Hulst RW, Zandstra DF, Geraedts AA, van der Ende A, Tytgat GN. Suppression of Helicobacter pylori infection during intensive care stay: Related to stress ulcer bleeding incidence? J Crit Care 2001;16 (4):182-7.  Back to cited text no. 7
Maury E, Tankovic J, Ebel A, Offenstadt G. An observational study of upper gastrointestinal bleeding in Intensive Care Units: Is Helicobacter pylori the culprit? Crit Care Med 2005;33 (7):1513-8.  Back to cited text no. 8
Miwa H, Go MF, Sato N. H. pylori and gastric cancer: The Asian enigma. Am J Gastroenterol 2002;97 (5):1106-12.  Back to cited text no. 9
Zaidi SF. Helicobacter pylori associated Asian enigma: Does diet deserve distinction? World J Gastrointest Oncol 2016;8 (4):341-50.  Back to cited text no. 10
Toubanakis G. Perforated chronic duodenal ulcer in children with coexistence of acute appendicitis. Aust Paediatr J 1988;24 (6):371-2.  Back to cited text no. 11
Hardin DM Jr. Acute appendicitis: Review and update. Am Fam Physician 1999;60 (7):2027-34.  Back to cited text no. 12
Singh JP, Mariadason JG. Role of the faecolith in modern-day appendicitis. Ann R Coll Surg Engl 2013;95 (1):48-51.  Back to cited text no. 13
Chandrasegaram MD, Rothwell LA, An EI, Miller RJ. Pathologies of the appendix: A 10-year review of 4670 appendicectomy specimens. ANZ J Surg 2012;82 (11):844-7.  Back to cited text no. 14
Marudanayagam R, Williams GT, Rees BI. Review of the pathological results of 2660 appendicectomy specimens. J Gastroenterol 2006;41 (8):745-9.  Back to cited text no. 15
Connell FG. Etiology of appendicitis. Am J Surg 1937;37 (2):232-8.  Back to cited text no. 16
Aaron CD. Chronic appendicitis, pylorospasm and duodenal ulcer. JAMA 1915;LXIV (22):1845.  Back to cited text no. 17
Burden VG. Chronic appendicitis-duodenal ulcer. Am J Surg 1933;21 (2):235-9.  Back to cited text no. 18
Zalecki M. The Influence of antral ulcers on intramural gastric nerve projections supplying the pyloric sphincter in the pig. PLoS One 2015;10 (5):e0126958.  Back to cited text no. 19
Deshmukh S, Verde F, Johnson PT, Fishman EK, Macura KJ. Anatomical variants and pathologies of the vermix. Emerg Radiol 2014;21 (5):543-52.  Back to cited text no. 20
Wangensteen OH, Buirge RE, Dennis C, Ritchie WP. Studies in the etiology of acute appendicitis: The significance of the structure and function of the vermiform appendix in the genesis of appendicitis a preliminary report. Ann Surg 1937;106 (5):910-42.  Back to cited text no. 21


  [Figure 1], [Figure 2]


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