Background: Acute mesenteric ischaemia and duodenal perforation are surgical emergencies with serious

consequences. Patients presenting with acute mesenteric ischaemia alone face a high mortality rate as high as 60%

whereas those presenting with peptic ulcer perforation the mortality rates range from 6-14%. There are very few

reported cases of patients presenting with this dual pathology.

Case presentation: We report a unique case of a 53 year old Italian lady who presented with acute mesenteric

ischaemia and duodenal perforation. This is the first report of massive bowel ischaemia and duodenal perforation

with no apparent underlying common pathophysiology leading to this presentation.

Conclusion: Early management in the intensive care unit and appropriate surgical intervention maximised the

patient’s chances of survival despite the poor prognosis associated with her dual pathology. The rare pathology of

the patient described can be explained by two possible hypotheses: peptic ulcer disease causing duodenal

ulceration, which precipitated ischaemic infarction of the small bowel. The second hypothesis is the patient

developed a stress related ulcer following ischaemic bowel infarction secondary to arterial thrombosis

A Sitges-Serra

Ahmed Aber

AW Bradbury

Farhan Rashid

G Lock

L Gunshefski

Lois Haruna

M Tun

MA Mansour

Marco Barreca

MG Wilcox

RA Abdu

RN Kaleya

TJ Howard

WA Oldenburg

PubMed

Springer - Publisher Connector

Haruna et al. BMC Surgery 2012, 12:21
http://www.biomedcentral.com/1471-2482/12/21CASE REPORT Open AccessAcute mesenteric ischemia and duodenal ulcer
perforation: a unique double pathology
Lois Haruna, Ahmed Aber, Farhan Rashid* and Marco BarrecaAbstract
Background: Acute mesenteric ischaemia and duodenal perforation are surgical emergencies with serious
consequences. Patients presenting with acute mesenteric ischaemia alone face a high mortality rate as high as 60%
whereas those presenting with peptic ulcer perforation the mortality rates range from 6-14%. There are very few
reported cases of patients presenting with this dual pathology.
Case presentation: We report a unique case of a 53 year old Italian lady who presented with acute mesenteric
ischaemia and duodenal perforation. This is the first report of massive bowel ischaemia and duodenal perforation
with no apparent underlying common pathophysiology leading to this presentation.
Conclusion: Early management in the intensive care unit and appropriate surgical intervention maximised the
patient’s chances of survival despite the poor prognosis associated with her dual pathology. The rare pathology of
the patient described can be explained by two possible hypotheses: peptic ulcer disease causing duodenal
ulceration, which precipitated ischaemic infarction of the small bowel. The second hypothesis is the patient
developed a stress related ulcer following ischaemic bowel infarction secondary to arterial thrombosis.
Keywords: Acute mesenteric ischaemia, Duodenal ulcer perforation, Mesenteric venous thrombosis, Ischemic bowel
infarction, Bowel necrosisBackground
Acute mesenteric ischemia (AMI) comprises a group of
pathophysiologic processes that have a common end
point—bowel necrosis. The survival rate has not
improved substantially during the past 70 years, and the
major reason is the continued difficulty in recognizing
the condition before bowel infarction occurs [1,2].
Clinical presentation is nonspecific in most cases and
can be characterized by an initial discrepancy between
severe abdominal pain and minimal clinical findings. In
general, patients with AMI have an acute onset of symp-
toms and a rapid deterioration in their clinical condition.
Complications such as ileus, peritonitis, pancreatitis, and
gastrointestinal bleeding may also mask the initial signs
and symptoms of AMI [2].
Acute mesenteric ischemia can be categorized into 4
specific types based on its cause. The most frequent
cause is arterial emboli. They are responsible for ap-
proximately 40% to 50% of cases [1,3]. Most mesenteric* Correspondence: farhan_rashid@hotmail.com
Department of General Surgery, Luton and Dunstable Hospital, Lewsey Road,
Luton, Bedfordshire LU4 ODZ, UK
© 2012 Harouna et al.; licensee BioMed Centra
Commons Attribution License (http://creativec
reproduction in any medium, provided the oremboli originate from a cardiac source. The second most
common cause is acute mesenteric thrombosis accounts
for 25% to 30% of all ischemic events [4,5]. Most of the
reported cases of mesenteric ischemia due to arterial
thrombosis occur with a background of severe athero-
sclerotic disease, the most common site near the origin
of the Superior Mesenteric Artery [6]. Commonly,
patients with this condition can tolerate major visceral
artery obstruction because the slow progressive nature
of atherosclerosis allows the development of important
collaterals. The third major cause is non-occlusive mes-
enteric ischemia. The pathogenesis of is poorly under-
stood but often involves a low cardiac output state
associated with diffuse mesenteric vasoconstriction.
Splanchnic vasoconstriction in response to hypovolemia,
decreased cardiac output, hypotension, or vasopressors
best explain the difference between this entity and other
forms of AMI [7,8]. Mesenteric venous thrombosis is
the least common cause of mesenteric ischemia, repre-
senting up to 10% of all patients with mesenteric ische-
mia and 18% of those with AMI. Most cases are thought
to be secondary to other intra-abdominal pathologicl Ltd. This is an Open Access article distributed under the terms of the Creative
ommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and
iginal work is properly cited.
Figure 1 CT scan of the abdomen showing free peritoneal
fluid.
Haruna et al. BMC Surgery 2012, 12:21 Page 2 of 4
http://www.biomedcentral.com/1471-2482/12/21conditions (such as malignancy, intra-abdominal sepsis,
or pancreatitis) or were classified as idiopathic [9].
Mesenteric venous thrombosis is usually segmental,
with oedema and hemorrhage of the bowel wall and
focal sloughing of the mucosa. Thrombi usually originate
in the venous arcades and propagate to involve the arcu-
ate channels. Hemorrhagic infarctions occur when the
intramural vessels are occluded [2]. Involvement of the
inferior mesenteric vein and large bowel is uncommon.
The transition from normal to ischemic intestine is more
gradual with venous embolism than with arterial embol-
ism or thrombosis.
Case presentation
A 53-year-old lady presented following a collapse at
home. In the ambulance she became unresponsive with
a temperature 33.4oC, heart rate of 95 beats per minute
and un-recordable blood pressure. On arrival active re-
suscitation commenced and a brief history of three days
of severe, intermittent abdominal pain, absolute consti-
pation, and reduced urine output was noted. Prior to
this recent deterioration the patient had been well, with
no weight loss or change in appetite. She had a past
medical history of hypertension, osteoporosis, a previous
appendicectomy; and a 20-pack year smoking history.
She denied any dyspeptic symptoms prior to her admis-
sion, and had never taken any antacids. Her medications
on admission were regular beta blocker, regular long
term bisphosphonates and paracetamol on as required
basis. On inspection the patient appeared of a normal
body habitus, with a BMI of 22 and examination
revealed a peritonitic abdomen.
Blood tests from admission revealed grossly elevated
inflammatory markers (CRP>500mg/L), neutrophilia and
acute kidney failure. Her blood gas showed metabolic
acidosis with a high lactate (12.7mmol/L), and low base
excess (−21.8 mmol/L) and bicarbonate (6.9mmol/L).
Due to her severe acute renal impairment no contrast
was initially used for imaging. CT scan of her abdomen
performed on admission revealed extensive free periton-
eal fluid and also fluid adjacent to the right kidney in the
retro peritoneum (Figure 1). There was no evidence of
any free air, obstruction, perforation or abdominal aortic
aneurysm, with no evidence for small bowel ischaemia.
Furthermore an ascitic tap was performed which
revealed a clear straw coloured fluid with a very high
lactate dehydrogenase, and normal protein. It did not
yield growth of any organisms.
Despite optimal management in the intensive care unit
the patient’s inflammatory markers, creatinine and ala-
nine aminotranserase all continued to rise, and urine
output remained minimal. In light of her clinical deteri-
oration, 12 hours after admission the patient underwent
an urgent diagnostic laparoscopy.Intraoperatively approximately 3 litres of free intraper-
itoneal purulent bile stained fluid filled the abdomen,
and multiple fibrinous exudates surrounded the entire
small bowel. A 162 cm section of distal small bowel
appeared ischemic, and an anterior duodenal (D1) per-
foration was identified. The procedure was converted to
a laparotomy in view of the findings. The D1 perforation
was repaired using an omental patch, and the ischemic
bowel wrapped in warm saline-soaked packs, with min-
imal benefit. The distal 162cm of dead small bowel was
resected, and because of her critical condition the neo-
distal small bowel had a few viable slightly dusky patches
left behind for a relook the following day. A washout
was performed and a laparostomy using a saline bag was
applied.
One day post-operatively the patient was dialysed and
kept intubated due to unresolving metabolic acidosis.
During the second laparotomy another 50cm of small
bowel appeared ischaemia and was resected. 2 meters of
healthy small bowel was left in situ. An ileocaecal anas-
tomosis was made, a washout performed, and the ab-
dominal wound closed.
Two weeks after her initial laparotomy the patient
had an endoscopy for a nasojejunal tube insertion. The
omental patch repair was performed during laparotomy
for duodenal perforated ulcer. However, once endos-
copy was performed few days after the first laparotomy
for naso-jejunal feeding tube insertion, a small hole
was identified near the D1 repair site and was clipped
(Figure 2). A repeat endoscopy a week later showed
closure of the duodenal defect and a 1cm healing
ulcer. The patient made a slowly recovery and she was
discharged few weeks later.
Histology showed haemorrhagic infarction in sections
of small bowel with ischaemic changes throughout the
submucosa and muscle coat, with normal appearing
Mesenteric vessels.
Figure 2 Endoscopic clipping of anterior duodenal perforation.
Haruna et al. BMC Surgery 2012, 12:21 Page 3 of 4
http://www.biomedcentral.com/1471-2482/12/21Discussion and conclusion
The unusual presentation of this patient raised an im-
portant question regarding her dual pathology: which
occurred first? Did she have a perforated duodenal ulcer,
causing sepsis and hypotension leading to small bowel
ischemia, or did she suffer from ischaemic bowel, and
subsequently developed a stress-related perforated ulcer?
After performing a through literature search, we did
identify a single case report that described a patient pre-
senting with acute abdomen and the subsequent inter-
vention revealed exactly the same double pathology of
Small bowel ischaemia and duodenal ulcer. However the
histopathology of the bowel in that particular case did
show evidence of polyarteritis nodosa explaining the
cause of the acute bowel ischaemia [10].
In order to explain this double pathology it is vital
to note that in peptic ulcer disease the two major pre-
cipitating factors are Helicobacter pylori infection and
non-steroidal anti-inflammatory drugs (NSAIDs). Ulcer
incidence increases with age and therapy with drugs
such as corticosteroids, anticoagulants and bisphosho-
nates. Complications (bleeding, perforation, obstruction)
can occur in patients with peptic ulcers of any aetiology.
Perforation occurs in about 5% to 10% of patients with
active ulcer disease [11].
With this background we are proposing two explana-
tions for this pathology. The first is that the patient had
been on long term bisphosphonates and this increased
her risk for peptic ulcer disease. If we assume that the
perforation of the duodenal ulcer occurred first, it was
likely that it led to mesenteric venous thrombosis caus-
ing ischaemic infarction of the small bowel. The hist-
ology results favour this theory as the patient had
segmental involvement of the small bowel with the spar-
ing of the large bowel and this commonly present in
acute ischaemia of the bowel that is associated with
mesenteric venous thrombosis.The second hypothesis is that the patient developed a
stress related duodenal ulcer post ischaemic bowel in-
farction and eventually this ulcer perforated. The cause
of the ischaemia is likely due to arterial thrombosis
with a background of severe atherosclerotic disease
caused by the patient‘s long history of hypertension and
smoking. Patients with this type of bowel ischaemia
present later as they can tolerate major visceral artery
obstruction because the slow progressive nature of ath-
erosclerosis allows the development of important collat-
erals. The patient had 3 days history of feeling unwell
and constipation with minimal urine output before she
collapsed.Consent
Written informed consent was obtained from the patient
for publication of this Case report and any accompany-
ing images. A copy of the written consent is available for
review by the Series Editor of this journal.
Abbreviations
AMI: Acute mesenteric ischaemia; NSAIDS: Non-steroidal anti-inflammatory
drugs.
Competing interests
The authors declare that they have no competing interests. No financial
support has been received.
Authors’ contribution
LH drafted the manuscript, and conducted a literature search. AA, FR and MB
conducted a literature search and contributed to drafting the manuscript. FR
monitored the drafting and assisted with the research. MB performed the
operation and reviewed the manuscript and gave final approval for
publication. All authors read and approved the final manuscript.
Received: 11 February 2012 Accepted: 11 October 2012
Published: 30 October 2012
References
1. Lock G: Acute intestinal ischaemia. Best Pract Res Clin Gastroenterol 2001,
15:83–98.
2. Oldenburg WA, Lau LL, Rodenburg TJ, Edmonds HJ, Burger CD: Acute
mesenteric ischaemia: a Clinical Review. Arch Intern Med 2004,
164:1054–1062.
3. Bradbury AW, Brittenden J, McBride K, Ruckley CV: Mesenteric ischaemia: a
multidisciplinary approach. Br J Surg 1995, 82:1446–1459.
4. Sitges-Serra A, Mas X, Roqueta F, Figueras J, Sanz F: Mesenteric infarction:
an analysis of 83 patients with prognostic studies in 44 cases
undergoing a massive small-bowel resection. Br J Surg 1988,
75:544–548.
5. Mansour MA: Management of acute mesenteric ischemia. Arch Surg 1999,
134:328–330.
6. Kaleya RN, Boley SJ: Acute mesenteric ischemia: an aggressive diagnostic
and therapeutic approach: 1991 Roussel Lecture. Can J Surg 1992,
35:613–623.
7. Wilcox MG, Howard TJ, Plaskon LA, Unthank JL, Madura JA: Current
theories of pathogenesis and treatment of nonocclusive mesenteric
ischemia. Dig Dis Sci 1995, 40:709–716.
8. Howard TJ, Plaskon LA, Wiebke EA, Wilcox MG, Madura JA: Nonocclusive
mesenteric ischemia remains a diagnostic dilemma. Am J Surg 1996,
171:405–408.
9. Abdu RA, Zakhour BJ, Dallis DJ: Mesenteric venous thrombosis: 1911 to
1984. Surgery 1987, 101:383–388.
Haruna et al. BMC Surgery 2012, 12:21 Page 4 of 4
http://www.biomedcentral.com/1471-2482/12/2110. Tun M, Malik AK: Massive small bowel infarction and duodenal
perforation due to abdominal polyarteritis nodosa: a case report.
Malays J Path 1994, 16(1):75–78.
11. Gunshefski L, Flancbaum L, Brolin RE, Frankel A: Changing patterns in
perforated peptic ulcer disease. Am Surg 1990, 56:270.
doi:10.1186/1471-2482-12-21
Cite this article as: Haruna et al.: Acute mesenteric ischemia and
duodenal ulcer perforation: a unique double pathology. BMC Surgery
2012 12:21.Submit your next manuscript to BioMed Central
and take full advantage of: 
• Convenient online submission
• Thorough peer review
• No space constraints or color ﬁgure charges
• Immediate publication on acceptance
• Inclusion in PubMed, CAS, Scopus and Google Scholar
• Research which is freely available for redistribution
Submit your manuscript at 
www.biomedcentral.com/submit


Acute mesenteric ischemia and duodenal ulcer perforation: a unique double pathology

Haruna, L.

Aber, A.

Rashid, F.

Barreca, M.

White Rose Research Online

Haruna et al. BMC Surgery 2012, 12:21http://www.biomedcentral.com/1471-2482/12/21CASE REPORT Open AccessAcute mesenteric ischemia and duodenal ulcerperforation: a unique double pathologyLois Haruna, Ahmed Aber, Farhan Rashid* and Marco BarrecaAbstractBackground: Acute mesenteric ischaemia and duodenal perforation are surgical emergencies with seriousconsequences. Patients presenting with acute mesenteric ischaemia alone face a high mortality rate as high as 60%whereas those presenting with peptic ulcer perforation the mortality rates range from 6-14%. There are very fewreported cases of patients presenting with this dual pathology.Case presentation: We report a unique case of a 53 year old Italian lady who presented with acute mesentericischaemia and duodenal perforation. This is the first report of massive bowel ischaemia and duodenal perforationwith no apparent underlying common pathophysiology leading to this presentation.Conclusion: Early management in the intensive care unit and appropriate surgical intervention maximised thepatient’s chances of survival despite the poor prognosis associated with her dual pathology. The rare pathology ofthe patient described can be explained by two possible hypotheses: peptic ulcer disease causing duodenalulceration, which precipitated ischaemic infarction of the small bowel. The second hypothesis is the patientdeveloped a stress related ulcer following ischaemic bowel infarction secondary to arterial thrombosis.Keywords: Acute mesenteric ischaemia, Duodenal ulcer perforation, Mesenteric venous thrombosis, Ischemic bowelinfarction, Bowel necrosisBackgroundAcute mesenteric ischemia (AMI) comprises a group ofpathophysiologic processes that have a common endpoint—bowel necrosis. The survival rate has notimproved substantially during the past 70 years, and themajor reason is the continued difficulty in recognizingthe condition before bowel infarction occurs [1,2].Clinical presentation is nonspecific in most cases andcan be characterized by an initial discrepancy betweensevere abdominal pain and minimal clinical findings. Ingeneral, patients with AMI have an acute onset of symp-toms and a rapid deterioration in their clinical condition.Complications such as ileus, peritonitis, pancreatitis, andgastrointestinal bleeding may also mask the initial signsand symptoms of AMI [2].Acute mesenteric ischemia can be categorized into 4specific types based on its cause. The most frequentcause is arterial emboli. They are responsible for ap-proximately 40% to 50% of cases [1,3]. Most mesenteric* Correspondence: farhan_rashid@hotmail.comDepartment of General Surgery, Luton and Dunstable Hospital, Lewsey Road,Luton, Bedfordshire LU4 ODZ, UK© 2012 Harouna et al.; licensee BioMed CentraCommons Attribution License (http://creativecreproduction in any medium, provided the oremboli originate from a cardiac source. The second mostcommon cause is acute mesenteric thrombosis accountsfor 25% to 30% of all ischemic events [4,5]. Most of thereported cases of mesenteric ischemia due to arterialthrombosis occur with a background of severe athero-sclerotic disease, the most common site near the originof the Superior Mesenteric Artery [6]. Commonly,patients with this condition can tolerate major visceralartery obstruction because the slow progressive natureof atherosclerosis allows the development of importantcollaterals. The third major cause is non-occlusive mes-enteric ischemia. The pathogenesis of is poorly under-stood but often involves a low cardiac output stateassociated with diffuse mesenteric vasoconstriction.Splanchnic vasoconstriction in response to hypovolemia,decreased cardiac output, hypotension, or vasopressorsbest explain the difference between this entity and otherforms of AMI [7,8]. Mesenteric venous thrombosis isthe least common cause of mesenteric ischemia, repre-senting up to 10% of all patients with mesenteric ische-mia and 18% of those with AMI. Most cases are thoughtto be secondary to other intra-abdominal pathologicl Ltd. This is an Open Access article distributed under the terms of the Creativeommons.org/licenses/by/2.0), which permits unrestricted use, distribution, andiginal work is properly cited.Figure 1 CT scan of the abdomen showing free peritonealfluid.Haruna et al. BMC Surgery 2012, 12:21 Page 2 of 4http://www.biomedcentral.com/1471-2482/12/21conditions (such as malignancy, intra-abdominal sepsis,or pancreatitis) or were classified as idiopathic [9].Mesenteric venous thrombosis is usually segmental,with oedema and hemorrhage of the bowel wall andfocal sloughing of the mucosa. Thrombi usually originatein the venous arcades and propagate to involve the arcu-ate channels. Hemorrhagic infarctions occur when theintramural vessels are occluded [2]. Involvement of theinferior mesenteric vein and large bowel is uncommon.The transition from normal to ischemic intestine is moregradual with venous embolism than with arterial embol-ism or thrombosis.Case presentationA 53-year-old lady presented following a collapse athome. In the ambulance she became unresponsive witha temperature 33.4oC, heart rate of 95 beats per minuteand un-recordable blood pressure. On arrival active re-suscitation commenced and a brief history of three daysof severe, intermittent abdominal pain, absolute consti-pation, and reduced urine output was noted. Prior tothis recent deterioration the patient had been well, withno weight loss or change in appetite. She had a pastmedical history of hypertension, osteoporosis, a previousappendicectomy; and a 20-pack year smoking history.She denied any dyspeptic symptoms prior to her admis-sion, and had never taken any antacids. Her medicationson admission were regular beta blocker, regular longterm bisphosphonates and paracetamol on as requiredbasis. On inspection the patient appeared of a normalbody habitus, with a BMI of 22 and examinationrevealed a peritonitic abdomen.Blood tests from admission revealed grossly elevatedinflammatory markers (CRP>500mg/L), neutrophilia andacute kidney failure. Her blood gas showed metabolicacidosis with a high lactate (12.7mmol/L), and low baseexcess (−21.8 mmol/L) and bicarbonate (6.9mmol/L).Due to her severe acute renal impairment no contrastwas initially used for imaging. CT scan of her abdomenperformed on admission revealed extensive free periton-eal fluid and also fluid adjacent to the right kidney in theretro peritoneum (Figure 1). There was no evidence ofany free air, obstruction, perforation or abdominal aorticaneurysm, with no evidence for small bowel ischaemia.Furthermore an ascitic tap was performed whichrevealed a clear straw coloured fluid with a very highlactate dehydrogenase, and normal protein. It did notyield growth of any organisms.Despite optimal management in the intensive care unitthe patient’s inflammatory markers, creatinine and ala-nine aminotranserase all continued to rise, and urineoutput remained minimal. In light of her clinical deteri-oration, 12 hours after admission the patient underwentan urgent diagnostic laparoscopy.Intraoperatively approximately 3 litres of free intraper-itoneal purulent bile stained fluid filled the abdomen,and multiple fibrinous exudates surrounded the entiresmall bowel. A 162 cm section of distal small bowelappeared ischemic, and an anterior duodenal (D1) per-foration was identified. The procedure was converted toa laparotomy in view of the findings. The D1 perforationwas repaired using an omental patch, and the ischemicbowel wrapped in warm saline-soaked packs, with min-imal benefit. The distal 162cm of dead small bowel wasresected, and because of her critical condition the neo-distal small bowel had a few viable slightly dusky patchesleft behind for a relook the following day. A washoutwas performed and a laparostomy using a saline bag wasapplied.One day post-operatively the patient was dialysed andkept intubated due to unresolving metabolic acidosis.During the second laparotomy another 50cm of smallbowel appeared ischaemia and was resected. 2 meters ofhealthy small bowel was left in situ. An ileocaecal anas-tomosis was made, a washout performed, and the ab-dominal wound closed.Two weeks after her initial laparotomy the patienthad an endoscopy for a nasojejunal tube insertion. Theomental patch repair was performed during laparotomyfor duodenal perforated ulcer. However, once endos-copy was performed few days after the first laparotomyfor naso-jejunal feeding tube insertion, a small holewas identified near the D1 repair site and was clipped(Figure 2). A repeat endoscopy a week later showedclosure of the duodenal defect and a 1cm healingulcer. The patient made a slowly recovery and she wasdischarged few weeks later.Histology showed haemorrhagic infarction in sectionsof small bowel with ischaemic changes throughout thesubmucosa and muscle coat, with normal appearingMesenteric vessels.Figure 2 Endoscopic clipping of anterior duodenal perforation.Haruna et al. BMC Surgery 2012, 12:21 Page 3 of 4http://www.biomedcentral.com/1471-2482/12/21Discussion and conclusionThe unusual presentation of this patient raised an im-portant question regarding her dual pathology: whichoccurred first? Did she have a perforated duodenal ulcer,causing sepsis and hypotension leading to small bowelischemia, or did she suffer from ischaemic bowel, andsubsequently developed a stress-related perforated ulcer?After performing a through literature search, we dididentify a single case report that described a patient pre-senting with acute abdomen and the subsequent inter-vention revealed exactly the same double pathology ofSmall bowel ischaemia and duodenal ulcer. However thehistopathology of the bowel in that particular case didshow evidence of polyarteritis nodosa explaining thecause of the acute bowel ischaemia [10].In order to explain this double pathology it is vitalto note that in peptic ulcer disease the two major pre-cipitating factors are Helicobacter pylori infection andnon-steroidal anti-inflammatory drugs (NSAIDs). Ulcerincidence increases with age and therapy with drugssuch as corticosteroids, anticoagulants and bisphosho-nates. Complications (bleeding, perforation, obstruction)can occur in patients with peptic ulcers of any aetiology.Perforation occurs in about 5% to 10% of patients withactive ulcer disease [11].With this background we are proposing two explana-tions for this pathology. The first is that the patient hadbeen on long term bisphosphonates and this increasedher risk for peptic ulcer disease. If we assume that theperforation of the duodenal ulcer occurred first, it waslikely that it led to mesenteric venous thrombosis caus-ing ischaemic infarction of the small bowel. The hist-ology results favour this theory as the patient hadsegmental involvement of the small bowel with the spar-ing of the large bowel and this commonly present inacute ischaemia of the bowel that is associated withmesenteric venous thrombosis.The second hypothesis is that the patient developed astress related duodenal ulcer post ischaemic bowel in-farction and eventually this ulcer perforated. The causeof the ischaemia is likely due to arterial thrombosiswith a background of severe atherosclerotic diseasecaused by the patient‘s long history of hypertension andsmoking. Patients with this type of bowel ischaemiapresent later as they can tolerate major visceral arteryobstruction because the slow progressive nature of ath-erosclerosis allows the development of important collat-erals. The patient had 3 days history of feeling unwelland constipation with minimal urine output before shecollapsed.ConsentWritten informed consent was obtained from the patientfor publication of this Case report and any accompany-ing images. A copy of the written consent is available forreview by the Series Editor of this journal.AbbreviationsAMI: Acute mesenteric ischaemia; NSAIDS: Non-steroidal anti-inflammatorydrugs.Competing interestsThe authors declare that they have no competing interests. No financialsupport has been received.Authors’ contributionLH drafted the manuscript, and conducted a literature search. AA, FR and MBconducted a literature search and contributed to drafting the manuscript. FRmonitored the drafting and assisted with the research. MB performed theoperation and reviewed the manuscript and gave final approval forpublication. All authors read and approved the final manuscript.Received: 11 February 2012 Accepted: 11 October 2012Published: 30 October 2012References1. Lock G: Acute intestinal ischaemia. Best Pract Res Clin Gastroenterol 2001,15:83–98.2. Oldenburg WA, Lau LL, Rodenburg TJ, Edmonds HJ, Burger CD: Acutemesenteric ischaemia: a Clinical Review. Arch Intern Med 2004,164:1054–1062.3. Bradbury AW, Brittenden J, McBride K, Ruckley CV: Mesenteric ischaemia: amultidisciplinary approach. Br J Surg 1995, 82:1446–1459.4. Sitges-Serra A, Mas X, Roqueta F, Figueras J, Sanz F: Mesenteric infarction:an analysis of 83 patients with prognostic studies in 44 casesundergoing a massive small-bowel resection. Br J Surg 1988,75:544–548.5. Mansour MA: Management of acute mesenteric ischemia. Arch Surg 1999,134:328–330.6. Kaleya RN, Boley SJ: Acute mesenteric ischemia: an aggressive diagnosticand therapeutic approach: 1991 Roussel Lecture. Can J Surg 1992,35:613–623.7. Wilcox MG, Howard TJ, Plaskon LA, Unthank JL, Madura JA: Currenttheories of pathogenesis and treatment of nonocclusive mesentericischemia. Dig Dis Sci 1995, 40:709–716.8. Howard TJ, Plaskon LA, Wiebke EA, Wilcox MG, Madura JA: Nonocclusivemesenteric ischemia remains a diagnostic dilemma. Am J Surg 1996,171:405–408.9. Abdu RA, Zakhour BJ, Dallis DJ: Mesenteric venous thrombosis: 1911 to1984. Surgery 1987, 101:383–388.Haruna et al. BMC Surgery 2012, 12:21 Page 4 of 4http://www.biomedcentral.com/1471-2482/12/2110. Tun M, Malik AK: Massive small bowel infarction and duodenalperforation due to abdominal polyarteritis nodosa: a case report.Malays J Path 1994, 16(1):75–78.11. Gunshefski L, Flancbaum L, Brolin RE, Frankel A: Changing patterns inperforated peptic ulcer disease. Am Surg 1990, 56:270.doi:10.1186/1471-2482-12-21Cite this article as: Haruna et al.: Acute mesenteric ischemia andduodenal ulcer perforation: a unique double pathology. BMC Surgery2012 12:21.Submit your next manuscript to BioMed Centraland take full advantage of: • Convenient online submission• Thorough peer review• No space constraints or color figure charges• Immediate publication on acceptance• Inclusion in PubMed, CAS, Scopus and Google Scholar• Research which is freely available for redistributionSubmit your manuscript at www.biomedcentral.com/submit

Abstract
          
            Background
            Acute mesenteric ischaemia and duodenal perforation are surgical emergencies with serious consequences. Patients presenting with acute mesenteric ischaemia alone face a high mortality rate as high as 60% whereas those presenting with peptic ulcer perforation the mortality rates range from 6-14%. There are very few reported cases of patients presenting with this dual pathology.
          
          
            Case presentation
            We report a unique case of a 53 year old Italian lady who presented with acute mesenteric ischaemia and duodenal perforation. This is the first report of massive bowel ischaemia and duodenal perforation with no apparent underlying common pathophysiology leading to this presentation.
          
          
            Conclusion
            Early management in the intensive care unit and appropriate surgical intervention maximised the patient’s chances of survival despite the poor prognosis associated with her dual pathology. The rare pathology of the patient described can be explained by two possible hypotheses: peptic ulcer disease causing duodenal ulceration, which precipitated ischaemic infarction of the small bowel. The second hypothesis is the patient developed a stress related ulcer following ischaemic bowel infarction secondary to arterial thrombosis.
          </jats:sec

Crossref

BMC Surgery

Abstract Background Acute mesenteric ischaemia and duodenal perforation are surgical emergencies with serious consequences. Patients presenting with acute mesenteric ischaemia alone face a high mortality rate as high as 60% whereas those presenting with peptic ulcer perforation the mortality rates range from 6-14%. There are very few reported cases of patients presenting with this dual pathology. Case presentation We report a unique case of a 53 year old Italian lady who presented with acute mesenteric ischaemia and duodenal perforation. This is the first report of massive bowel ischaemia and duodenal perforation with no apparent underlying common pathophysiology leading to this presentation. Conclusion Early management in the intensive care unit and appropriate surgical intervention maximised the patient’s chances of survival despite the poor prognosis associated with her dual pathology. The rare pathology of the patient described can be explained by two possible hypotheses: peptic ulcer disease causing duodenal ulceration, which precipitated ischaemic infarction of the small bowel. The second hypothesis is the patient developed a stress related ulcer following ischaemic bowel infarction secondary to arterial thrombosis.</p

Haruna Lois

Aber Ahmed

Rashid Farhan

Barreca Marco

Directory of Open Access Journals

Acute intestinal ischaemia. Best Pract Res Clin Gastroenterol

Boley SJ: Acute mesenteric ischemia: an aggressive diagnostic and therapeutic approach:

CD: Acute mesenteric ischaemia: a Clinical Review. Arch Intern Med

DJ: Mesenteric venous thrombosis:

JA: Current theories of pathogenesis and treatment of nonocclusive mesenteric ischemia. Dig Dis Sci

JA: Nonocclusive mesenteric ischemia remains a diagnostic dilemma.

Management of acute mesenteric ischemia. Arch Surg

Mesenteric infarction: an analysis of 83 patients with prognostic studies in 44 cases undergoing a massive small-bowel resection.

Ruckley CV: Mesenteric ischaemia: a multidisciplinary approach.

https://eprints.whiterose.ac.uk/118590/1/Acute%20mesenteric%20ischemia%20and%20duodenal%20ulcer%20perforation%3A%20a%20unique%20double%20pathology.pdf

Acute mesenteric ischemia and duodenal ulcer perforation: a unique double pathology

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Directory of Open Access Journals

Springer - Publisher Connector