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Dig Dis Sci
DOI 10.1007/s10620-017-4807-4
ORIGINAL ARTICLE
Clinical Features and Outcomes of Gastric Ischemia
Ayush Sharma1 • Saurabh Mukewar1 • Suresh T. Chari1 • Louis M. Wong Kee Song1
Received: 25 May 2017 / Accepted: 11 October 2017
Ó Springer Science+Business Media, LLC 2017
Abstract
Background and Aims Gastric ischemia is a rare condition
associated with poor prognosis. Our study aim was to
highlight the clinical features and outcomes of patients
with gastric ischemia.
Methods A retrospective review of patients diagnosed with
isolated gastric ischemia at our institution from January 1,
2000, to May 5, 2016, was performed. Demographic,
clinical, endoscopic, radiologic, and outcome variables
were abstracted for analysis.
Results Seventeen patients (65% men) with mean age of
69.3 ± 11.3 years and body mass index of 28.8 ± 11.1
were identified. The etiologies for gastric ischemia included local vascular causes (n = 8), systemic hypoperfusion
(n = 4), and mechanical obstruction (n = 5). The most
common presenting symptoms were abdominal pain
(65%), gastrointestinal bleeding (47%), and altered mental
status (23%). The typical endoscopic appearance was
mucosal congestion and erythema with or without ulceration. Gastric pneumatosis and portal venous air were more
commonly seen on CT imaging. Radiologic and/or surgical
intervention was needed in 9 patients, while the remaining
8 patients were managed conservatively with acid suppression, antibiotics, and nasogastric tube decompression.
The median duration of hospital stay was 15 days (range
1–36 days). There were no cases of rebleeding and the
Electronic supplementary material The online version of this
article (doi:10.1007/s10620-017-4807-4) contains supplementary
material, which is available to authorized users.
& Louis M. Wong Kee Song
wong.louis@mayo.edu
1
Division of Gastroenterology and Hepatology, Mayo Clinic,
200 First Street SW, Rochester, MN 55905, USA
mortality rate as a direct result of gastric ischemia was 24%
within 6 months of diagnosis.
Conclusion Although uncommon, gastric ischemia is
associated with significant mortality. Endoscopy and CT
imaging play an important role in its diagnosis. The management of gastric ischemia is dictated by its severity and
associated comorbidities.
Keywords Ischemic gastropathy Gastric necrosis Upper
gastrointestinal bleeding Stomach apoplexy
Abbreviations
BMI Body mass index
GI
Gastrointestinal
IR
Interventional radiologic
NG
Nasogastric
PPI
Proton pump inhibitor
UGI Upper gastrointestinal
Introduction
The occurrence of gastric ischemia is rare due to the rich
vascular supply to the stomach [1]. The stomach is vascularized from the celiac trunk and its branches, which
include the left gastric, splenic, and common hepatic
arteries (Supplementary Figure 1). Only a handful of cases
of gastric ischemia have been reported in the literature in
patients with predisposing factors, such as atherosclerosis
[2], vasculitis [3], paraesophageal hernia [4], gastric
volvulus [5], gastric dilation [6], disseminated intravascular coagulation, shock [3, 7], and postoperatively [8, 9].
Gastric ischemia has also been described in case reports of
patients undergoing therapeutic interventions, such as
endoscopic submucosal dissection [10], sclerosant [11, 12]
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Dig Dis Sci
and epinephrine [13, 14] injection for non-variceal upper
gastrointestinal bleeding, and transarterial chemoembolization for hepatocellular cancer [15]. Due to the rarity
of gastric ischemia, there is limited understanding of its
etiopathogenesis, clinical features, endoscopic/radiologic
findings, and patient outcomes. Herein, we describe our
experience with regard to patients with gastric ischemia
managed in a tertiary care hospital over the past 15 years.
Methods
Study Design
A retrospective case series study was undertaken. We
searched in-patient and out-patient electronic medical
records at Mayo Clinic, Rochester, Minnesota, from January 1, 2000, to May 5, 2016, to identify patients with
diagnosis of ‘‘vascular insufficiency’’ and ‘‘other disorders
of stomach’’ using ICD-9 codes 557.1 and 537.8, respectively. We searched the terms ‘‘gastric ischemia’’ or ‘‘ischemic gastropathy’’ in the clinical notes, endoscopy notes,
and pathology reports to identify a total of 35 patients. Of
those, 18 patients were excluded as they did not meet
inclusion criteria (Fig. 1). The study was approved by the
Institutional Review Board (IRB# 16-003399) of Mayo
Clinic.
Fig. 1 Flow diagram for
selection of patients with gastric
ischemia
123
Inclusion and Exclusion Criteria
We included adult patients (C 18 years) diagnosed with
gastric ischemia based on the presence of at least 2 or more
features: (1) clinical (e.g., abdominal pain, GI bleeding),
(2) radiographic (e.g., gastric pneumatosis, portal venous
gas), and (3) endoscopic (e.g., ischemic-appearing mucosal
changes or necrosis) findings. We excluded patients with
discrete gastric ulcers secondary to causes such as Helicobacter pylori and non-steroidal anti-inflammatory drugs,
patients with mesenteric ischemia without gastric
involvement, and those with symptomatic paraesophageal
hernias with no endoscopic signs of gastric ischemia. We
also excluded patients with associated esophageal or duodenal ischemia on endoscopy and focused on the cohort of
patients with isolated gastric ischemia.
Study Variables
We abstracted various demographic and clinical variables,
including age, sex, body mass index (BMI), clinical features, and putative risk factors (e.g., thromboembolic disease, vasculitis, septic or hemorrhagic shock,
paraesophageal hernia, underlying malignancy, recent
surgery). We noted radiologic (e.g., portal venous air,
gastric pneumatosis), endoscopic (e.g., discoloration—
pallor or congestion or necrosis of gastric mucosa;
Dig Dis Sci
ulcerations—location, extent, and bleeding stigmata), and
histopathological findings. Specific management details,
including medications [e.g., proton pump inhibitor (PPI),
antibiotics], nasogastric (NG) tube decompression, nutritional support, radiologic and/or surgical intervention, were
recorded, as well as morbidity and mortality data at last
follow-up.
Table 1 Patient demographics and features
Features
n = 17
Demographics
Male
11 (65%)
Age (years), mean ± SD
69.3 ± 11.3
2
28.8 ± 11.1
Body mass index (kg/m ), mean ± SD
Clinical features
Statistical Analysis
Descriptive statistics were used for the study, with all
parameters expressed as means (standard deviations) or
medians (ranges), as appropriate. Data analysis was performed using JMPÒ, version 10 software (SAS Institute,
Cary, NC).
Results
Seventeen patients (65% men) were diagnosed with gastric
ischemia, 15 endoscopically and 2 intraoperatively, with
mean age of 69.3 ± 11 years and BMI of 28.8 ± 11.1
(Table 1 and supplementary Table 1). Ten patients (58%)
were diagnosed in an in-patient setting, while 7 (42%) were
diagnosed in an out-patient setting. Among these patients,
9 (53%) had a history of smoking, 8 (47%) had hypertension, 7 (41%) had hyperlipidemia, and 6 (35%) had diabetes mellitus. The most common presenting symptoms
were abdominal pain and acute GI bleeding in 11 (65%)
and 8 (47%) patients, respectively. Five (29%) patients had
a history of weight loss. Hypotension prior to diagnosis
was documented in 6 (35%) patients and 3 (50%) of these
patients required blood transfusion.
Abdominal pain
11 (65%)
Gastrointestinal bleeding
8 (47%)
Altered mental status
4 (23%)
Shock
4 (23%)
Thromboembolism
2 (12%)
Comorbidities
Smoking
9 (53%)
Hypertension
8 (47%)
Hyperlipidemia
7 (41%)
Diabetes
6 (35%)
Celiac ostial stenosis
4 (23%)
Paraesophageal hernia
3 (18%)
Postoperative
2 (12%)
Gastric outlet obstruction
2 (12%)
CT findings
Gastric pneumatosis
9 (54%)
Portal venous air
6 (34%)
Treatment
Conservative
8 (47%)
Interventional radiology
3 (18%)
Surgery, gastric resection
6 (35%)
Outcomes
Follow-up duration (months), median (range)
Died directly to due to gastric ischemia
21 (0–116)
4 (24%)
Etiology and Risk Factors
The etiologies for gastric ischemia included local vascular
causes (n = 8; 47%), systemic hypoperfusion (n = 4;
23%), and mechanical obstruction (n = 5; 30%). Among
the patients with local vascular causes, 4 had celiac ostial
stenosis, 2 were surgically related (status post-Ivor-Lewis
with gastric pull-up for esophageal cancer in one patient
and status post-total pancreatectomy with celiac axis
resection for metastatic renal cell cancer to the pancreas in
another), 1 had portal vein thrombosis, and 1 had undergone hepatic artery embolization. Systemic hypoperfusion
was seen in those with shock (n = 4; 2 sepsis, 1 hypovolemic and 1 cardiogenic). Among the 5 patients with
mechanical obstruction, 3 had paraesophageal hernias and
2 had gastric outlet obstruction causing gastric distension.
HIV testing was available in 4 patients, and all were negative. Bacterial cultures were obtained in 3 patients with no
growth in all.
Endoscopic Appearance
Endoscopy was performed in 15 (88%) patients. The typical appearance of ischemic gastropathy on endoscopy was
congestion and hemorrhagic (purplish hue) mucosa, with or
without ulceration or frank necrosis (Fig. 2 and Supplementary Video 1). The most common site was the greater
curvature of the body (n = 10; 66%) along the posterior
wall (n = 7; 47%). Other affected areas were the fundus
(n = 5; 33%), cardia (n = 3; 20%), antrum (n = 5; 33%),
anterior wall (1; 6%), and lesser curvature (1; 6%) of the
gastric body. Active bleeding was found in 5 (29%) cases
in the form of oozing. Biopsy was obtained in 3 (20%)
cases and was consistent with ischemic injury in all at
histopathology. The most common feature on histology
was reactive gastric mucosa with erosion and ulceration.
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Dig Dis Sci
Fig. 2 a, b Ischemic gastropathy with hemorrhagic congested mucosa, erosions, and ulcerations in the gastric body. c, d Complete mucosal
healing with scarring at 3 months follow-up
Imaging
Treatment and Outcomes
CT with and without angiography was performed in 15
(88%) patients. Findings suggestive of gastric ischemia
included gastric pneumatosis and portal venous gas
(Fig. 3). In patients in whom imaging was performed, it
was helpful in detecting the etiology in almost half of the
cases; 4 had ostial stenosis, 2 paraesophageal hernias, 1
portal vein thrombosis and 1 gastric dilatation due to gastric outlet obstruction. Two patients with paraesophageal
hernias had signs of incarceration on imaging. On CT, 4
(27%) patients had critical or severe atherosclerosis, 3
(20%) had mild-to-moderate degree of atherosclerosis, and
5 (33%) had no atherosclerosis. In 3 patients, due to poor
quality of scan we could not asses the degree of
atherosclerosis.
Eight (47%) patients were managed conservatively with
intravenous PPI, antibiotics, and NG tube decompression.
Four (24%) patients required total parenteral nutrition
(TPN), of whom 2 (50%) died at 28 and 79 days after
diagnosis. Nine (53%) patients required an intervention: 3
underwent interventional radiologic stent placement for
high-grade ostial stenosis followed by vascular surgery in
1; 6 underwent gastric resection (5 partial gastrectomy and
1 gastroplasty). One patient underwent IR stent placement
followed by gastrectomy. Among patients who underwent
gastric surgery, 3 had paraesophageal hernias, 1 had a
postoperative anastomotic leak, 1 had resection of a previous Mason shunt, and 1 had gastric perforation. In the
patients who underwent surgery, 2 were lost to follow-up, 1
died after 5 months due to esophageal cancer, and 2 had no
123
Dig Dis Sci
Fig. 3 a CT scan showing gastric pneumatosis and portal vein gas. b CT scan coronal section showing extensive portal vein gas with hepatic
infiltration. c CT scan coronal section showing extensive gastric wall pneumatosis
recurrence of symptoms. The median duration of hospitalization for our patient cohort was 15 days (range 1–36).
The median follow-up following diagnosis was 21
(range 0–116) months. Repeat endoscopy was performed in
5 patients at a mean 2.6 (range 1.6–18) months’ time
interval post-diagnosis. Four patients had complete healing
of gastric mucosa with or without obvious scarring, and 1
patient had a persistent small fundic clean-base ulcer.
Among those conservatively managed, none of the patients
had rebleeding. Six (35%) patients died on follow-up: 4
died secondary to gastric ischemia and sepsis or multiorgan failure, whereas 2 died from progression of underlying malignancy.
Discussion
To our knowledge, this study represents the largest case
series of patients with gastric ischemia. In our patient
population, the typical clinical presentation was abdominal
pain and GI bleeding, with the majority of patients having a
history of chronic smoking. The most common etiologies
were celiac ostial stenosis and systemic hypoperfusion. On
endoscopy, the mucosa appeared congested, hemorrhagic,
and ulcerated, mostly involving the posterior wall of the
stomach along the greater curvature of the body and fundus. Nearly half of the patients required radiologic and/or
surgical intervention. Among those conservatively or nonsurgically managed, there were no cases of recurrent
bleeding. Nearly one-third of patients died on follow-up
mostly within the first 2 months of diagnosis.
Gastric ischemia usually occurs due to decrease in
gastric blood flow by vascular insufficiency or by reperfusion injury [16]. Vascular insufficiency can be due to
local or systemic causes. In a series by Tang et al. [3], the
majority (* 65%) of cases had systemic hypoperfusion as
a cause for gastric ischemia. Another series by Herman
et al. [17] observed stress ulcers in 50% of patients as the
most common etiology. In our study, local vascular causes
(75%) were identified as the most common etiology for
gastric ischemia. Systemic hypoperfusion was observed in
25% of our patients, presenting predominantly as septic
shock. Rarely, therapeutic interventions such as endoscopic
submucosa dissection [10], injection sclerotherapy
[11, 12], intra-arterial infusion of vasopressors in the left
gastric artery [18], and epinephrine injection for GI
bleeding [13, 14] may result in gastric ischemia, though we
did not observe any such interventional cause for gastric
ischemia in our study. Gastric ischemia may occur after GI
surgery, such as post-vagotomy [9], gastric pull-up surgery
[19], and pancreatectomy with celiac axis resection [8]. We
observed gastric ischemia in 2 postoperative patients after
esophagectomy with gastric pull-up for esophageal cancer
and post-pancreatectomy with celiac axis resection for
metastatic renal cell carcinoma.
Factors such as advancing age, smoking, atherosclerosis,
diabetes, and hypertension predispose to ischemia by
causing a decrease in gastric and splanchnic blood flow
[2, 20, 21]. A decrease in blood flow causes an increase in
intramucosal acidosis and ulcer formation [22]. Aging and
diabetes may decrease gastric motility and delay gastric
emptying, leading to gastric distension and increased
intragastric pressure which is also shown to reduce gastric
blood flow in animal models [20, 23]. Smoking increases
acid and pepsin secretion and levels of oxygen-free radicals; it decreases prostaglandin synthesis, gastric blood
flow, and mucus secretion [24]. Hypertension, diabetes,
and hyperlipidemia accelerate the atherosclerotic process,
which may affect the celiac axis leading to reduced gastric
blood flow. In patients with portal hypertension or
obstruction, there is decreased gastric blood flow due to
vascular congestion predisposing to gastric ischemia [25].
123
Dig Dis Sci
We observed gastric ischemia in one patient with portal
venous thrombosis presenting with sepsis.
CT imaging plays an important role in the assessment of
gastric ischemia, with the most common suggestive findings being gastric wall pneumatosis and portal venous gas
[26]. In the study by Tang et al., 30% of cases had gastric
pneumatosis and portal venous gas on imaging [3]. In our
study, a higher proportion of patients with gastric pneumatosis (54%) and portal venous gas (31%) were observed.
However, these findings are not specific for gastric ischemia since bacterial infections or increased intragastric
pressures can present similarly [7]. CT can also be helpful
in determining the etiology in some cases [17] as in the
current study; 61% of cases had CT findings pointing to an
identifiable cause for gastric ischemia including celiac
ostial stenosis and gastric outlet obstruction. However, a
negative CT scan does not rule out the potential for gastric
ischemia and endoscopy is more sensitive at detecting early
ischemic changes.
At endoscopy, ischemic changes include mucosal congestion, erythematous or purplish hue of the mucosa, large
surface ulcerations with or without bleeding stigmata, and
frank necrosis with black/gray eschar. The areas of
involvement are most commonly seen in the region of
anastomosis of arterial branches from lesser to greater
curvatures, along the anterior and posterior gastric wall [3].
In our study, the most common location of ischemic ulcers
involved the greater curvature of the gastric body and
fundus along the posterior wall of the stomach. The body
and fundus form the dependent parts of the stomach and
have increased risk for acid pocket formation causing
ulceration [3]. Therefore, early acid suppression is considered important in the management of gastric ischemia.
Conservative management of gastric ischemia includes
acid suppression and gastric decompression [3, 6]. As
mentioned previously, gastric acid suppressive therapy
reduces the formation of large acid pockets along the
dependent parts of the stomach [3]. Gastric ischemia
impairs motility of the stomach causing fluid and food
accumulation leading to stomach distension and worsening
of ischemia [6]. Thus, NG tube decompression alleviates
gastric distention and may reduce the extent of ischemia.
The use of antibiotics is recommended in patients with
gastric pneumatosis and portal venous gas to prevent
infection as these patients are at a higher risk for perforation [7]. In our series, one patient with gastric pneumatosis
developed perforation, further complicated by bacteremia
and gastric abscess formation, eventually leading to the
patient’s demise.
In some patients, specific intervention aimed at restoring
blood flow can be performed. Four patients in our series
underwent IR-guided stent placement for celiac stenosis.
Surgical intervention is indicated for gastric ischemia
123
caused by an incarcerated paraesophageal hernia or gastric
volvulus. As described above, most patients did not require
gastrectomy for management of gastric ischemia. In our
series, three of 17 patients required surgery for complications of gastric ischemia, including refractory bleeding,
full-thickness gastric necrosis, and gastric perforation.
The risk of rebleeding in gastric ischemia is not known.
In a study by Herman et al. [17], 43% of cases developed
significant upper GI rebleeding requiring repeat endoscopy,
whereas none of the patients was reported to develop
rebleeding in the study by Tang et al. [3]. Our results are
similar to the latter study with no episodes of rebleeding. It
is noteworthy, however, that in the study by Herman et al.
[17], the majority of cases with rebleeding had duodenal
ischemia (67%), suggesting that small bowel ischemia is
more likely to rebleed than gastric ischemia. Gastric
ischemia may be complicated by perforation, resulting into
shock and fatal outcomes [27]. In our series, 2 (12%)
patients developed perforation from gastric ischemia and
both died in hospital. Delay in the diagnosis of gastric
ischemia can lead to severe complications with high mortality rates.
Despite the inherent limitations related to the retrospective nature of our study, the latter gives an insight into
the natural history of gastric ischemia with a wide range of
etiological factors. Although there is an increasing awareness of this condition, it is critical to recognize the ischemia in an early stage to improve outcomes. Additional
study limitations include the non-standardized descriptive
features of ischemic gastropathy by different endoscopists
performing the procedure and lack of biopsy-proven
ischemic injury in all patients. Due to rarity of patients with
gastric ischemia and small proportion, the results and
conclusion of this study are based on limited numbers and
should be interpreted cautiously.
In conclusion, gastric ischemia is an uncommon condition that is associated with a variety of causative factors.
Cross-sectional imaging and endoscopy play an important
role in the assessment of ischemic gastropathy and help to
guide the type of intervention required. Conservative
management includes acid suppression and NG tube
decompression, with or without antibiotic therapy, based
on the severity of ischemic injury involving the gastric
wall. Specific interventional radiologic and/or surgical
management depends on the etiology of gastric ischemia.
Gastric perforation as a result of gastric ischemia carries
high morbidity and mortality.
Author’s contribution AS and SM were involved in study concept
and design; AS was involved in acquisition of data; AS and SM
analyzed and interpreted the data; all the authors drafted the manuscript; all the authors revised critically and approved the final
manuscript.
Dig Dis Sci
Compliance with ethical standards
Conflict of interest All the authors declare that they have no conflict
of interest.
References
1. Lanciault G, Jacobson ED. Progress in gastroenterology. Gastroenterology. 1976;71:851–873.
2. Casey KM, Quigley TM, Kozarek RA, Raker EJ. Lethal nature of
ischemic gastropathy. The American Journal of Surgery.
1993;165:646–649.
3. Tang SJ, Daram SR, Wu R, Bhaijee F. Pathogenesis, diagnosis,
and management of gastric ischemia. Clinical Gastroenterology
and Hepatology. 2014;12:246-52 e1.
4. Shafii AE, Agle SC, Zervos EE. Perforated gastric corpus in a
strangulated paraesophageal hernia: a case report. Journal of
Medical Case Reports. 2009;3:1.
5. Peterson CM, Anderson JS, Hara AK, Carenza JW, Menias CO.
Volvulus of the gastrointestinal tract: appearances at multimodality imaging 1. Radiographics. 2009;29:1281–1293.
6. Sahoo MR, Kumar AT, Jaiswal S, Bhujabal SN. Acute dilatation,
ischemia, and necrosis of stomach without perforation. Case
Reports in Surgery. 2013;2013:984594.
7. Patel RM, DeSoto-LaPaix F, Mallaiah LR. Gastric infarction: a
complication of endocarditis due to Staphylococcus aureus.
Journal of Clinical Gastroenterology. 1983;5:159–164.
8. Kondo S, Katoh H, Hirano S, et al. Ischemic gastropathy after
distal pancreatectomy with celiac axis resection. Surgery Today.
2004;34:337–340.
9. Schein M, Saadia R. Postoperative gastric ischaemia. British
Journal of Surgery. 1989;76:844–848.
10. Probst A, Maerkl B, Bittinger M, Messmann H. Gastric ischemia
following endoscopic submucosal dissection of early gastric
cancer. Gastric Cancer. 2010;13:58–61.
11. Molina-Infante J, Fernandez-Bermejo M, Vinagre-Rodrı́guez G.
Severe gastric ischemia after combined sclerotherapy for bleeding gastric ulcer. Endoscopy. 2011;43:E191-E.
12. Dorta G, Michetti P, Burckardt P, Gillet M. Acute ischemia
followed by hemorrhagic gastric necrosis after injection sclerotherapy for ulcer. Endoscopy. 1996;28:532.
13. Hilzenrat N, Lamoureux E, Alpert L. Gastric ischemia after
epinephrine injection for upper GI bleeding in a patient with
unsuspected
amyloidosis.
Gastrointestinal
Endoscopy.
2003;58:307–308.
14. Kim SY, Han S-H, Kim KH, et al. Gastric ischemia after epinephrine injection in a patient with liver cirrhosis. World Journal
of Gastroenterology: WJG. 2013;19:411.
15. Morante A, Romano M, Cuomo A. Massive gastric ulceration
after transarterial chemoembolization for hepatocellular carcinoma. Gastrointestinal Endoscopy. 2006;63:718–720.
16. Wadhwa SS, Perry MA. Gastric injury induced by hemorrhage,
local ischemia, and oxygen radical generation. American Journal
of Physiology-Gastrointestinal
and Liver
Physiology.
1987;253:G129–G133.
17. Herman J, Chavalitdhamrong D, Jensen DM, Cortina G, Manuyakorn A, Jutabha R. The significance of gastric and duodenal
histological ischemia reported on endoscopic biopsy. Endoscopy.
2011;43:365–368.
18. Sweren BS, Bohlman ME. Gastric and splenic infarction: a
complication of intraarterial vasopressin infusion. Cardiovascular and Interventional Radiology. 1989;12:207–209.
19. Oezcelik A, Banki F, Ayazi S, et al. Detection of gastric conduit
ischemia or anastomotic breakdown after cervical esophagogastrostomy: the use of computed tomography scan versus early
endoscopy. Surgical Endoscopy. 2010;24:1948–1951.
20. Lovat L. Age related changes in gut physiology and nutritional
status. Gut. 1996;38:306–309.
21. Iwao T, Toyonaga A, Ikegami M, et al. Gastric mucosal blood
flow after smoking in healthy human beings assessed by laser
Doppler
flowmetry.
Gastrointestinal
Endoscopy.
1993;39:400–403.
22. Takala J. Determinants of splanchnic blood flow. British Journal
of Anaesthesia. 1996;77:50–58.
23. Varhaug J, Svanes K, Lysen L, Holm P. The effect of intragastric
pressure on gastric blood flow after partial devascularization of
the stomach in cats. European Surgical Research.
1980;12:415–427.
24. Andrews F, Malcontenti-Wilson C, O’brien P. Protection against
gastric ischemia-reperfusion injury by nitric oxide generators.
Digestive Diseases and Sciences. 1994;39:366–373.
25. Iwao T, Toyonaga A, Ikegami M, et al. Reduced gastric mucosal
blood flow in patients with portal-hypertensive gastropathy.
Hepatology. 1993;18:36–40.
26. Binmoeller KF, Benner KG. Emphysematous gastritis secondary
to gastric infarction. American Journal of Gastroenterology.
1992;87:526–529.
27. Santos T, Freitas C, Pinto-de-Sousa J. Gastric wall ischemia
following massive gastric distension due to peptic pyloric
stenosis: a case report. Journal of Surgical Case Reports. 2016.
doi:10.1093/jscr/rjw008.
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