CASE REPORTS
Feline Emphysematous Gastritis in a Cat with
Pancreatitis and Secondary Hepatic Lipidosis
Emily Fulton, BVSc, Gawain Hammond, MA, VetMB, MVM, CertVDI, DECVDI, FHEA,
ndez Pe
Francesco Marchesi, DVM, PhD, DECVP, Marta Herna rez, DVM,
Alison E. Ridyard, BVSc, DSAM, DECVIM-CA
ABSTRACT
A 7 yr old female neutered domestic shorthair was presented with a 2 mo history of lethargy and hyporexia progressing
to anorexia. Initial diagnostics indicated pancreatitis with secondary hepatic lipidosis. Supportive care, including the
placement of an esophageal feeding tube, was initiated. The feeding tube was removed traumatically by the cat and thus
replaced. The cat acutely deteriorated while hospitalized, developing marked hypersalivation and an obtunded menta-
tion. Radiographs were taken to confirm placement of the feeding tube in case tube dislodgement was contributing to
the hypersalivation; results confirmed appropriate positioning and gastric pneumatosis. Despite intensified medical man-
agement, the patient suffered cardiopulmonary arrest 7 days after hospital admission. Post-mortem examination con-
firmed necrotizing gastritis with emphysema alongside segmental mucosal necrosis in the jejunum, focal pancreatic
necrosis, and diffuse hepatic lipidosis. Gas in the gastric wall is a rare finding in veterinary medicine and can arise due to
gastric pneumatosis or emphysematous gastritis; there are scant reports of either in feline medicine. This report docu-
ments a case of emphysematous gastritis in a cat with concurrent pancreatitis and hepatic lipidosis. The cat developed
emphysematous gastritis without undergoing gastrointestinal surgery which is currently the only reported feline predis-
posing factor for development. (J Am Anim Hosp Assoc 2022; 58:207–212. DOI 10.5326/JAAHA-MS-7228)
Introduction pressures leading to weaknesses in the mucosa, enabling the entrance
The presence of air within any tissue is known as pneumatosis. Air of air. In humans, this condition has been associated with severe
can rarely occur within the wall of any portion of the gastrointestinal vomiting, pyloric stenosis, and anorexia nervosa among other predis-
tract. In human literature, the colon is the most frequently reported posing factors.3–5 Conversely, emphysematous gastritis is defined by
site for pneumatosis, with gastric pneumatosis occurring much less the presence of bacteria within the gastric wall. Various bacteria have
1
commonly. There are two categories of gastric pneumatosis been implicated in human emphysematous gastritis, with Streptococci
reported in human medicine; the first is gastric emphysema, carrying sp, Escherichia coli, Enterobacter spp, Clostridium welchii, and Staph-
a favorable prognosis, and the second is emphysematous gastritis, ylococcus aureus being most frequently reported.6 Predisposing fac-
which is a much more critical condition, with reported mortality tors include ingestion of corrosive substances, alcoholism, abdominal
2
rates of between 33.3 and 59.4%. The distinction between emphyse- surgery, and diabetes mellitus.7 Reports of emphysematous gastritis
matous gastritis and gastric emphysema is largely based on the pres- in veterinary medicine are scant. In the cat, there have been just
ence or absence of gas-forming organisms. In the case of gastric seven reports of gastric pneumatosis and a single report of pneuma-
emphysema, bacteria are absent; an increase in gastric intraluminal tosis intestinalis.8–14 The single reported predisposing factor in cats
pressure is hypothesized to be the underlying trigger, with increased for the development of emphysematous gastritis is gastrointestinal
From the University of Glasgow, Glasgow, Scotland. FNA (fine-needle aspirate)
Correspondence: [email protected] (E.F.) Accepted for publication: June 3, 2021.
© 2022 by American Animal Hospital Association JAAHA.ORG 207
surgery.8 Canine gastric pneumatosis is also uncommon, and its cytology revealed no cells or microorganisms. Cytology of the liver
occurrence is most often associated with the presence of gastric dila- aspirates was most consistent with hepatic lipidosis. Culture of an
15
tion and volvulus. Here, we report a case of emphysematous gastri- FNA of the liver parenchyma (placed into an enriched medium
tis in a cat who had been diagnosed with pancreatitis with secondary blood culture bottlea) yielded a nonhemolytic Staphylococcus, which,
hepatic lipidosis; the cat was medically managed and had not under- in the absence of an inflammatory component to the FNAs, was
gone gastrointestinal surgery. most likely to represent contamination. The investigations concluded
that the cat had developed hepatic lipidosis resulting from anorexia
Case Report due to pancreatitis.
A 7 yr old female neutered domestic shorthair was referred to the To facilitate nutritional support and management of hepatic lipi-
Internal Medicine Department at the University of Glasgow for dosis, an esophageal feeding tube was placed using a standard curved
investigation of raised hepatic enzymes and increased total bilirubin. forceps technique and was secured in place with a finger trap suture.
The cat’s appetite had been slightly reduced for the previous 2 mo, Supportive therapy was then initiated for the treatment of suspected
with a significant deterioration in her condition noted over the 2 wk pancreatitis with secondary hepatic lipidosis. Buprenorphineb
before presentation, with hyporexia progressing to anorexia and leth- (0.2 mg/kg q 6 hr) and maropitantc (1 mg/kg q 24 hr) were adminis-
argy. Two days before referral, the owners had noticed that her pin- tered IV, and IV fluid therapyd was initiated (4 mL/kg/hr). Unfortu-
nae and mucous membranes had become icteric. nately, due to the fractious nature of the patient, the feeding tube was
On physical examination, the cat was quiet but alert. Her sclera, traumatically removed by the cat shortly after recovery, necessitating
pinnae, and mucous membranes were all confirmed to be jaundiced; replacement of the tube the following day with no complications
the rest of the examination was unremarkable; the cat had a body incurred during placement or recovery. Radiographs were taken and
condition score of 5/9.16 Routine clinicopathological testing was confirmed successful placement, and at that point there were no
performed. Hematology documented only a mild lymphopenia abnormalities within the cranial abdomen. Feeding via the esophageal
(0.617 3 109/L; reference range, 1.5–7 3 109/L). Serum biochemistry tube was started at a third of resting energy requirements because of
showed marked increases in alkaline phosphatase (458 U/L; reference the previous anorexia and was initially tolerated well. Oral ursodeoxy-
range, 0–100 U/L), aspartate transaminase (94 U/L; reference range, cholic acide (15 mg/kg q 24 hr) and S-adenosyl methionine/silybinf
0–30 U/L), and alanine transaminase (252 U/L; reference range, (90 mg/cat q 24 hr) were also introduced. Within 24 hr of initiation
0–35 U/L); gamma-glutamyl transferase activity was within normal of tube feeding, the cat began to develop marked hypersalivation.
limits (15 U/L; reference range, 0–15 U/L); total bilirubin was mark- Hematology and serum biochemistry were repeated and were
edly increased (180 mmol/L; reference range 0–10 mmol/L). Addi- unchanged aside from the development of mild hypokalemia
tionally, mild hypertriglyceridemia (1.06 mmol/L; reference range, (3.2 mmol/L; reference range 3.5–5.8 mmol/L). The opioid dose was
0–0.6 mmol/L), mild total hypercalcemia (2.89 mmol/L; reference halved and IV omeprazoleg (1 mg/kg q 12 hr) started in case of
range, 1.6–2.65 mmol/L), mild hyperglycemia (8.9 mmol/L; reference esophagitis; potassium supplementation was also added to the IV
range, 4.3–6.6 mmol/L), and hypophosphatemia (0.83 mmol/L; refer- fluid therapy. Mild hyperammonemia was detected (109 mmol/L; ref-
ence range, 1.29–2.84 mmol/L) were noted. Urinalysis was unre- erence range, ,60 mmol/L) raising the possibility of hepatic encepha-
markable aside from the presence of bilirubinuria. lopathy contributing to the cat’s clinical presentation.
A coagulation profile was performed and showed mild prolon- Overnight on day 6 of hospitalization (3 days after the feeding
gation in prothrombin time (19.3 s; reference range 9–14 s); activated tube placement), the cat deteriorated significantly, becoming severely
partial thromboplastin time and fibrinogen were within normal lim- depressed and unwilling to stand. Indirect blood pressure measure-
its. Abdominal ultrasonography was performed on the day of ments documented marked hypotension with a reading being unob-
admission and revealed changes compatible with hepatic lipidosis tainable. Repeat serum biochemistry showed a moderate azotemia
and pancreatitis: The liver was enlarged and diffusely hyperechoic, (creatinine 224 mmol/L; reference range, 71–212 mmol/L and urea
and the pancreas was mildly enlarged with a diffusely hypoechoic 24.9 mmol/L; reference range, 5.7–12.9 mmol/L), which was thought
appearance with the surrounding mesentery being marginally to be prerenal in origin. Hematology showed a persistent lymphope-
hyperechoic. There was no evidence of dilation of the biliary tract, nia, and, although the neutrophil count remained within the refer-
and the stomach was noted to be normal. ence range, there was a left shift with a significant band neutrophilia
To further define the cause of the serum biochemical changes, (2.08 3 109/L; reference range: 0–0); on smear analysis, the neutro-
cholecystocentesis and liver fine-needle aspirates (FNAs) were per- phils showed marked toxic changes. Thoracic radiographs were
formed under general anesthesia. Bile culture was sterile, and repeated to assess for aspiration pneumonia and to again check the
208 JAAHA | 58:4 Jul/Aug 2022
Feline Emphysematous Gastritis
position of the feeding tube, which confirmed appropriate feeding curvature, particularly in the antrum region. Approximately 80 mL of
tube placement to the level of the 9th rib. Although there was no gray/green fluid content was noted in the gastric lumen. The gastric
overt pulmonary or intrathoracic pathology, there was moderate gas- mucosa showed extensive green/yellow to dark red discoloration with
tric dilation due to gas (with the stomach extending beyond the 13th sparse small foci and irregular areas of red discoloration suggestive of
rib), and intramural gas was present in the ventral and caudo-lateral mucosal erosions (Figure 2A). In the areas of mucosal discoloration,
regions the gastric wall (Figure 1A), consistent with gastric pneuma- the gastric wall was thickened with slight crepitation at touch (emphy-
tosis. Functional ileus was also suspected based on the radiographic sema). Histological examination confirmed extensive necrosis of the
findings. Repeat abdominal ultrasounds showed an unchanged gastric mucosa with superficial bacteria including gram-positive cocci
appearance to the liver; assessment of the stomach showed gas infil- and gram-negative rods and slender bacilli (Figure 2B); there were
tration into the wall along a substantial area of the greater curvature multifocal and extensive round or irregular clear spaces in the submu-
of the stomach (Figure 1B). The jejunum and ileum were moderately cosa (Figure 2C), consistent with gas bubbles (emphysema) and diffuse
distended with fluid; there was no evidence of obstruction, although, edema affecting the submucosa and variably extending to the muscu-
as with the radiographs, there was suggestion of ileus. Because of the laris. There was variable sparse infiltration of hypersegmented and
clinical suspicion of sepsis, blood and urine samples were then col- degenerate neutrophils in the submucosa and most prominently asso-
lected and submitted for culture; both were reported to be sterile. ciated with the disrupted muscularis mucosae (Figure 2D). Focally
The patient received several fluidd boluses (5–10 mL/kg over extensive mucosal necrosis with associated gram-positive and
20 min) to positive effect and was then started on 6 mL/kg/hr of con- gram-negative bacteria was also present in the proximal jejunum.
tinued fluid therapy; serial blood pressure readings were taken, and Changes in the pancreas included a focal area of acinar necrosis and
systolic blood pressure was maintained above 60 mm Hg. IV cefurox- necrosis with saponification of adjacent peripancreatic adipose tissue.
imeh (20 mg/kg q 8 hr) and metronidazolei (10 mg/kg q 12 hr) Microscopic changes in the liver were consistent with hepatocellular
were administered because of the suspicion of sepsis; sucralfatej lipidosis.
(250 mg/cat q 8 hr) was administered via the feeding tube. Despite Fluorescence in situ hybridization analysis was performed on
intensification of medical management, the cat suffered cardiopul- tissue sections from the stomach and proximal jejunum and indi-
monary arrest 24 hr after the documentation of gastric pneumatosis. cated that the majority of bacteria present were E coli alongside clus-
Post-mortem evaluation was performed within 24 hr of death. ters of clostridia.
There was mild pale-yellow discoloration of subcutaneous and visceral
adipose tissue (jaundice). Approximately 40 mL of straw-colored fluid Discussion
was present in the abdominal cavity. The stomach showed focally There are sparse reports of feline gastric pneumatosis in veterinary
extensive red discoloration of the serosal surface along the greater literature. There are four reports of emphysematous gastritis, two of
FIGURE 1
Imaging. (A) Radiograph of the thorax and cranial abdomen demonstrating gastric pneumatosis (solid arrow). (B) Short-axis ultrasound
scan of the body of the stomach showing intramural hyperechogenicities (arrow heads) with distal reverberation indicating gastric
pneumatosis.
JAAHA.ORG 209
FIGURE 2
Cat stomach. (A) Macroscopic findings at postmortem examination: The necrotic mucosal surface shows an extensive area of green discolor-
ation with peripheral and sparse red mottling. (B) Large numbers of bacteria associated with the necrotic mucosa, including gram-positive
cocci (dark blue dots) and gram-negative rods (red) either sparse or in clusters. Gram stain. Original magnification 340. (C) Diffuse necro-
sis of the mucosa (arrowheads). The submucosa is expanded by multifocal irregular and variably coalescing clear spaces consistent with gas
bubbles (asterisks). HE stain. Original magnification 31.25. (D) Diffuse necrosis of the mucosa (asterisk). Diffuse necrosis of the muscularis
mucosae and submucosa with associated infiltration of degenerate neutrophils (arrowheads). HE stain. Original magnification 310. HE,
hematoxylin and eosin.
which were associated with abdominal surgery; one cat underwent In the current case, the cat was diagnosed with pancreatitis
exploratory laparotomy to obtain biopsies (including gastric biopsy) causing secondary hepatic lipidosis and underwent neither gastroin-
and the other to remove foreign material from the gastrointestinal testinal surgery nor any sampling of the gastrointestinal tract, thus
tract.8,9 In a third case, FNAs were taken from a thickened portion representing a case of emphysematous gastritis without any previous
10
of small intestine. The fourth case occurred in a cat with concur- interference to the abdominal gastrointestinal tract. Although the
rent hepatic portal venous gas; this cat had undergone endoscopy placement of the esophageal feeding tube and subsequent need for
retrieval of gastric foreign material alongside endoscopic biopsies of replacement was initially considered as a potential reason for the
the stomach and duodenum.14 In all cases, gastrointestinal tract development of gastric pneumatosis in this case, the lack of submu-
intervention was thought to be at least partially responsible for the cosal gas tracking on radiographs and the unremarkable appearance
development for feline emphysematous gastritis; this is also a of the esophagus and surrounding tissue at postmortem made this
7
reported risk factor in humans. unlikely. Gastric emphysema has been reported as a complication of
210 JAAHA | 58:4 Jul/Aug 2022
Feline Emphysematous Gastritis
nasogastric tube placement in a human, resulting from extension of Although feline emphysematous gastritis is a rare occurrence, if
the nasogastric tube into the gastric mucosa.17 However, direct gas- encountered in the future, rapid administration of antibiotic therapy
tric trauma during feeding tube placement in this case was consid- as in humans is also advocated. Culture and sensitivity was unfortu-
ered unlikely. nately not performed either ante- or postmortem in this case; how-
In human medicine, emphysematous gastritis has been reported ever, fluorescence in situ hybridization analysis indicated E coli as
secondary to acute pancreatitis.18 In this case, it was hypothesized the predominant bacteria present in association with the mucosal
that age-related immunocompromise and patient co-morbidities had lesions; clusters of clostridia were also noted. Previous reports of
led to compromise of the protective function of the stomach wall. feline emphysematous gastritis implicate Enterococcus sp., E coli,
Interestingly, pancreatitis was also present in a previous case of feline Candida albicans, Lactobacillus minitus, and Clostridium perfringens
emphysematous gastritis as well as in the case of feline gastric Type A as causative agents.8–10 Therefore, a broad-spectrum antibi-
emphysema.8,11 In the current case, it is likely that the cause of otic such as amoxicillin-clavulanate should be considered as a first
emphysematous gastritis was multifactorial, but we hypothesize that choice to cover for the range of organisms that may be present. In
regional peritonitis secondary to pancreatitis, hypotension, and local humans, culture and sensitivity of the gastric fluid has reported to be
vascular events such as thromboembolism contributed to compro- of use for tailoring antibiotic therapy.25
mise of the gastric mucosa allowing colonization with bacteria. The Administration of nutrition bypassing the stomach is also of
use of omeprazole could have contributed to gastrointestinal dysbio- importance. Total parenteral nutrition in veterinary medicine can be
sis, leading to the proliferation of noncommensal bacteria within the complex and is not without its own inherent risk, such as the devel-
stomach. In humans, the use of proton pump inhibitors is linked to opment of sepsis.26 In one previous feline case report in which the
gastric bacterial overgrowth and development of enteric infection, cat survived to discharge, a jejunostomy tube was placed to allow
such as enteric C difficile, due to the reduced increased gastric pH food to bypass the stomach, and thus this procedure may worth con-
that results from proton pump inhibitor use.19 Alternatively, the sidering in future cases.8
development of ileus could have altered the bacterial population pre- Of the previously reported case of feline emphysematous gastri-
sent within the stomach; several studies in both the cat and dog have tis, two survived and the third was euthanized. Emphysematous
shown that acute gastrointestinal disease can be linked with changes gastritis proved fatal in this case, thus providing a reminder of the
within the gastrointestinal microbial population.20 severity of the condition. This case represents a cat with emphysema-
Differentiation of emphysematous gastritis from gastric emphy- tous gastritis with no prior abdominal surgery or procedures related
sema based on radiography alone can be challenging. In cases of to the gastrointestinal tract. The cat had been diagnosed with pancre-
emphysematous gastritis in humans, numerous mottled cystic lesions atitis, and therefore it is suggested that emphysematous gastritis may
are usually observed within the wall of the gastric mucosa on radio- represent a rare and severe complication of this condition.
graphs in comparison to the linear pattern that is more commonly
associated with gastric emphysema.21 However, the linear pattern We gratefully acknowledge Lynn Oxford, Frazer Bell, and Lynn
seen with gastric emphysema is not pathognomonic and can also be Stevenson (Veterinary Diagnostic Services, University of Glas-
observed in cases of emphysematous gastritis.21 In the majority of gow School of Veterinary Medicine) for technical support with
cases, it falls to the clinical assessment of the patient to determine tissue processing for histopathology. In addition, we thank
whether gastric emphysema or emphysematous gastritis seems most Elspeth Waugh and the Clinical Pathology team for their assis-
likely. In this case, because of the rapid deterioration, development tance with the cytology. We thank Debbie Langton and Tristan
of sepsis, and ultimately fatal outcome, emphysematous gastritis was Cogan (Langford Vets Diagnostic Services, University of Bristol)
strongly suspected. for their support with FISH analysis.
Historically, in human medicine, emphysematous gastritis was
managed with surgical debridement of necrotic tissue. However, FOOTNOTES
a
more recently, there has been a switch toward early medical manage- Signal Blood Culture System; Oxoid LTD, Basingstoke, Hampshire,
United Kingdom
ment and endoscopic evaluation to assess for the need for surgical b
Vetergesic; Ceva Animal Health, Ltd., Amersham, Buckinghamshire,
intervention (for example, evidence of gastric infarction or perfora- United Kingdom
c
tion); this change in approach has been credited with a reduction in Cerenia; Zoetis UK, Ltd., Leatherhead, Surrey, United Kingdom
d
Vetivex (Hartmann’s) 11 Solution for Infusion; Dechra Veterinary Prod-
mortality rates.2 Medical management in humans often consists of
ucts, Shrewsbury, Shropshire, United Kingdom
broad spectrum antibiotics, supportive IV fluid therapy, and the use e
Destolit; Norgine Pharmaceuticals, Ltd., Harefild, Uxbridge, United Kingdom
23,24 f
of parenteral nutrition to permit gastrointestinal tract to recover. Denamarin; Protexin Veterinary, Somerset, United Kingdom
JAAHA.ORG 211
g
Omeprazole; Servipharm Limited, Harrow, Greater London, United clinical and imaging characteristics: Five cases. Vet Radiol Ultrasound
Kingdom 2019;60:136–44.
h
Zinacef; GlaxoSmithKline UK, Brentford, Middlesex, United Kingdom 13. Walczak R, Paek M, Suran J, et al. Radiography and ultrasonography of
i
Metronidazole 5 mg/mL; B. Braun Melsungen AG, Melsungen, Germany pneumatosis intestinalis in a cat. Vet Radiol Ultrasound 2018;61:E26–30.
j
Antepsin; Laboratoria Baldacci S.P.A., Pisa, Italy 14. Spiller KT, Eiseberg BW. Extensive hepatic portal venous gas and gastric
pneumatosis in a cat. Vet Med Sci 2021;7:593–9.
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