A 5-month-old 1.9-kg (4.2-lb) spayed female Siamese cat was referred to the Mississippi State University Animal Health Center for evaluation because of intermittent vomiting, regurgitation, decreased appetite, and lack of weight gain. The clinical signs were first observed after an ovariohysterectomy performed by the referring veterinarian 22 days earlier. Regurgitation occurred after feeding, and the cat was vomiting approximately 3 times daily. Dietary changes were unsuccessful in resolving the decreased appetite. At the time of evaluation at the referral hospital, the owners had been spoon-feeding the cat 1 tablespoon of a canned high-calorie dieta every 2 to 4 hours. Examination revealed that the cat was approximately 5% dehydrated and lethargic, with a body condition score of 4 (scale, 1 to 9).1 The abdomen was tense when palpated. A CBC, serum biochemical analysis, urinalysis, fecal flotation, and FIV, FeLV, and feline heartworm antigen tests were performed, and survey abdominal radiographs were obtained.
Clinicopathologic abnormalities included neutropenia (1,353 cells/μL; reference range, 2,500 to 12,500 cells/μL), lymphocytosis (9,348 cells/μL; reference range, 1,500 to 7,000 cells/μL), slight anisocytosis, and poikilocytosis. Hypoglobulinemia (2.7 g/dL; reference range, 4.1 to 6.0 g/dL) and low total protein concentration (5.3 g/dL; reference range, 6.5 to 8.4 g/dL) were also present. Urine specific gravity was 1.027, and hematuria (50 to 100 RBCs/hpf; reference range, 0 to 5 RBCs/hpf) was detected. Results of fecal flotation were positive for Toxocara spp. Results of FIV, FeLV, and feline heartworm antigen tests were negative.
Radiographic findings included decreased detail in the midabdominal region, a fluid- and gas-distended stomach with a small accumulation of mineral opacities, and caudal displacement of other abdominal viscera (Figure 1). On the basis of these findings, a tentative diagnosis of pyloric outflow obstruction was made. Severe fluid distention of the stomach was also observed during ultrasonographic examination of the abdomen. Additionally, multiple well-defined and hyperechoic structures were detected within the gastric lumen, and the circumferentially thickened pylorus (wall thickness, approx 6 mm) was seen invaginating into the gastric lumen (Figure 2). Real-time ultrasonographic investigation revealed normal pylorogastric serosal continuity. Subjectively, both kidneys were mildly decreased in size, with mild dilation of the left renal pelvis. A minimal amount of anechoic free fluid was found within the abdomen. Ultrasonographic diagnoses included pyloric outflow obstruction with abnormal pyloric wall thickness and mild left renal pyelectasia.
Survey abdominal radiographs (ventrodorsal [A], right lateral [B], and left lateral [C] views) of a 5-month-old spayed female Siamese cat evaluated because of intermittent vomiting, regurgitation, decreased appetite, and lack of weight gain. A—The stomach (arrowheads) is severely distended with fluid and gas, and other abdominal organs are displaced caudally. B—With the patient in right lateral recumbency, the distended pylorus (arrowheads) can be seen as a soft tissue opacity. C—With the patient in left lateral recumbency, the gas-filled lumen of the stomach (arrowheads) is evident, and a small accumulation of faint, pinpoint mineral opacities is present within the pylorus (circle). This finding, known as a gravel sign, is supportive of pyloric outflow obstruction.11
Citation: Journal of the American Veterinary Medical Association 242, 6; 10.2460/javma.242.6.792
Ultrasonographic image of the stomach and pylorus of the same cat as in Figure 1, with the patient in dorsal recumbency (left side of the image is cranial). The pylorus is seen protruding into the gastric lumen, mimicking the appearance of an intussusception. The pyloric wall is thickened, and severe gastric distention with echogenic fluid and small hyperechoic structures are present.
Citation: Journal of the American Veterinary Medical Association 242, 6; 10.2460/javma.242.6.792
The cat was anesthetized for endoscopic evaluation of the upper gastrointestinal tract. Following premedication with dexmedetomidine (5 μg/kg [2.3 μg/lb]) and butorphanol tartrate (0.4 mg/kg [0.18 mg/lb]), IM, an over-the-needle catheter was inserted in a cephalic vein, and anesthesia was induced via IV administration of propofol (2.5 mg/kg [1.1 mg/lb]). The cat was intubated, and anesthesia was maintained with isoflurane in oxygen. A flexible gastrointestinal videoscopeb with an insertion tube (outer diameter, 8.6 mm; working length, 1,030 mm) was used to evaluate the upper gastrointestinal tract. Results of esophageal evaluation were unremarkable. The stomach was dilated with liquid and ingesta. The pyloric antrum was abnormally shortened, and the pylorus was very difficult to identify; careful probing with a blunt-tipped forceps revealed the pyloric outflow orifice. The diameter of the pyloric antrum was estimated to measure 2 mm. These findings confirmed stenosis of the pyloric outflow tract.
On the basis of these results, a pylorectomy and gastroduodenostomy (Billroth I) procedure was recommended to the owner. The owner elected to pursue surgery, which was performed under the same anesthetic episode. Cefazolin (22 mg/kg [10.0 mg/lb]) was administered IV. Exploratory surgery via a ventral midline celiotomy revealed palpable thickening of the pyloric region of the stomach. All other organs were grossly normal. Stay sutures (4-0 polydioxanone) were placed in the stomach and duodenum adjacent to the proposed pylorectomy site. These sutures were used to manipulate the stomach and duodenum throughout the procedure. Margins of resection for the pylorectomy were visualized 1 to 2 cm orad and aborad of the pylorus. Branches of the right gastric and gastroepiploic arteries and veins supplying the pylorus were identified, isolated, and cauterized by means of bipolar electrocautery. The cauterized vessels were then sharply divided. During dissection, care was taken to avoid the common bile duct and disruption of the blood supply to adjacent structures. Doyen forceps were placed orad and aborad to the planned area of resection. A straight Kelly forceps was then placed opposite each Doyen forceps across the area to be resected. The pylorus was transected orad and aborad to the Kelly forceps with a No. 15 scalpel blade. Starting from the lesser curvature, the pyloric antrum was closed in a simple interrupted pattern with 4-0 polydioxanone suture, leaving a stoma with approximately the same diameter as the duodenum. The duodenum and pyloric antrum were anastomosed with 4-0 polydioxanone suture in a simple interrupted pattern.
A purse string suture of 3-0 polydioxanone was then placed in the gastric body, and a full-thickness stab incision was made within the purse string. A 16F, 39-cm-long silicone gastrostomy tube was introduced into the gastric lumen, and the purse string suture was tied. A stab incision was made in the left body wall, just caudal to the last rib, and the gastrostomy tube was passed through this stab incision site. Gastropexy to the left abdominal wall was performed with 3-0 polydioxanone suture in an interlocking box pattern. Nylon suture (3-0) was used to secure the tube to the skin at the exit site in a fingertrap pattern. Lavage of the surgical region and peritoneal cavity was performed with sterile saline (0.9% NaCl) solution, and the abdomen was closed routinely. Recovery from anesthesia was uneventful.
Immediate postoperative care included IV fluid therapy with lactated Ringer's solution (3 mL/kg/h [1.4 mL/lb/h]) and a constant rate infusion of fentanyl (5 μg/kg/h, IV) for analgesia. Maropitant citrate (1.0 mg/kg [0.45 mg/lb], q 24 h) and famotidine (0.1 mg/kg [0.05 mg/lb], q 12 h) were administered SC. Pyrantel pamoate (10 mg/kg [4.5 mg/lb]) was administered via the gastrostomy tube for treatment of the Toxocara spp infection. Gastric contents were aspirated via the gastrostomy tube, and the tube was flushed with 5 mL of warm water every 4 hours. The fentanyl infusion was incrementally decreased and was discontinued 24 hours after surgery. Beginning at that time, buprenorphine (0.01 mg/kg [0.005 mg/lb], IV) was administered every 8 hours. Sucralfate suspension (200 mg; 105.3 mg/kg [47.86 mg/lb]) was administered every 8 hours via the gastrostomy tube as prophylaxis against gastrointestinal ulceration, and feeding was reinstituted, starting with one-fourth of a can of a high-calorie moist dieta every 6 hours via the gastrostomy tube. On the second day following surgery, the maropitant citrate was discontinued because of the cat's excellent appetite and lack of vomiting.
Six days after admission, the cat was discharged to the owner. At that time, the cat was eating and drinking normally and the gastrostomy tube was only being used for administration of medications. The owner was instructed to administer famotidine (0.5 mg/kg [0.23 mg/lb], q 12 h) and sucralfate (200 mg, q 8 h) through the gastrostomy tube and buprenorphine (0.01 mg/kg, PO, q 8 h) and to return the cat for examination in 1 week.
One day after discharge, the cat was reevaluated at the veterinary medical teaching hospital because it had disrupted the sutures securing the gastrostomy tube to the skin. These sutures were replaced, and at the owner's request, the cat was readmitted to the hospital. All medications were continued at the same dosages. The cat was fed the same high-calorie canned dieta (one-fourth of a can, q 6 h) and remained hospitalized for 5 days, at which time the gastrostomy tube was removed. Upon discharge, the owner was instructed to continue famotidine administration (0.5 mg/kg, PO, q 12 h) and to have a follow-up evaluation by the referring veterinarian in 5 to 7 days for assessment of the gastrostomy stoma and again in 3 weeks for a second treatment for Toxocara spp infection.
Histologic evaluation of the resected tissue revealed that the wall of the pylorus was abruptly and irregularly thickened by haphazardly arranged bundles of smooth muscle with some subdividing bands of fibrous connective tissue (Figure 3). Scattered lymphocytic aggregates, usually associated with blood vessels, were interspersed among these tissues. The submucosa also contained fibrovascular tissue with numerous profiles of arteries and veins, interspersed with mesenchymal cells, and minimal mononuclear infiltrates. Many of these mesenchymal cells tested positive for smooth muscle actin via immunohistochemical analysis,c indicating smooth muscle myofiber or myofibroblast origin (Figure 4). A focus of mucosal ulceration, covered by a coagulum of fibrin, necrotic cellular debris, and small numbers of degenerate leukocytes, was detected. Histologic and immunohistochemical findings were consistent with a diagnosis of hypertrophy of the tunica muscularis of the surgically excised pyloric tissue.
Photomicrograph of a section of the resected pylorus from the cat in Figure 1. The tunica muscularis is focally and irregularly thickened, and smooth muscle bundles are moderately disorganized. Scattered lymphocytic aggregates (arrows), usually associated with blood vessels, are interspersed within the muscularis. H&E stain; bar = 500 μm.
Citation: Journal of the American Veterinary Medical Association 242, 6; 10.2460/javma.242.6.792
Photomicrograph of a section of the resected pylorus from the cat in Figure 1 obtained at the juncture of the submucosa and tunica muscularis. Immunostaining (dark brown) demonstrates irregular smooth muscle bundles and likely myofibroblasts at the juncture of thickened tunica muscularis and submucosa. Immunohistochemical stain for smooth muscle actin with hematoxylin counterstain; bar = 200 μm.
Citation: Journal of the American Veterinary Medical Association 242, 6; 10.2460/javma.242.6.792
Results of a follow-up physical examination by the referring veterinarian 3 weeks after surgery were normal. The owner reported no vomiting at that time, and the cat's appetite was good. Approximately 2 months after surgery, the owner reported occasional vomiting. Famotidine treatment was reinstituted at the described dose; because of problems with twice-daily pill administration, famotidine was discontinued, and treatment was initiated with an omeprazole suspension (0.6 mg/kg [0.27 mg/lb], PO, q 24 h). Approximately 3 months after surgery, the omeprazole was changed to every-other-day dosing, to be continued indefinitely. Through continued telephone communication up to 15 months following surgery, the owners reported that the cat seemed completely normal both in appearance and behavior.
Discussion
Pyloric stenosis of young cats has been reported rarely. In 1970, Twaddle2 reported pyloric stenosis in 3 cats that were between 11 and 14 months of age at the time of initial evaluation; 2 of these were sexually intact female Siamese, and 1 was a neutered male domestic shorthair. Two additional sexually intact female Siamese cats with the condition were reported by Twaddle3 in 1971; these kittens were 6 months old at the time of evaluation and were offspring of one of the female Siamese cats treated previously. The clinical signs described in those reports2,3 included persistent vomiting, a good appetite despite vomiting, thin body condition, and regurgitation of any solid food. Radiographic examinations of the upper gastrointestinal tract following oral administration of barium sulfate contrast medium were performed in all of those patients.2,3 A tentative diagnosis of pyloric stenosis was made on the basis of prolonged gastric emptying times and clinical history.2,3 All 5 cats were treated via Heineke-Mikulicz pyloroplasty. After surgery, one of the older cats vomited occasionally, with complete resolution after 1 month.2 In 2 of the younger cats, vomiting was seen 2 to 3 times daily during the first 10 days but became progressively less frequent, with complete resolution 2 months after surgery.3 Follow-up time was variable, but was as long as 1 year, and all cats were reported to be clinically normal when the last update was obtained.2,3
In 1974, Pearson et al4 described 13 cats with delayed gastric emptying. All cats were ≤ 2 years of age, and 11 of 13 were of the Siamese breed. Nine of these 13 cats also had some degree of esophageal dilatation or dysfunction, determined on the basis of esophagoscopy results. All of these cats were treated via a Fredet-Ramstedt pyloromyotomy. Five cats were clinically normal following recovery from surgery, and 5 had intermittent vomiting or regurgitation; 3 had no improvement and died or were euthanized because of their clinical signs.
Overall, the previous reports2–4 of pyloric stenosis in cats treated by means of pyloroplasty or pyloromyotomy revealed favorable outcomes in many cases, with resolution or improvement of clinical signs. Because of the young ages of cats in reported cases and apparent heritability of the condition, a congenital etiology has been assumed. However, determining a specific etiology is difficult because no histopathologic findings have previously been described for patients with this condition.
Pyloric stenosis also occurs in dogs and is also known as antral pyloric hypertrophy syndrome or chronic hypertrophic pyloric gastropathy. The congenital form of the disease is less common and is characterized by selective hypertrophy of the muscularis of the pylorus; this most commonly develops in Boxers and Boston Terriers.5 The acquired form of the disease is more common in male dogs and small breeds such as Lhasa Apso, Shih Tzu, Pekingese, and Miniature Poodle.6 With this form of the disease, mucosal hypertrophy is present, with or without hypertrophy of the muscularis.5,6 In humans, pyloric stenosis is a frequently encountered condition of newborns and infants. It is characterized by hypertrophy of the pyloric musculature and typically treated via pyloromyotomy.7
In the cat described in the present report, a presumptive diagnosis of congenital pyloric outflow obstruction was made on the basis of the clinical history of intermittent vomiting and anorexia and progressive weight loss, along with radiographic and ultrasonographic evidence of gastric distension. Diagnostic imaging of the abdomen facilitates the diagnosis of mechanical pyloric outflow obstruction. Abdominal radiographs reveal marked gastric distention with fluid and gas, as in the patient of this report. Ultrasonography is used in the evaluation of gastric wall thickness and the presence of intramural or extramural lesions, which may contribute to decreased gastric outflow.
The normal ultrasonographic appearance of the feline gastrointestinal tract has been described. The pylorus lies slightly more on the midline in cats than in dogs, with gastric wall thickness measuring between 1.1 and 3.6 mm.8 Measurements may be greater if obtained when the stomach is empty and may also vary depending on whether the measurement is made in the region of a rugal fold or interrugal area. To the authors' knowledge, the ultrasonographic appearance of pyloric stenosis in cats has not been described. In dogs, congenital pyloric hypertrophy can be visualized ultrasonographically as a localized, circumferential thickening of the pylorus.9 The thickened pylorus can protrude into the gastric lumen and mimic the appearance of an intussusception.10 In 1 study,11 gastric wall thickness was > 9 mm in all dogs evaluated. In the cat of the present report, the pylorus was moderately thickened, measuring approximately 6 mm, with a multilayered puckered pattern protruding into the gastric lumen. Gastric body wall thickness measured up to 3 mm, but the lumen was severely distended with fluid and ingesta. Upon further ultrasonographic evaluation, the serosal margins of the wall of the pylorus were identified and found to be contiguous with the gastric wall, eliminating the suspicion of intussusception. Although not pathognomonic for obstruction or hypertrophy in animals, food and fluid were not observed to pass through the lumen of the pylorus during ultrasonography, supporting decreased peristalsis. In a previous report11 that described ultrasonographic examination of 6 dogs with pyloric hypertrophy, 5 were noted to have no movement of gastric contents through the pylorus despite peristaltic activity. Additionally, a fluid- or food-distended stomach can aid in determining delayed gastric emptying, especially if the time of previous feeding is known.11 In children, diagnosis of pyloric stenosis is usually made ultrasonographically, and for experienced evaluators, accuracy of diagnosis approaches 100%.7 In these cases, the lesion can be seen as a thickened prepyloric antrum bridging the distended stomach and duodenal ampulla.7 Results of upper gastrointestinal endoscopy were definitive for stenosis in the cat of this report and prompted surgery.
To the best of the authors' knowledge, this is the first report of a cat with histologic findings of smooth muscle hypertrophy and fibrosis supporting the clinical diagnosis of pyloric stenosis. This is most analogous to the congenital form of pyloric stenosis found in young Boxers and Boston Terriers and in human infants.5,7
In addition to the previously mentioned treatment options of Heineke-Mikulicz pyloroplasty and Fredet-Ramstedt pyloromyotomy described for cats with pyloric stenosis,2–4 reported treatments for dogs with pyloric stenosis have included Y-to-U pyloroplasty and pylorectomy.5 With pylorectomy, resected tissue can be submitted to help provide a definitive diagnosis. Pylorectomy has been used for primary treatment and as a revision surgery for the treatment of this condition in dogs. In 1 report,12 pylorectomy was advocated for as the best initial treatment for dogs with pyloric stenosis involving either large amounts of redundant mucosa or thickened pyloric musculature. Treatment of pyloric stenosis with a Billroth I procedure has not been previously reported in cats. In this case, it is the authors' opinion that the stenosis was so severe that pyloromyotomy or pyloroplasty procedures may not have provided adequate relief from the outflow obstruction.
Pylorectomy in cats has been described in 2 clinical reports.13,14 Runk et al13 described the use of this technique with a favorable outcome in a 1-year-old cat for treatment of duodenal perforation associated with oral administration of carprofen following ovariohysterectomy. After prolonged treatment for septic peritonitis, the cat recovered fully and was apparently normal according to the owners 6 months after surgery. A report by Shimamura et al14 described use of the Billroth I procedure in a 7-year-old cat for treatment of a pyloric mass, which was histologically confirmed as lymphoma. Although recovery from surgery was excellent, the patient began vomiting intermittently approximately 3 weeks after surgery. The vomiting was attributed to megaesophagus, which was reported as a complication of the pylorectomy, although the relationship between that condition and the surgery was not clear.
The prognosis following pylorectomy in dogs for benign causes of gastric outflow obstruction is good.12,15 However, complications can occur, including dehiscence and septic peritonitis, gastric atonia, persistent or recurrent outflow obstruction, and inadvertent common bile duct trauma.12,15 Although the technique for gastroduodenostomy is similar to an intestinal end-to-end anastomosis, a thorough knowledge of pyloric anatomy is necessary to avoid serious surgical errors because of the proximity of the pancreas, bile duct, and major vessels.12,15
Congenital pyloric stenosis in cats is rare. However, it should be considered when a young cat, particularly of Siamese breed lineage, is evaluated because of signs of pyloric outflow obstruction. To the authors' knowledge, this is the first report that describes ultrasonographic and histologic changes associated with pyloric stenosis in a cat. Additionally, this is the first report of use of the Billroth I procedure to treat this condition in a cat, and the treatment resulted in resolution of the clinical signs associated with pyloric obstruction.
Science Diet a/d, Hill's Pet Nutrition, Topeka, Kan.
Evis Exera Gastrointestinal Videoscope GIF Type 160, Olympus America Inc, Melville, NY.
Smooth muscle actin antibody, DAKO North America Inc, Carpinteria, Calif.
References
1. LaFlamme DP. Development and validation of a body condition score system for cats: a clinical tool. Feline Pract 1997; 25(5–6):13–18.
2. Twaddle AA. Pyloric stenosis in three cats and its correction by pyloroplasty. N Z Vet J 1970; 18: 15–17.
3. Twaddle AA. Congenital pyloric stenosis in two kittens corrected by pyloroplasty. N Z Vet J 1971; 19: 26–27.
4. Pearson H, Gaskell CJ, Gibbs C, et al. Pyloric and oesophageal dysfunction in the cat. J Small Anim Pract 1974; 15: 487–501.
5. Guilford W. Antral pyloric hypertrophy syndrome (pyloric stenosis). In: Strombeck DR, ed. Small animal gastroenterology. 3rd ed. Philadelphia: WB Saunders Co, 1996; 296–300.
6. Matthiesen DT, Walter MC. Surgical treatment of chronic hypertrophic pyloric gastropathy in 45 dogs. J Am Anim Hosp Assoc 1985; 22: 241–247.
7. Aspelund G, Langer JC. Current management of hypertrophic pyloric stenosis. Semin Pediatr Surg 2007; 16: 27–33.
8. Newell SM, Graham JP, Roberts GD, et al. Sonography of the normal feline gastrointestinal tract. Vet Radiol Ultrasound 1999; 40: 40–43.
9. Pennick DG, Nyland TG, Kerr LY, et al. Ultrasonographic evaluation of gastrointestinal disease in small animals. Vet Radiol 1990; 31: 134–141.
10. Pennick D. Gastrointestinal tract. In: Pennick D, d'Anjou M-A, eds. Atlas of small animal ultrasonography. Ames, Iowa: Blackwell Publishing, 2008;287.
11. Biller DS, Partington BP, Miyayashi T, et al. Ultrasonographic appearance of chronic hypertrophic pyloric gastropathy in the dog. Vet Radiol Ultrasound 1994; 35: 30–33.
12. Walter MC, Matthiesen DT, Stone EA. Pylorectomy and gastroduodenostomy in the dog: technique and clinical results in 28 cases. J Am Vet Med Assoc 1985; 187: 909–914.
13. Runk A, Kyles AE, Downs MO. Duodenal perforation in a cat following the administration of nonsteroidal anti-inflammatory medication. J Am Anim Hosp Assoc 1999; 35: 52–55.
14. Shimamura S, Shimizu M, Hirao H, et al. Megaesophagus was complicated with Billroth I gastroduodenostomy in a cat. J Vet Med Sci 2005; 67: 935–937.
15. Eisele J, Kovak McClaran J, Runge JJ, et al. Evaluation of risk factors for morbidity and mortality after pylorectomy and gastroduodenostomy in dogs. Vet Surg 2010; 39: 261–267.
