Pylorogastric intussusception in a Chihuahua puppy. A case report

Abstract

A three-month-old Chihuahua dog was presented with acute abdominal pain, vomiting and cardiovascular shock. Abdominal ultrasound (US) and iodated contrast gastrogram revealed suspected pylorogastric intussusception. Because of the poor prognosis the dog was euthanatized. Diagnosis of pylorogastric intussusception was confirmed at necropsy. Parasitological, virological, serological and histological examinations were also performed. This report documents the sixth case of pylorogastric (i.e. duodenogastric, gastrogastric) intussusception in the veterinary medical literature and it is the first report on a puppy dog in which US and radiographic diagnosis were confirmed post mortem.

Introduction

Intussusception is defined as a prolapse of a part of the intestine into the lumen of an immediately adjoining part and has been reported in both humans and animals. In dogs and cats intussusception most commonly occurs at the ileocecocolic junction where invagination is usually in the normal direction of peristalsis. Occasionally invaginations occur in the reverse direction (oral direction) within the small intestine and in other parts of the alimentary tract (i.e. gastroesophageal, pylorogastric or duodenogastric intussusceptions) [1,3,5,7,10]. Our report describes the first case of pylorogastric intussusception in a puppy of a small-breed dog along with clinical, radiological, US and post mortem findings.

Case history

A three-month-old, female Chihuahua dog, 650 g body weight (BW), with an acute history of abdominal pain, vomiting and hypovolemic shock was presented to our clinic. The vomiting had occurred on a few occasions during the previous week.

At the time of the examination, clinical findings included lethargy, dehydration (approximately 8%) and hypothermia (36.5 °C). The dog’s abdomen was tense on palpation. A complete blood count (CBC), serum biochemical analysis (SBA) and urinalysis (UA) were performed, and therapy with intravenous (IV) lactated Ringer’s solution (LRS) was administered.

Clinicopathological abnormalities included moderate leukocytosis (21.07 × 10³/μL; reference range (RR): 5.5–16.9 × 10³/μL), high neutrophil count (13.82 10³/μL; RR: 2–12 × 10³/μL) and monocytosis (3.26 × 10³/μL; RR: 0.1–1.4 × 10³/μL). Serum biochemical abnormalities included hypoproteinemia (4 g/dL; RR: 5.7–7.7 g/dL), hypoalbuminemia (1.6 g/dL; RR: 2.6–4 g/dL), low calcium levels (7.6 mg/dL; RR: 8–12 mg/dL) and hypocholesterolemia (73 mg/dL; RR: 110–300 mg/dL). Electrolytes presented moderate hyponatriemia (140 mmol/L; RR: 146–154 mmol/L), hypochloridemia (97 mmol/L; RR: 107–125 mmol/L) and mild metabolic alkalosis (27 mmol/L; RR: 14–24 mmol/L), while hematic pH was 7.44. UA showed a specific gravity of 1.015 with aciduria (urine pH 6).

Intravenous fluid therapy was continued using 0.9% sodium chloride solution (6 mL/kg BW/hour), ranitidine (4 mg/kg BW) and cefazolin (22 mg/kg BW).

Abdominal radiograph showed distension of the gastric area. Abdominal US examination was performed (General Electric Logic 5 Expert) using a 7.5–10 MHz convex probe in order to evaluate the cause of the abdominal pain; the stomach was distended and filled with fluid, and the pyloric region appeared laminated, while the pylorus and proximal duodenum were displaced into the pyloric antrum and fundus. In addition, multiple concentric echogenic and echolucent rings were visible. A severe hypoechoic gastric mucosal layer caused by edema was also present (Fig. 1).

Fig. 1.

US examination of the pylorogastric intussusceptions. (a) Transverse image of the pyloric region. Multiple concentric echogenic and echolucent rings were visible. (b) Longitudinal image of intussusceptions seen in (a); pylorus and proximal duodenum were displaced into the pyloric antrum and fundus; severely hypoechoic gastric mucosal layer caused by edema (arrow).

Radiographic evaluation of the stomach and duodenum using iodated contrast medium showed double lines into the gastric lumen associated with abnormal distension of the stomach. Radiographic analysis 45 and 120 min after ingestion of iodated contrast media demonstrated weak propulsion of the contrast medium and a double layer into the gastric lumen.

Diagnosis of pylorogastric intussusception was made, and the dog was euthanatized because of the poor prognosis. Diagnosis was subsequently confirmed at necropsy, but the clear causes were not found. Parasitological, serological and virological examinations were negative, while histological examination revealed diffuse superficial erosion of the gastric mucosal layer (Fig. 2).

Fig. 2.

Diffuse superficial erosion of the gastric mucosal layer, sub-mucosal congestion and mild edema.

Discussion

Previous reports have described pylorogastric intussusception in dogs, where the distal segment (duodenum) was the intussusceptum prolapsing into the stomach [1,6,14].

Intestinal intussusception is usually described in dogs of less than one year of age and it commonly occurs at the ileocecocolic junction. The vast majority of cases of intussusception is of unknown origin [5,9,11,12,14]. In young dogs, enteritis (viral, parasitic or immunomediated) and general anesthesia, with or without abdominal surgical procedures, have been identified as possible predisposing factors. In dogs with pylorogastric intussusception, the cause or underlying etiological factors are unknown. Most cases of intussusception occur within the small bowel in the aboral direction. In this case, the dog presented pylorogastric intussusception in which the pylorus and proximal duodenum were invaginated in the oral (i.e. retrograde) direction into the body of the stomach. There are only five previously reported cases of pylorogastric/duodenogastric intussusceptions in the veterinary medical literature.

The case reported in this paper had marked similarities with the precedents: all dogs presented acute, severe vomiting, marked dehydration, tachycardia and abdominal pain [1]. Applewhite et al. [2] sustain that diagnosis of pylorogastric intussusception is difficult to confirm without exploratory celiotomy, but we affirm that diagnosis could be confirmed at US and radiographic examinations. In our dog, US and radiographic procedures confirmed the diagnosis of pylorogastric intussusception, and exploratory celiotomy was not required for diagnostic purposes. Our US findings support the US results obtained by Lee et al. [6]. Furthermore, positive-contrast gastrogram and necropsy also confirmed the diagnosis (Fig. 3).

Fig. 3.

Comparison between iodinated contrast enhanced X-ray 120 min after ingestion (b) and necropsy finding (a); there is a close correspondence between the two images.

Treatment of pylorogastric intussusception was not successful in two of the previously reported cases. Two dogs underwent celiotomy with surgical reduction of intussusception, and post-operative follow-up was 20 and 4 months, respectively. Only one dog had spontaneous resolution [6]. The five dogs with diagnosis of this pathology were a 2-year-old neutered female English Sheepdog, a 7-year-old female Basset Hound, a 3-year-old male Rottweiler, a 10-month-old neutered male Saint Bernard and a 7-year-old female Maltese.

Our case was a 3-month-old puppy dog of a very small breed (Chihuahua, 650 g BW) with severe pylorogastric intussusception, whose poor condition prevented us from performing surgery.

None of the reported canine cases presented foreign bodies within the stomach or anywhere else in the gastrointestinal tract that could constitute predisposing causes. In our patient, histopathological evaluation of the stomach, pylorus, bowel, liver, spleen, kidney and lung showed no identifiable predisposing abnormalities. However, the stomach presented diffuse superficial erosion of the mucosal layer. Fecal parasitological and virological electron microscope examinations were negative. A possible etiological factor could be the presence of a predisposing inflammation due to a primary gastritis that could have stimulated the release of inflammatory mediators and vasoactive compounds from a variety of cell types (e.g. neutrophils, mast cells, platelets, endothelial cells, neurons). Exfoliation of the superficial gastric epithelial cells and destruction of the normal mucosal barrier resulted in gastric acid, pepsin and gastric lipase back-diffusion. This inflammatory cascade may have stimulated further acid secretion and mucosal damage and may thus have increased cell membrane permeability, altering the microvascular blood flow and gastric motility [4,8,13,15].

In conclusion, pylorogastric intussusception is a very rare condition described in the veterinary medical literature (6 documented cases in the last 26 years), as the event is often transitory and resolves on its own. In some cases the stenosis is partial leaving a possibility for the food bolus to pass causing nonspecific transitory symptoms with partial solution of the problem. This pathology is not often described or studied due to the dog’s young age; it generally dies after the initial therapies and further investigation is therefore interrupted. Etiological factors are unknown in absence of a gastrointestinal mass; predisposing factors include gastric inflammation, intestinal parasitism, viral enteritis, gastrointestinal foreign body and intraluminal and extraluminal mass lesions [2]. Our case confirms gastric inflammation as a possible predisposing etiological factor for pylorogastric intussusception. It also confirms that US and radiographic examinations are valid diagnostic tools for reaching a clinical diagnosis. However, prognosis is very poor in these patients, and further investigation is therefore required to identify effective curative treatment options.

Conflict of interest statement

The authors have no conflict of interest.