Subclinical cecal impaction in a dog

Abstract

A 7-year-old, bichon frise dog was incidentally diagnosed with cecal impaction. Typhlectomy was performed as cecal rupture and resultant septic peritonitis appeared to be imminent. Histopathological evaluation did not identify an underlying cause for impaction and cecal dysmotility was suspected. Subclinical cecal impaction has not previously been reported in dogs.

A 7-year-old, castrated male bichon frise dog was presented to the family veterinarian for its annual physical examination. A firm, caudal abdominal mass was palpated. The dog did not have any clinical signs at the time of presentation. Abdominal radiographs revealed a mineralized mass in the right caudolateral abdomen.

Case description

Upon presentation to the Ontario Veterinary College Health Sciences Centre (OVCHSC), the patient was bright and alert, and vital parameters were normal. A firm, round mass was palpated in the caudal abdominal region. The results of the remainder of the physical examination were unremarkable. Abdominal radiographs were repeated, and the abdominal mass appeared to be of similar size when compared to the radiographs performed by the family veterinarian. A mineralized, heterogeneous oval-shaped mass approximately 10 × 7 cm was visualized in the right caudal abdomen (Figure 1). The mass was well-demarcated and confined by a thin, soft tissue wall. Three-view thoracic radiographs were taken and were normal. An abdominal ultrasound revealed the presence of a markedly dilated cecum that was filled with fecal material. Due to the marked dilation of the cecum and the risk of rupture and secondary septic peritonitis, an exploratory celiotomy and typhlectomy were recommended to the owner. In preparation for general anesthesia, a complete blood (cell) count (CBC), serum biochemical profile, and urinalysis were performed and found to be within normal limits.

Figure 1.

Right lateral abdominal radiograph demonstrating a mineralized, heterogeneous oval-shaped mass visualized in the caudal abdomen.

The following day, the patient was premedicated with hydro-morphone (Sandoz, Boucherville, Quebec), 0.05 mg/kg body weight (BW), and general anesthesia was induced with pro-pofol (APP Pharmaceuticals, Schaumburg, Illinois, USA), 2 mg/kg BW, and midazolam (Sandoz), 0.2 mg/kg BW. An exploratory celiotomy was performed through a ventral midline abdominal incision. Abdominal exploration revealed a markedly enlarged (10 × 7 cm), thin-walled cecum (Figure 2), filled with formed fecal material. The remainder of the abdominal exploration did not reveal any other abnormal findings. A typhlectomy was performed using a thoracoabdominal stapling device (Multifire Endo TA30; Covidien, Mansfield, Massachusetts, USA) that was applied across the base of the cecum. The resected cecum was fixed in 10% neutral buffered formalin for 24 h, and routinely processed for histologic examination. The abdominal cavity was lavaged with warm physiologic saline and the edges of the rectus abdominus fascia were infiltrated with bupivacaine (Hospira, Lake Forest, Illinois, USA). The abdominal incision was then closed in a routine fashion. The dog recovered without complication and analgesia was provided using intravenous fentanyl (Sandoz), 2 to 3 μg/kg BW per hour. The dog was discharged 24 h after surgery, eating and drinking normally, and showed no signs of abdominal discomfort. At last follow-up 4 mo after surgery, the patient was doing clinically well.

Figure 2.

Intra-operative picture demonstrating a markedly enlarged, thin-walled cecum, filled with formed fecal material. TA-30 Stapling Device visualized.

On light microscopic examination, all tissue layers of the cecum were present and intact but uniformly thinned (Figure 3). Within the tunica muscularis there was patchy fibrosis, with individual and clustered myofibers isolated from one another by fibrous connective tissue. Numerous morphologically normal submucosal and myenteric plexi were identified within all sections. There was no evidence of inflammatory, degenerative, or dysplastic changes within the nervous tissue compartment of the cecum.

Figure 3.

Light microscopic examination of the cecal wall. All tissue layers of the cecum were present and intact but uniformly thinned. There was no evidence of inflammatory, degenerative, or dysplastic changes within the nervous tissue compartment of the cecal wall. Hematoxylin and eosin stain. Original magnification 100×.

Discussion

Diseases of the cecum, including inversion (1), neoplasia (2), and impaction (3–5) have been reported in dogs. There have been 3 previous reports of cecal impaction in the dog (3–5). The most common clinical signs associated with cecal impaction include: vomiting, diarrhea, anorexia, and feces containing blood or mucus (3–5). These signs have been reported as beginning over a period of several weeks (3), or intermittently over the course of several months (4,5). To the authors’ knowledge, this is the first report of cecal impaction in a dog that did not result in clinical signs. This may indicate that cecal impaction occurs more commonly than previously thought, but remains undiagnosed.

Similar to previous reports (3,4), histopathological evaluation of the cecum in this case failed to identify an underlying cause for impaction. The extensive fibrosis identified within the tunica muscularis was interpreted as being the result of ischemia secondary to increased luminal pressure, which would have resulted in collapse of the local venous circulation. The fact that there was no indication of ongoing necrosis in any tissue compartment indicates that such pressure spikes were intermittent, likely relieved by a combination of myodegeneration (resulting in relaxation and further dilation of the cecum) and possibly release of some cecal content via the cecocolic orifice. The degree of fibrosis present would have interfered with normal peristalsis, and likely contributed to the propagation of cecal dilation. It is likely that abnormal motility of the cecum was the predisposing factor; however, this is difficult to substantiate. In our case, the histological diagnosis of cecal smooth muscle atrophy and fibrosis is similar to that from a previous case report on cecal impaction by Eastwood et al (5), who suggested that these findings are comparable to those of visceral myopathies in humans.

Visceral myopathies are characterized histologically by degeneration and progressive replacement of intestinal smooth muscle cells with fibrosis that typically affects the longitudinal layers (6). Although this condition is generally diffuse throughout the entire intestine in humans, segmental forms do occur and may be similar to the isolated disease of the cecum in the case of this report (7). Biopsy and histopathological examination of the remaining portion of the gastrointestinal tract have been recommended in cases of cecal impaction to further characterize a suspected motility disorder (2). Full-thickness biopsies of the remaining portions of the GI tract may have been helpful in determining an underlying cause in the present case. Visceral myopathies in humans are generally given a poor prognosis. Surgery is avoided in cases of diffuse disease, but can be effective in segmental forms of the disease (7). Caution must be exercised when attempting to compare visceral myopathies in humans with cases of cecal impaction in dogs as the smooth muscle atrophy and fibrosis could be secondary changes from impaction and not the underlying cause.

The cause of cecal impaction in the absence of any apparent predisposing factor is difficult to determine. Motility in the intestine is complex and is initiated by the interstitial cells of Cajal (ICC), which are the intestinal pacemaker cells and are a specialized population of smooth muscle cells that control intestinal motility (8). Interstitial cells of Cajal contain large numbers of mitochondria, endoplasmic reticulum, and have relatively few contractile elements compared with other smooth muscle cells (8). These cells are responsible for slow wave production which initiates spiking activity in the intestines, generating contractions (8). Isolated smooth muscle cells rarely generate spontaneous electrical activity (9), but an isolated ICC can and will allow for efficient and normal peristalsis (9,10). These pacemaker cells can direct motility orally or aborally, which results in retention during digestion, as well as transit aborally. If ICC are unable to normally coordinate oral and aboral transit of feces through the cecum, retention of feces may become pathologic leading to impaction.

Cecal impaction occurs in several species, and is well-recognized in horses (11). There are 2 distinct classifications of cecal impaction in horses; type I — which results from the cecum being packed with ingesta, or type II — a massively distended cecum as a result of a motility disorder (12). In horses, all efforts are made to try and preserve the cecum and typhlectomy is rarely performed because of the importance of the cecum in a hindgut fermenter. Indications for surgical intervention in horses with cecal impaction include an elevated heart rate, evidence of progressive impaction, and systemic deterioration (13). Surgery in horses typically consists of a typhlotomy if a type I impaction is suspected, or a typhlotomy and cecal bypass procedure for type II impactions (12). If this classification of cecal impaction was used in our case, it seems likely that a type II impaction occurred as a result of cecal dysmotility.

Cecal impactions have been described in other species including humans (14), horses (15), cows (16), and llamas (17). The cause in all of these species is poorly understood (14–17). In the absence of mechanical obstruction of cecal outflow, dysmotility must be considered as the primary cause. In dogs, typhlectomy appears to be curative. In the dog of this report, cecal impaction and marked dilation did not result in clinical signs; however, elective typhlectomy was performed as cecal rupture and resultant septic peritonitis appeared to be imminent.