Case Report

A 17 wk old 1.3 kg (2.8 lb) sexually intact female domestic shorthair kitten was examined because of a history of constipation. A common anogenital orifice was noted on physical examination. The referring veterinarian performed abdominal radiographs and a barium study and suspected atresia ani with possible rectovaginal communication. The cat was referred to the University of Florida College of Veterinary Medicine for further evaluation.

On presentation, the cat was bright, alert, and responsive with a body condition score of 5/9 and normal vital signs. The owner reported that the patient was defecating out of her vulva and would occasionally vocalize and strain during defecation. The patient had two previous urinary tract infections that resolved with appropriate antibiotic administration. During the physical examination, the kitten was noted to have fecal material in the vulva. An anogenital cleft was noted, as there was no distinction between the anus and vulva externally. Upon digital rectal examination, there was good anal tone, the rectum was patent, and no stricture or other abnormalities were present.

Abdominal radiography revealed two distinct colons, both filled with a moderate amount of formed fecal material (Figure 1A). Computed tomography (CT)^a of the caudal abdomen and pelvis was performed to further determine the extent of the congenital anomalies and enhance surgical planning. Administration of a nonionic, iodinated contrast medium, iohexol^b, at a dosage of 36.9 g/kg was performed through the common anovulvar orifice. Images were obtained before and after contrast administration. Helical CT images were obtained in a volume data set and were reconstructed in soft tissue and bone algorithms and then reformatted in transverse, dorsal, and sagittal planes. Beginning at the junction of the transverse and descending colon and ending 1 cm proximal to the pelvic canal, there was a segmental duplication the descending colon (Figure 1B). The right-sided colon diameter measured 15–16 mm, and the left-sided colon diameter measured 11–13 mm along their respective lengths. This represented a 19–27% relative size reduction of the left compared with the right colon depending on where the axial plane of the image was measured. The structures diffusely contained heterogeneous soft tissue and scant mineral attenuating material (−90,177, average = 124, standard deviation = 51 HU) in the left colon and (−68,178, average = 99, standard deviation = 39 HU) in the right colon consistent with partially desiccated feces, potentially indicating fecal retention or constipation. There was also a common anovulvar orifice with no evidence of contrast medium entering the uterus or ureters. No other abnormalities were noted. The colonic duplication was confirmed at the time of surgery (Figure 1C).

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Surgical removal of the accessory colon and reconstruction of the anovulvar cleft was discussed with the owner and consent was given. A packed cell volume 32% (reference range 37–54%), total protein 5.9 g/dL (reference range 5.4–7.1 g/dL), and blood urea nitrogen 20 mg/mL (15–26 mg/mL reference range) were performed prior to induction of anesthesia. Premedication with 0.5 mg/kg of midazolam^c and 0.3 mg/kg of methadone^d was administered intramuscularly. Induction of general anesthesia was performed with 2.3 mg/kg of ketamine^e and 4.6 mg/kg of propofol^f IV. A 3.0 mm cuffed endotracheal tube was placed to establish a patent airway. Isoflurane^g inhalant was delivered ranging from 1 to 2% and oxygen at 1 L/min for the duration of the advanced imaging series. Heart rate, electrocardiogram, indirect oscillometric blood pressure, oxygen saturation (by means of pulse oximetry), and end-tidal CO₂ were monitored throughout the procedure. Dopamine^h (7 μg/kg/min) and fentanylⁱ (0.4 μg/kg/min) were administered to the patient during the procedure.

The anogenital cleft was carefully visualized prior to surgery (Figure 2A) and was reconstructed via perineoplasty. The patient was positioned in dorsal recumbency with the perineum elevated 30 degrees. Bilateral 1.5 cm vertical incisions were made in the mucocutaneous junction on each side of the anogenital cleft. The rectal mucosa was divided from the vulvar mucosa with scissors, undermined, and apposed side to side in tubular fashion using 4-0 polydiaxanone^j using a simple interrupted suture pattern. Similarly, the vestibular-vulvar mucosa was apposed side to side in tubular fashion with simple interrupted 4-0 polydiaxanone sutures. A cutaneous shelf was fashioned to cover the anal and vulvar reconstructions by undermining and mobilizing skin from the lateral aspects of the perineal wound and closing with 4-0 polypropylene^k in a simple interrupted pattern.

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The table was leveled and then a celiotomy was performed. The uterine body was located intrapelvically, so an ovariectomy and partial hysterectomy were performed. Both ovaries and approximately 75% of the uterine horns were ligated and excised. A dominant right colon and a smaller accessary left colon were confirmed during abdominal exploration. The colonic duplication originated at the junction of the transverse and descending colon and ended 1 cm cranial to the brim of the pubis. Communication between the duplicate colons was present both proximally and distally. The smaller left colon was emptied by manipulating feces into the dominant right colon at both locations. A 30 mm thoracoabdominal autostapler^l was used to apply staple lines across the left accessary colon at its proximal and distal aspects, respectively. The accessary colon was excised and the staple lines oversewn with 4-0 polydiaxanone in a simple continuous suture pattern and wrapped with greater omentum. The abdomen was closed in a routine fashion.

Postoperatively, the patient was placed on 32 mg of cefoxitin^m (22 mg/kg) IV q 6 hr and 0.2 mg of methadone (0.15 mg/kg) IV q 6 hr for 72 hr postoperatively. The patient had an episode of diarrhea about an hour postoperatively and continued to pass small amounts of formed feces frequently for several days. By 4 days postoperatively, the patient was defecating larger volumes of formed feces at normal intervals and was released from the hospital. At discharge, she was switched to oral medications including 27 mg of clavamoxⁿ (20.7 mg/kg) orally q 12 hr and 0.03 mg of buprenorphine^o (0.02 mg/kg) orally q 8 hr for 6 days.

The patient underwent some minor transient stranguria and tenesmus in the first week postoperatively, which had resolved by suture removal 14 days postoperatively. Both surgical sites healed by primary intention, and at 6 mo postoperatively, the anogenital cleft repair had remained intact (Figure 2B). The patient had no gross evidence of recurrent urinary tract infection and showed no clinical signs of urinary or fecal incontinence. The use of stool softeners or gastrointestinal motility medications were not necessary based on clinical evaluation of the patient.

Discussion

The case described here represents a unique combination of anatomic anomalies including a communicating colonic duplication and a concomitant anogenital cleft. Reports of gastrointestinal duplication in the veterinary literature are limited, encompassing few canine and feline cases.^1–13 The majority of the literature depicts feline patients with noncommunicating enteric duplications that are cystic in appearance but resemble normal gastrointestinal tract histologically. An anogenital cleft is a rare congenital anomaly in dogs and cats and embryologically occurs as a result of incomplete closure of the dorsal urogenital folds.^12,14 In females, incomplete occlusion of the skin between the dorsal vulvar commissure and the anus is observed exposing the bottom of the vaginal vestibule and the clitoris. This defect can also be seen in males with hermaphroditism. These malformations can lead to ascending infection of the urinary tract via fecal contamination.¹²

There are previous case reports describing attempted surgical correction of noncommunicating intestinal duplication in cats. These patients can display various clinical presentations from clinically normal with the diagnosis of enteric duplication being a completely incidental finding to abdominal pain, constipation, vomiting, dyspnea, tenesmus, and difficult hind limb ambulation due to concomitant vertebral malformation. The duplication itself can involve any part of the gastrointestinal tract and has been reported in the esophagus, duodenum, jejunum, and colon, although it is more commonly reported in the colon. The majority of the literature depicts feline patients with noncommunicating enteric duplications that are cystic in appearance but resemble normal gastrointestinal tract histologically. Surgical resolution has been attempted multiple ways, including draining or resection of the cystic region followed by omentalization, or complete resection and anastomosis.^5,6,9–11 In all of these previous case reports involving feline enteric duplications, none of the duplications communicated with the corresponding gastrointestinal tract lumen as seen in this patient.

The literature on surgical management of colonic duplication in canine patients is even more uncommon.^4,13 There is one case report depicting successful surgical repair of a tubular colonic duplication in a 6 mo old intact female Boston terrier who had suffered from tenesmus since weaning.⁴ No other skeletal or urogenital abnormalities were identified in this patient, and a good result was obtained.⁴ A noncommunicating small intestinal duplication was diagnosed and treated surgically in a 9 yr old spayed female Yorkshire terrier with acute onset of anorexia and diarrhea, but the animal did not survive the early postoperative period.¹⁴ Successful correction of an anogenital cleft via perineoplasty has been reported in a pug, but the dog did not have concomitant colonic duplication.¹³

Numerous reports describe rectal or colonic duplications in humans.^15–17 These malformations are usually more complex congenital anomalies than those reported in canines or felines and often involve the colon and the urinary and genital tracts.¹⁵ Embryonically, there are three different mechanisms for colonic duplication reported in the literature, including persistence of vacuoles present among epithelial cells during intestinal development, twinning of the primitive colon and rectum after division of the cloaca by the urorectal folds, and splitting of the notochord during embryological development.^2,17 It is not known if this embryonic mechanism occurs similarly in veterinary patients with enteric duplications.

A classification scheme for colonic duplication has also been reported in people.¹⁶ Type I colonic duplications may involve spherical, tubular, double-barreled, loop, or multiple duplications. Type II colonic duplications are described as a double-barreled duplication with duplications of the urinary or genital tracts. With type II duplications, the genitals, urethra, or bladder may also be duplicated and the anal openings may be located on either side of midline.² None of those classifications completely describes the anatomic anomalies seen in this cat.

To the authors’ knowledge, this case represents the first report of a communicating colonic duplication and a concomitant anogenital cleft reported in a cat in the veterinary literature.

Conclusion

A unique communicating colonic duplication and concomitant anogenital cleft is described in a 17 wk old female cat. The congenital anomaly led to recurrent urinary tract infections and constipation early in life. Advanced CT imaging was used to enhance surgical planning. The anogenital cleft malformation was corrected by surgical separation and tubular reconstruction of rectal and vestibular mucosa, respectively, and adjacent skin was used to create a perineal shelf between the anus and vulva. A unilateral colectomy was performed to remove the communicating left accessory colon. A partial ovariohysterectomy was also performed. The patient had no detectable evidence of recurrent urinary tract infections and had complete fecal and urinary continence 6 mo postoperatively. The complex process of abnormal embryologic development of the alimentary tract is also discussed.