Atresia Ani in the Dog: A Retrospective Study

Introduction

Congenital anomalies of the rectum and anus are rare in dogs.¹ The most frequently reported anomaly in dogs is atresia ani.² Atresia ani is caused by failure of the urorectal fold to completely separate the primitive cloaca, or failure of the anal membrane to perforate after anal formation. In the canine embryo, the gastrointestinal, urinary, and reproductive tracts initially communicate. At 7 weeks of development, the urorectal fold grows caudally, separating the urogenital and rectal tracts and their shared cloaca horizontally [Figure 1]. The anal membrane eventually thins and ruptures, forming an anus.^3,4

Four types of atresia ani have been reported [Figure 2], including congenital anal stenosis (Type I); imperforate anus alone (Type II) or combined with more cranial termination of the rectum as a blind pouch (Type III); and discontinuity of the proximal rectum with normal anal and terminal rectal development (Type IV).⁵ Animals with Type IV atresia ani may have normal development of the anus and terminal rectum.⁵ Types III and IV have also been classified as rectal atresia or segmental rectal aplasia.⁶

Clinical signs of atresia ani usually begin within a few weeks of birth. Dogs with congenital stenosis (Type I) may develop constipation and tenesmus soon after weaning.⁵ Dogs with Types II, III, and IV atresia ani usually have perineal swelling or anal membrane protrusion from accumulation of meconium and feces within the rectum. Affected puppies may be restless and stand with an arched back. Other findings include abdominal enlargement, absence of defecation, and an anal dimple [Figure 3]. If obstruction is longstanding, vomiting and dehydration can develop. Many animals with atresia ani have multiple congenital anomalies at the time of birth (e.g., cleft palates, open fontanelles, hypospadia) and therefore should be fully evaluated before surgical correction is considered.⁵

There are few reports of atresia ani in dogs in the literature.^7–11 Reports may be rare because the incidence is low or because affected dogs are euthanized at an early age based on the perception that surgical correction is unrewarding. To make recommendations regarding treatment, prognosis, and heritability, veterinarians need information on incidence and clinical outcome. The purposes of this study were to determine the incidence, gender, and breed predisposition of atresia ani in dogs from a multi-institutional database and to report the clinical outcome of affected dogs presented to a veterinary teaching hospital.

Materials and Methods

The Veterinary Medical Data Base^a (VMDB) was searched from March 1964 to July 2003 using the terms canine, congenital, atresia, anus, and rectum. Data collected included signalment, diagnosis, and discharge status of dogs diagnosed with congenital atresia ani. Total number of dogs and number of each breed were recorded. Dogs seen multiple times were counted only once during the specified time period.

Odds ratios and confidence intervals were calculated with a commercial statistical software program.^b Statistical significance was set at P<0.05.

A retrospective study of the records from the University of Tennessee Veterinary Teaching Hospital (UTVTH) from February 1976 to December 2003 was also performed, using canine atresia ani and atresia rectum as the search criteria. Data collected included signalment, diagnosis, type of treatment, discharge status, and clinical outcome. Follow-up information was obtained by contacting owners, contacting referring veterinarians, or by physical examination at UTVTH.

Results

From 1964 to 2003, records of 1,624,499 dogs were included in the VMDB. Of these dogs, 119 (0.007%) were diagnosed with atresia ani (atresia of the anus and/or rectum). Forty-four breeds were affected. Breeds reported more than once included miniature or toy poodle (n=17), Boston terrier (n=8), miniature schnauzer (n=5), chow chow (n=4), Maltese (n=4), rottweiler (n=4), American cocker spaniel (n=4), Australian shepherd (n=3), Doberman pinscher (n=3), German shorthaired pointer (n=3), Labrador retriever (n=3), and boxer, German shepherd dog, standard poodle, Shetland sheepdog, and the Finnish spitz (n=2 each). Seven breeds had significantly increased incidence of atresia ani compared to mixed-breed dogs (incidence 0.004%), including the Finnish spitz (incidence 0.0935%; odds ratio [OR] 19.401; 95% confidence interval [CI] of 2.182 to 81.114; P=0.0058); Boston terrier (incidence 0.066%; OR 13.766; 95% CI 5.178 to 33.28; P<0.000001); Maltese (incidence 0.064%; OR 13.385; 95% CI 3.294 to 40.649; P=0.00004); chow chow (incidence 0.043%; OR 8.902; 95% CI 1.142 to 11.001; P=0.0018); German shorthaired pointer (incidence 0.028%; OR 5.787; 95% CI 1.092 to 19.828; P=0.02); miniature or toy poodle (incidence 0.02%; OR 4.278; 95% CI 2.072 to 8.798; P=0.000046); and miniature schnauzer (incidence 0.019%; OR 3.936; 95% CI 1.142 to 11.002; P=0.0154).

There were 69 females and 36 males. Genders of 14 dogs were not recorded. Females were significantly more likely to be affected than males (OR 1.796; 95% CI 1.2 to 2.687; P=0.0053). The most common age ranges at presentation were 8 to 24 weeks (43%), 2 to 8 weeks (42%), and 0 to 2 weeks (15%). Five dogs were between 1 and 2 years of age, and one was >4 years of age at presentation. Of the 119 dogs, 80 were specifically coded as having partial or complete congenital atresia ani,^c and 39 were coded as having congenital atresia rectum.^d Treatments were not recorded, and limited information regarding outcome was available from the VMDB. Regarding outcome, 40 dogs were euthanized, 69 were released, and nine died.

From 1976 to 2003, 67,681 dogs were seen at the UTVTH. Of these canine cases, 11 (0.0002%) were diagnosed with atresia ani/rectum. Seven of these dogs were also included in the VMDB records. There were four females and six males, and the gender of one dog was not recorded. The average age of nine dogs at the time of presentation was 5 weeks. Age was not recorded for two dogs. Clinical signs included straining to defecate (n=11), recognizable anal dimple (n=5) [Figure 3], fecal material within the vulva (n=3), thin body condition (n=2), and regurgitation (n=1). One dog developed an anal stricture after a previous anoplasty and a rectal pull-through procedure. The diagnosis of atresia ani in all 11 dogs was made on physical examination. In addition, survey abdominal radiography was performed in four dogs in an attempt to confirm the specific type of atresia ani. Anal stenosis (Type I), imperforate anus (Type II), and Type III atresia ani with rectovaginal fistula were reported in three dogs. The type of atresia ani was not recorded in the other eight dogs.

Five dogs were euthanized at presentation. One dog underwent anoplasty, and five dogs underwent anoplasty with rectal pull-through [Figure 4].⁵ In the three dogs with rectovaginal fistulas, the fistulas were ligated, transected, and oversewn.⁵ In one dog with rectovaginal fistula and Type III atresia ani, the anal dimple was not present, and the anal sphincter was located by application of an electrical stimulus.^e One dog with Type II atresia ani required subtotal colectomy 2 weeks after initial anoplasty and rectal pull-through because of segmental colonic distension and persistent constipation [Figure 5].

Follow-up information was available on four dogs. The dog that underwent anoplasty alone was discharged 1 day after surgery but returned 16 days later because of anal stricture. Anoplasty was repeated, and 1 month after the second surgery, the dog was fecally continent and had no recurrence of the anal stricture. One dog with atresia ani and rectovaginal fistula was euthanized 3 months after surgery because of anal stricture and fecal incontinence. Another dog with Type III atresia ani and rectovaginal fistula (this dog did not have a visible anal dimple at the time of surgery) was fecally incontinent for 6 months after surgery. By 12 months after surgery, this dog had recovered some fecal control and was trained to defecate on newspapers indoors. The dog that underwent anoplasty with rectal pull-through and subsequent subtotal colectomy was fecally continent 9 months after surgery but continued to have constipation from mega-colon. The dog was maintained on lactulose (0.5 mL/kg q 24 hours) to help soften fecal consistency. This dog was initially presented with regurgitation that persisted after surgery and was subsequently diagnosed with generalized megaesophagus. One dog that underwent anoplasty and rectal pull-through was lost to follow-up but was continent at the time of discharge 5 days after surgery.

Discussion

The true incidence of congenital abnormalities of the rectum and anus in dogs is difficult to determine, since many dogs may be euthanized before being evaluated at an institution linked to the VMDB. In the study reported here, incidence of atresia ani in dogs was approximately 0.007%. Of domestic animals, atresia ani has a relatively high incidence in pigs and is the cause of mortality in 3% of piglets that die on breeding farms.¹² In one study, 0.27% to 0.29% of Landrace piglets were born with atresia ani.¹³ Atresia ani is considered a highly heritable trait in pigs, and a chromosomal abnormality with a recessive mode of inheritance and 50% penetrance is suspected.^14–16 Selective breeding of pigs has reduced the frequency of atresia ani by 0.01% per year.¹⁷

Atresia ani in dogs has been previously described as having no sex or breed predilection.⁶ The data in the present study, however, found that females were 1.79 times more likely to develop atresia ani than males and that several breeds, including poodles and Boston terriers, were predisposed to the condition. Breeds previously reported in the literature as having atresia ani included the miniature poodle, Doberman pinscher, German shepherd dog, French poodle, boxer, Siberian husky, and mixed-breed dogs.^7–11

The type of atresia ani could not be definitely identified from VMDB or UTVTH records. Of the dogs treated surgically at UTVTH, Type II or III atresia ani was presumed to be most common, since five dogs underwent a rectal pull-through procedure. Prassinos et al. reported six dogs with atresia ani, including one with anal stenosis and five with imperforate anus (Type II or Type III atresia ani).⁷ Survey radiography of the caudal abdomen and perineal region may be helpful in determining the extent of rectal atresia and the type of atresia ani, but it was performed in only four of 11 dogs at the UTVTH. Radiography would also be helpful in identifying colonic distension, since chronic colonic dilatation may result in hypomotility that requires additional medical or surgical management. In addition, contrast radiography (i.e., retrograde vaginography) would be useful in dogs with rectovaginal fistula for determining the location of the fistula and detecting rectal atresia.

Surgery is the treatment of choice for atresia ani, although anal stenosis has been treated with bougienage.⁵ In dogs with imperforate anus (Type II), the location of the anus can sometimes be identified by the presence of an anal dimple. Some authors also recommend application of an electrical stimulus or pinching the vulva to look for subtle contractions in the area of the anus.^18,19 During surgery, a cruciate incision is made over the anal dimple, and the rectal pouch is identified and mobilized through the external anal sphincter with stay sutures.⁵ The rectum is opened and sutured to the skin after trimming any excess skin flaps.⁵ If a concurrent rectovaginal fistula is present, the incision is extended toward the vulva, and the fistula is identified, transected, and oversewn.⁵

The most commonly reported complications after corrective surgery have included wound dehiscence, incontinence from inadequate sphincter function, and secondary colonic atony from prolonged distension.^7–11 These complications may necessitate a second surgery, such as a subtotal colectomy or anoplasty, or lead to euthanasia of the animal. In the present study, five dogs were euthanized at presentation. Of the six dogs that underwent surgical treatment, three required anoplasty revision or subtotal colectomy. Three dogs were fecally continent at the time of release or follow-up, but one of these dogs continued to have constipation from chronic colonic dilatation and required stool softeners to reduce clinical signs.²⁰

The high incidence of fecal incontinence after surgery may have occurred from a congenital lack of a functional anal sphincter or direct damage to the innervation of the sphincter muscle from surgical dissection.⁷ Care must be taken during dissection to minimize the incidence of incontinence after anorectal surgery. Interestingly, one dog had gradual improvement of fecal control 1 year after the surgery. This improvement may have been associated with the weight gain that occurred following ovariohysterectomy 8 months after anoplasty; the additional perineal and intrapelvic fat may have added pressure to the rectal and anal region.

Conclusion

Atresia ani was diagnosed in 0.007% of cases recorded in the VMDB and in 0.0002% of dogs examined at UTVTH over a 27-year period. Based on the results of this study, the incidence of atresia ani was greater in female dogs and in certain breeds of dogs. Because of low numbers and limited diagnostic information, it was difficult to correlate outcome with type of atresia ani. A multicenter study would be useful for defining prognostic indicators.