Transmural rectal intestinal evisceration associated with parturition in a primiparous mare

Abstract

A 6-year-old, primiparous standardbred mare was presented with a history of intestinal protrusion from the rectum shortly after parturition. A subacute grade IV rectal tear was diagnosed. The unusual nature of the tear led to speculation of a possible owner palpation accident. A grave prognosis was given and the mare was euthanized.

A 6-year-old, primiparous standardbred mare was referred to the Atlantic Veterinary College (AVC) ~ 3 h after foaling with a history of suspected extensive rectal prolapse. The mare had given birth to a normal, healthy filly and, reportedly, was found by the owners, lying in the stall with a substantial amount of bowel protruding from the anus (Figure 1). The owner's son reported that a lapse in the monitoring of the mare had resulted in unobserved parturition. At the farm, the referring veterinarian (rDVM) found the mare recumbent with signs of shock, thrashing violently, and struggling to get to her feet. Due to the mare's distress, the rDVM was unable to perform a complete vaginal and rectal examination. A rectovaginal tear with prolapse of ~ 30 cm of rectum and ~ 4 m of bowel from the anus was suspected. A poor prognosis was given and euthanasia suggested. The owners declined and requested further evaluation at the AVC.

Figure 1. Caudal view of the recumbent mare at the time of examination by the referring veterinarian. Note the rectal prolapse, eviscerated small intestine, and placental membranes entwined around the intestine.

The rDVM elected not to perform epidural anesthesia due to concerns that it may have exacerbated the hindquarter weakness, preventing the mare from rising or increasing the risk of recumbency during transportation to the AVC. The mare was sedated with detomidine HCl (Pfizer, Kirkland, Quebec), 0.01 mg/kg body weight (BW), IV, and butorphanol tartrate (Wyeth-Ayerst, Markham, Ontario), 0.02 mg/kg BW, IV. A nasotracheal tube was placed to prevent the mare from closing the glottis and straining. The exposed viscera were lavaged with sterile isotonic saline and replaced via the anus into the rectum. The rectal prolapse was reduced and a purse string suture was placed in the anus for temporary retention. Flunixin meglumine (Vetrepharm Canada, London, Ontario), 1 mg/kg BW, IV; gentamicin sulfate (Schering-Plough, Kenilworth, New Jersey, USA), 6.6 mg/kg BW, IV; sodium penicillin (Novopharm, Toronto, Ontario), 22 000 IU/kg BW, IV; and 2 L of 7.2% hypertonic saline (Vetrepharm Canada), IV, were administered by the rDVM before transportation to the AVC.

On admission to the AVC, the mare was depressed and sweating. There were bilateral edema and abrasions of the upper eyelids. The mare had an increased heart rate (60 beats/min; reference range: 28 to 40 beats/min); rapid, shallow respiration (rate: 24 breaths/min; reference range: 10 to 14 breaths/min); and a rectal temperature of 37.5°C (reference range: 37.3°C to 38.3°C). On abdominal auscultation, borborygmi were absent in all quadrants. Dehydration was ~ 8% to 10%, based on the pale, tacky mucous membranes and a capillary refill time of ~ 3 s. The packed cell volume was 0.40 L/L (reference range: 0.32 to 0.52 L/L) and the plasma total protein was 54 g/L (reference range: 64 to 77 g/L). An epidural injection of lidocaine HCl (Vétoquinol, Lavaltrie, Quebec), 5 mL, was administered. The purse string suture was removed and the rectum palpated carefully. A large circular defect (10 to 15 cm diameter) was found in the rectal wall, ~ 40 cm cranial and ventrolateral to the anus at the 4 to 5 o'clock position. The defect communicated with the peritoneal cavity, and distended loops of bowel could be palpated through the rent. Placental membranes were found in the vagina.

A hematogram revealed a moderate leukopenia characterized by a moderate neutropenia, a degenerative left shift with a 4+ toxic change, and a moderate lymphopenia (Table 1). This was indicative of severe acute inflammation. Significant serum biochemical findings are listed in Table 1 and were consistent with shock, dehydration, stress, and muscle damage.

Table 1.

The history, clinical signs, and laboratory findings supported a diagnosis of retained placenta, an intraperitoneal grade IV rectal tear, prolapse of the rectum, and intestinal evisceration. Peritonitis and septicemia, secondary to intra-abdominal contamination with fecal matter, were suspected. A grave prognosis was given and the owner requested euthanasia.

On necropsy, moderate, acute hemoperitoneum (~ 5 to 6 L), acute small intestinal and rectal infarction and necrosis, with acute peritonitis and a grade IV rectal tear, were the significant findings. The hemoperitoneum was thought to be due to ruptured blood vessels within the mesentery or rectal wall. A segment of distal jejunum, ~ 3 m in length, was dark red and moderately distended with fluid and gas. There were also small amounts of fibrin adherent to the serosa of the jejunum. Blood vessels along the mesenteric border of the intestinal wall were thin and friable. A full thickness perforation in the rectal wall was found, ~ 40 cm proximal to the anus. The defect was irregularly circular in shape and measured ~ 15 cm at its greatest width. The rectal mucosa surrounding the tear was dark red, friable, and markedly edematous. The rectal mucosa extending for ~ 60 cm proximal to the lesion was dark red, and the lumen contained a small amount of firm, dry, green forage. There were several small partial thickness tears in the rectal wall, proximal to the larger defect. The rectal serosa had moderate amounts of adherent fibrin, pieces of hair, and straw. The connective tissues on the dorsal surface of the uterus and surrounding the rectum had coalescing areas of extensive hemorrhage. The uterine wall in this area was thin. There was extensive tearing and hemorrhage of the muscles lining the floor of the pelvis, attributed to possible dystocia. The postmortem diagnoses were infectious peritonitis, secondary to abdominal contamination, and a subacute grade IV rectal tear.

Several findings pointed to the atypical nature of the rectal tear in this case. These included the ventrolateral location and circular shape of the tear; the lack of confirmation of a history of recent rectal palpation, assisted parturition, or previous trauma to the rectum; and the lack of significant injury to the vagina and vulva. In contrast to the present case, the most common site for rectal tears has been reported to be the dorsal rectum between 10 and 2 o'clock, usually in a longitudinal orientation, ~ 25 to 30 cm from the anus and cranial to the peritoneal reflection at the pelvic inlet (1,2,3,4). An inherent weakness of the intestinal wall in this area, due partly to the direct penetration of short terminal arteries on either side of the mesenteric tenia and partly to the lack of serosa on this segment of bowel where it is enclosed by the mesorectum, has been hypothesized (1,2,3). The prevalence of ventral rectal tears is low (< 10%), and tears of this type have been poorly documented (2). The prognosis for ventral and lateral tears is worse than for dorsal tears, due to the lack of suspending mesentery, which provides a protective barrier to peritoneal contamination for tears of the dorsal aspect of the rectum (2). The more circular shape of the tear in this case may suggest that a focal area of pressure had been exerted on the rectal wall resulting in injury. The other small, partial thickness rectal lesions that were found lend support to the possibility that the traumatic insult originated within the lumen of the rectum.

The vast majority of rectal tears seen in horses are inadvertently caused by veterinarians during routine rectal palpation (5). A retrospective study conducted at the University of California-Davis (UCD) of 42 cases of rectal tears between 1967 and 1977 determined that 60% of rectal tears were produced iatrogenically by experienced clinicians (2). Other causes included student palpation accidents (17%), owner palpation accidents (5%), breeding accidents (5%), enemas (5%), dystocia (2%), pelvic and vertebral fractures (2%), trailer accidents (2%), and spontaneous rupture (2%) (2). Of the causes of rectal tears listed, all except spontaneous rupture, dystocia, and an owner palpation accident could be ruled out as potential causes of the grade IV rectal tear that occurred in the current case.

Spontaneous and noniatrogenic rupture of the rectum has been documented less commonly as a cause of rectal tears in the horse (2,6). Pre-existing bowel weakness due to previous palpations, breeding trauma, and foaling injuries have been reported to increase the risk of non iatrogenic rectal tears (2,6). Horses with neurogenic fecal impaction of the rectum resulting from injuries to the caudal spinal cord, and older horses with intraluminal growths are at increased risk of spontaneous rectal rupture due to extreme impaction of the rectum with feces (2,8). Ischemic vascular disease leading to devitalization of the rectal tissue has also been reported as a predisposing cause of spontaneous rectal tears (3). Ischemic necrosis and thrombosis of the caudal mesenteric artery and its branches following infection with Salmonella spp. has been incriminated as a cause of rupture of the rectal wall (3). It has also been speculated that a nonocclusive form of vascular disease resulting from the migration of Strongylus vulgaris through the caudal mesenteric artery and its branches may lead to devitalization and ischemic necrosis of the rectal tissue, thereby creating a focal area of weakness in the rectal wall and subsequently increasing the risk of spontaneous rupture (3). There was no pathologic evidence in the present case to suggest that the cause of the rectal tear was due to necrosis as a result of rectal impaction or obstruction. It is also unlikely that there was either a focal area of weakening in the rectal wall or intestinal infarction due to an ischemic vascular disease, as such factors would be expected to produce lesions of a chronic or progressive nature. In the case presented, the lesions identified at necropsy were consistent with an acute to subacute process.

Parturition induced trauma is a relatively common cause of rectal tears (8,9). It is often associated with dystocia as a result of delivery of a malpositioned or oversized fetus and, occasionally, from overzealous assistance during foaling (8,9). Such tears often result in rectovestibular fistulas, which occur when the forefoot of the fetus catches on the dorsal transverse fold of the vaginovestibular junction (8,9). Continued contractions and straining by the mare provides the force that drives the foot up through the dorsal wall of the vestibule and through the ventral wall of the rectum (8,9). In the case presented, the necropsy findings of traumatic injury of the pelvic musculature and the dorsal aspect of the uterus are suggestive that the mare had dystocia. As well, the rectal prolapse identified on initial examination was most likely a result of prolonged, forceful straining by the mare during a difficult delivery process characterized by dystocia, or secondary to the rectal tear (10). However, in the case presented here, the normal size of the foal at birth, the lack of an obvious rent in the vagina, and the absence of significant injury to the vaginal mucosa, confirmed that a rectovestibular fistula was not present.

The study at the UCD indicated that one of the more common causes of rectal tears in horses was owner palpation accidents (2). The author speculates that, in this case, the rectal tear may have been the result of a rectal palpation performed by the owner. It is possible that the person monitoring the foaling perceived that the mare had dystocia and attempted to manipulate the uterus and fetus per rectum, which resulted in tearing of the rectal wall. Supporting this hypothesis is the abnormal location of the rent in the rectal wall, and the acute and extensive nature of the tear. An owner palpation accident would seem the most likely cause of the grade IV rectal tear in this case, although the person responsible for observing the mare was reluctant to provide a complete account of the events associated with the mare's parturition.

The exact cause of rectal tear in this case cannot be defined with certainty, but it is important to note that rectal tears pose serious and often life threatening situations requiring immediate assessment and medical attention. The greatest complication associated with grade IV rectal tears is the development of severe peritonitis resulting from perforation of the rectum and contamination of the abdominal cavity with fecal matter. The prognosis for a grade IV rectal tear is extremely poor. Owners and managers of pregnant mares need to be advised of the risks associated with inexperienced persons assisting mares during parturition.