History
A 10-year-old 550-kg (1,210-lb) multiparous Standardbred mare was referred for examination at the Cornell University Hospital for Animals because of signs of colic, ventral abdominal edema, and a high concentration of serum amyloid A. The mare was pregnant (336 days of gestation) and had a 2-day history of inappetence and increasing signs of discomfort and edema along the ventral aspect of the abdomen. The mare had no history of other medical problems or abnormalities during previous pregnancies. The mare had received altrenogest (0.88 mg/kg [0.4 mg/lb], PO) and flunixin meglumine (1.1 mg/kg [0.5 mg/lb], IV) prior to referral.
On initial referral examination the day of admission (day 1), the mare had persistent signs of colic, including pawing with the forelimbs and frequently standing in a stretched-out position. The mare was tachycardic (56 beats/min; reference range, 28 to 44 beats/min) and had hyperemic mucous membranes, with a capillary refill time within reference limits. Physical examination revealed substantial amounts of warm, pitting edema along the ventral aspect of the caudal portion of the abdomen. The mare had no discharge from the vulva or mammary glands. A CBC revealed mild neutrophilia (7,300 neutrophils/μL; reference range, 2,700 to 6,600 neutrophils/μL) with a left shift (200 neutrophil band cells/μL; reference range, 0 to 100 neutrophil band cells/μL) and toxic changes. Serum biochemical analyses revealed high serum amyloid A concentration (944 μg/mL; reference range, 5 to 20 μg/mL) and high serum activities of creatine kinase (4,207 U/L; reference range, 142 to 548 U/L) and aspartate aminotransferase (602 U/L; reference range, 199 to 374 U/L).
Transabdominal ultrasonography revealed no free fluid or distended viscera and a live fetus with a mildly elevated heart rate (120 beats/min; reference range, 74 to 106 beats/min). A nasogastric tube was passed in the mare; however, no gastric reflux was obtained. Transrectal palpation revealed no abnormal abdominal viscera and a gravid uterus with an active fetus. Transrectal ultrasonography revealed that the combined thickness of the uterus and placenta was slightly high (13.4 mm; upper reference limit, 12 mm) and that the allantoic fluid was subjectively more hyperechoic than anticipated and had multifocal, small, echogenic speckles that swirled in the allantoic space. These findings were suggestive of placentitis.
Question
What are the differential diagnoses for colic in a periparturient mare? Please turn the page.
Answer
Differential diagnoses for colic in a periparturient mare are small and large intestinal abnormalities (eg, intestinal strangulation, volvulus, impaction, torsion, or ischemic injury), uterine torsion, hydrops condition, or abdominal wall disruption.
Results
The mare was hospitalized, and because survival of the foal was a high priority for the owners, conservative treatment that allowed progression through the remaining gestational period was elected. A belly band was placed on the mare for abdominal support, and IV fluids were administered to correct mild dehydration. Penicillin G potassium (22,000 U/kg [10,000 U/lb], IV, q 6 h, for 6 days), ceftiofur (2.2 mg/kg [1.0 mg/lb], IV, q 12 h, for 2 days), and pentoxyphylline (10.2 mg/kg [4.64 mg/lb], PO, q 12 h, for 6 days) were administered for treatment of suspected placentitis. In addition, the mare was fitted with ice boots to help prevent laminitis, and pain management included administration of flunixin meglumine (1.1 mg/kg [0.5 mg/lb], IV, q 12 h, for 4 days), a continuous rate infusion of 2% lidocaine (0.05 mg/kg/min [0.023 mg/lb/min], IV, for 3 days), and butorphanol tartrate (0.01 to 0.02 mg/kg [0.0045 to 0.0091 mg/lb], IV, q 6 h, for 5 days, or as needed). Fetal heart rate was assessed every 2 hours with ECG to monitor for signs of stress.
On day 3, ceftiofur was discontinued and replaced with gentamicin (6.6 mg/kg [3.0 mg/lb], IV, q 24 h, for 5 days) for broader antimicrobial coverage. On day 4, the mare had slight development of the mammary glands and minimal mammary gland secretions. The amount of these secretions was only sufficient to allow us to monitor pH, which was 7.8, suggestive of imminent foaling and not conducive to safe induction of parturition. The mare was monitored closely, and signs of abdominal discomfort were noted frequently. The edema on the ventrum of the abdomen had progressed and extended more cranially.
Ultrasonographic examination of the ventral abdominal musculature on day 4 revealed bilateral abdominal wall tears. These tears were focal, partial tears of the external abdominal oblique muscles, with the right side more severely affected than the left (Figure 1). The lesions appeared as focal hypoechoic areas (right side, 2.2 × 11.5 × 12 cm; left side, 1.0 × 6.2 cm) with multiple linear hyperechoic tags. The rectus abdominis muscles were intact, and the intestines did not appear to herniate through the tears.
Transabdominal ultrasonographic images of the left (A) and right (B) external abdominal oblique muscles of a pregnant multiparous Standardbred mare on day 4 of hospitalization for signs of colic, edema on the ventrum of the abdomen, and high concentration of serum amyloid A. The images were obtained at the level of the cranial aspect of the mammary glands. There are bilateral partial tears (arrows) in the external abdominal oblique muscles, with the right side more severely affected. The scale on the right of each image is in centimeters.
Citation: Journal of the American Veterinary Medical Association 256, 3; 10.2460/javma.256.3.309
On day 5, development of the mammary glands had progressed, and there were hemorrhagic secretions from the right mammary gland. A CBC was repeated and revealed a neutrophil count within reference limits and resolution of toxic changes; therefore, treatment with ice boots was discontinued. Serum amyloid A concentration was higher than on admission and peaked at 1,811 μg/mL. Transabdominal ultrasonography was repeated and revealed enlargement of the abdominal wall tears on the right side of the abdomen (Figure 2). Because the mare showed signs of increasing discomfort, an epidural catheter was placed for administration of morphine (0.10 mg/kg [0.05 mg/lb]) and detomidine (0.006 mg/kg [0.003 mg/lb]). Shortly afterward, the mare was noted to have had a wet perineum and fluid on the tuber calcanei and mammary glands. Vaginal examination (digital) confirmed rupture of the chorioallantois, full cervical dilation, and a live foal; however, no abdominal contractions or outward signs of impending parturition were detected. The fetus was in the anterior longitudinal dorsopubic position and was manipulated within 5 minutes following the vaginal examination to achieve dorsosacral positioning. An assisted vaginal delivery was performed. Within 22 minutes after fetal manipulations were started, a live 41.7-kg (91.7-lb) filly was delivered.
Ultrasonographic images of the left (A) and right (B) external abdominal oblique muscles of the mare of Figure 1 on day 5. The abdominal wall rupture (arrows) has enlarged bilaterally from that imaged the previous day (Figure 1), and the right side is still more severely affected than the left side. Blood (b; B) is collected near the site of the rupture. The scale on the right of each image is in centimeters.
Citation: Journal of the American Veterinary Medical Association 256, 3; 10.2460/javma.256.3.309
The filly was active and breathing and had a heart rate within reference limits. However, results of arterial blood gas analysis performed on the filly indicated that it had poor oxygenation. Therefore, the filly received supplemental oxygen for 4 days. In addition, an indwelling nasogastric tube was placed because the filly was unable to stand and suckle, consistent with neonatal maladjustment syndrome. Colostrum and hyperimmune plasma were administered to the filly to achieve a plasma IgG concentration > 1,000 mg/dL. A blood sample collected from the filly soon after birth was submitted for bacterial culture and yielded growth of Pantoea agglomerans. The filly was treated with broad-spectrum antimicrobials (penicillin G potassium, amikacin, and metronidazole), fluid therapy, and gastrointestinal protectants and an adsorbent.a The filly required intensive care in the neonatal unit for the first 16 days after birth.
The mare had no complications attributable to parturition and received a single dose of domperidone (25 mL of an 11% gel) because of a lack of milk production. In addition, after foaling, the mare also received misoprostol (2 μg/kg [0.91 μg/lb], PO, q 12 h, for 7 days) to help protect against gastric ulcers that could develop with prolonged administration of flunixin meglumine and to treat suspected mild colitis of the right dorsal colon.
Gross examination of the fetal membranes (expelled within 4 hours after foaling) confirmed complete expulsion and no apparent abnormalities. Nonetheless, the fetal membranes were submitted for bacterial culture and histologic examination because of placentitis suspected in the mare at the time of admission. Histologic examination revealed no evidence of an infectious process or placental insufficiency; however, multifocal areas of blunted villi, a few areas of eroded epithelium, and mild multifocal expansion of the chorioallantoic membrane by granulation tissue were detected. Evidence of small mineral deposits and meconium were noted, and most sites of hemorrhage within the allantois were small. Therefore, the fetal membranes were considered to have been clinically normal.
On day 6 (postpartum day 1), the mare had hemorrhagic secretions from the left mammary gland. The mare also developed an intermittent fever that peaked at 39.8°C (103.6°F) and was responsive to treatment with flunixin meglumine. Thoracic ultrasonography performed on the mare revealed moderate hyperechoic reflection bilaterally, with a right-sided, focal area of mild consolidation in the cranioventral aspect and pleural roughening, suggestive of pneumonia. A transtracheal wash was performed; however, examination of the recovered fluid revealed no active inflammation, and bacterial culture of the recovered fluid yielded no growth. Because the origin of the mare's fever was unknown, metronidazole (15.0 mg/kg [6.8 mg/lb], PO, q 8 h, for 5 days) was administered as a broad-spectrum antimicrobial treatment.
On day 8 (postpartum day 3), ventral edema of the mare's abdominal wall had subsided, and the mammary glands appeared cranially displaced. Transabdominal ultrasonography was repeated and revealed enlargement in the tears of the internal and external abdominal oblique muscles bilaterally and herniation of the small intestine and right horn of the uterus through the tears (Figure 3). Serum biochemical analyses revealed continued high activities of aspartate aminotransferase (peak, 893 U/L) and creatine kinase (peak, 3,229 U/L), which were indicative of further muscle damage. Supportive care continued, and the mare was monitored (physical and ultrasonographic examinations combined with serial measurement of peritoneal and blood lactate concentrations) for signs of intestinal strangulation.
Ultrasonographic images of the left (A) and right (B) external abdominal oblique muscles of the mare of Figures 1 and 2 on day 8 (postpartum day 3). Tears (arrows) in the musculature of the ventral aspect of the abdominal wall (AW; A and B) appear to have progressed to complete rupture of the left and right prepubic tendons, with jejunum (J; B) herniating through the right abdominal body wall. There is no evidence of small intestinal strangulation. The scale on the right of each image is in centimeters.
Citation: Journal of the American Veterinary Medical Association 256, 3; 10.2460/javma.256.3.309
Discussion
Differential diagnoses for colic signs in a periparturient mare include 2 broad categories: intestinal causes (including large intestinal and small intestinal abnormalities) and extraintestinal causes (eg, uterine torsion, placental hydrops, and abdominal wall disease [including prepubic tendon rupture or abdominal wall tear]1). On the basis of the clinical signs combined with clinicopathologic and ultrasonographic findings in the mare of the present report, the most likely source of colic signs was abdominal wall disease. It was likely that the abdominal wall tears were too small to detect during the initial examinations but enlarged during hospitalization and were evident on day 4.
The underlying cause of abdominal wall disease is not well understood; however, many predisposing factors exist,2 and although draft breed horses are overrepresented,3 the mare of the present report was a Standardbred. It is unknown whether there is a genetic predisposition for abdominal wall disease in Standardbreds; however, we were aware of a recent case report4 of a Standardbred mare that had a live foal a month after prepubic tendon rupture. Other predisposing factors include hydrops allantois, hydrops amnion, twins, fetal giants, and recent trauma.3 The inciting cause for the abdominal wall disease of the mare in the present report was undetermined, and it was unknown whether the mare's age, breed, or prior history of multiple pregnancies and parturitions was involved in development of abdominal wall disease.
A report5 of 13 late-term pregnant mares that had abdominal wall disease shows positive outcomes for most (10/13) of the mares but fewer positive outcomes for the foals (6/13). Conservative medical management of the mare was associated with good foal survival (6/8 surviving foals), compared with results after interventional management (induction of parturition, elective cesarean section, or elective euthanasia of the mare) in which none of the foals survived. However, the authors of that report5 did not differentiate between mares with prepubic tendon involvement or other abdominal wall muscle tears.
To allow for maximal development of the foal, parturition was not induced in the mare of the present report. In addition, calcium concentration and pH of the mammary gland secretions, assessments of which are paramount for safe induction of parturition,6 could not be accurately measured because of blood in the secretions.
The mare of the present report required assistance during foaling. Not only was the foal malpositioned, but the mare's abdominal contractions were likely weakened because of the muscle tears and epidural treatments.
Bilateral tears in the external abdominal oblique muscles were diagnosed by use of transabdominal ultrasonography. Initially, a partial tear in the prepubic tendon was suspected because of the development of hemorrhagic secretions from the right mammary gland and the fact that the mammary glands were not displaced cranially at the time. The tears in the external and internal abdominal oblique muscles progressively worsened, as determined during subsequent ultrasonographic examinations, and were accompanied by high activities of serum aspartate aminotransferase and creatine kinase. The abdominal wall tear progressed until hemorrhagic secretions were detected in both mammary glands of the mare in the present report. Blood in mammary gland secretions may result from a disruption in the blood supply of the mammary gland or rupture of the adjacent musculature caused by the abdominal wall defect.7 Despite the bilateral nature of the prepubic tendon rupture in the mare of the present report, cranial displacement of the mammary gland was obvious only after resolution of the marked edema along the ventral aspect of the mare's abdomen.
Long-term survival after foaling for mares with a severe abdominal wall defect that involves the prepubic tendon is unknown because many such horses are ultimately euthanized. However, a mare with complete rupture of the prepubic tendon survived for > 2 years after hospitalization.8 Regardless of prognosis, affected mares should not be rebred to become pregnant and carry foals to term but could be used as embryo transfer donors.3
Outcome
All antimicrobials administered to the mare of the present report were discontinued on day 10. Because of the mare's lack of milk production and to avoid inadvertent trauma to the mare's abdomen during nursing, the filly was fostered to a nurse mare on day 20 (postpartum day 15). On day 23, the mare was discharged to the owner with a belly band for abdominal support during transport, and the owner was instructed to closely monitor the mare for signs of colic. The filly thrived and on day 28 (postpartum day 23) was discharged to the owner.
Two years later, the mare of the present report was alive and had no history of recurrent colic. Because the mare was considered desirable as a donor for an embryo transfer program, multiple reproductive examinations had been performed during the interim to monitor ovarian structures and uterine edema. During the breeding season immediately after hospital discharge, urine pooling in the cranial aspect of the vagina because of poor perineal conformation was diagnosed in the mare, as was chronic endometritis. A single embryo was obtained from the mare during that breeding season; however, the embryo did not result in a pregnancy. Treatment of the endometritis followed by additional attempts to obtain embryos was planned.
Acknowledgments
No external funding support was provided for this report. The authors declare that there were no conflicts of interest.
Presented in abstract form at the Annual Conference of the Society for Theriogenology, Milwaukee, August 2018.
The authors thank Dr. Mike Miller for assistance with aftercare of the patients and Dr. Assaf Lerer for assistance with interpretation of the transabdominal ultrasonographic images.
Footnotes
Bio-Sponge, Platinum Performance, Buellton, Calif.
References
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8. Diel de Amorim M, Chenier T, Card C, et al. Treatment of hydropsical conditions using transcervical gradual fetal fluid drainage in mares with or without concurrent abdominal wall disease. J Equine Vet Sci 2018;64:81–88.
