Straining and abdominal distension in a 2-day-old Appaloosa filly

Rosalie Fortin-Trahan Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada

Search for other papers by Rosalie Fortin-Trahan in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
Emma Jessop Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada

Search for other papers by Emma Jessop in
Current site
Google Scholar
PubMed
Close
 BVSc
,
Alejandro Merchán Muñoz Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada

Search for other papers by Alejandro Merchán Muñoz in
Current site
Google Scholar
PubMed
Close
 LV, DVSc, DACVS
, and
Luis G. Arroyo Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada

Search for other papers by Luis G. Arroyo in
Current site
Google Scholar
PubMed
Close
 LMV, DVSc, PhD, DACVIM

Click on author name to view affiliation information

History

A 2-day-old 50-kg Appaloosa filly was referred to the Ontario Veterinary College for evaluation of straining. Upon presentation, the foal was bright and nursing well. Vital parameters revealed tachycardia (130 beats/min; reference range [RR], 92 to 100 beats/min), but the respiratory rate (40 beats/min; RR, 37 to 51 breaths/min) and rectal temperature (38.8 °C; RR, 37 to 39 °C) were within normal limits. The filly presented moderate abdominal distension and pain upon abdominal palpation. Mild bilateral increased bronchial sounds were auscultated.

A CBC revealed leukopenia (3,200 cells/μL; RR, 5,100 to 11,000 cells/μL) characterized by neutropenia (2,210 cells/μL; RR, 2,800 to 7,700 cells/μL) and lymphopenia (860 cells/μL; RR, 1,300 to 4,600 cells/μL). Venous blood gas and electrolyte analysis revealed hyponatremia (120 mmol/L; RR, 133 to 138 mmol/L), hypochloremia (86 mmol/L; RR, 97 to 102 mmol/L), and hyperkalemia (5.4 mmol/L; RR, 3.5 to 4.4 mmol/L). Serum creatinine (189 μmol/L; RR, 80 to 130 μmol/L) and urea (5.8 mmol/L; RR, 4.2 to 8.9 mmol/L) were increased on serum biochemistry profile. Abdominal ultrasonography was performed (Figure 1).

Figure 1
Figure 1
Figure 1

Transverse plane abdominal ultrasonographic images at the level of the umbilicus (A) and the caudal ventral aspect of the abdomen (B) in a 2-day-old 50-kg Appaloosa filly referred for evaluation of straining.

Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.09.0502

Diagnostic Imaging Findings and Interpretation

Thoracic ultrasonography revealed no significant abnormalities. Abdominal ultrasonography showed a large amount (approximately 7 cm in depth) of homogeneous anechoic free peritoneal fluid with aggregation of the intestinal tube, without ascites separation, containing a hyperechoic structure suspected to be omentum. The urinary bladder was distended and well rounded (6 cm diameter; Figures 1 and 2), which likely indicated an intact urinary bladder wall. Ultrasonography of the umbilical structures and bladder revealed a small urachal tear, at the level of the fundus of the bladder, immediately ventral to the right umbilical artery (Figures 1 and 2). Under ultrasonographic guidance, peritoneal fluid was retrieved from the caudal ventral aspect of the abdomen. The fluid was clear and yellow, with a nucleated cell count of 550 cells/μL (RR, 341 to 2,495 cells/μL), a predominance of neutrophils (90%; RR, 0% to 35.7%), and total proteins of < 20 g/L (RR, 11 to 25 g/L). The creatinine concentration in the peritoneal fluid (700 μmol/L) was 3.7 times higher than in serum (189 μmol/L); uroperitoneum was diagnosed.

Figure 2
Figure 2
Figure 2

Same image as in Figure 1. A—Intact urinary bladder wall (arrowhead), surrounded by a marked amount of free peritoneal fluid (asterisk). B—A small urachal defect (arrow) ventral to the right umbilical artery communicating with the peritoneal cavity (asterisk).

Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.09.0502

Treatment and Outcome

The filly was treated with intravenous isotonic fluid therapy. The hyperkalemia (6.0 mmol/L; RR, 2.5 to 5.2 mmol/L), straining, and abdominal distension progressively worsened over the following hours while the urinary bladder wall remained intact. Considering the latter, the owner elected to attempt medical management despite suggesting cystoplasty. Broad-spectrum systemic antimicrobials were initiated. A 14-French-Foley urinary catheter was placed at the level of the neck of the bladder and the cuff was filled with 5 mL of sterile saline. The urinary catheter was left in place to allow closure of the urachal tear and resolution of the uroperitoneum.

The uroperitoneum resolved within 24 hours. On day 5, fluoroscopic imaging of positive contrast retrograde cystography was performed and confirmed the absence of leakage into the peritoneal space (Figure 3). The urinary catheter was removed, and the filly was monitored for urination for 48 hours. Ultrasonographic examination after micturition revealed partial emptying of the bladder. On day 7, the size of the bladder was increased (8 cm X 13 cm), therefore the bladder was emptied with an aseptic urinary catheter. Bethanechol treatment (0.4 mg/kg, PO, q 8 h; Paladin Labs, Inc) was initiated to promote detrusor muscle (bladder) contraction and facilitate urination. Over the next 24 hours, the filly’s bladder size remained stable (between 4 and 7 cm in diameter).

Figure 3
Figure 3

Right lateral fluoroscopic image of positive contrast retrograde cystography of the same filly, 5 days after abdominal ultrasonography depicted in Figure 1, showing an intact urinary bladder and urachus as the contrast media was retained within those structures. Cr = Cranial. D = Dorsal.

Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.09.0502

Comments

Uroperitoneum is reported in approximately 0.5% to 2.5% of foals.1 The hallmark of uroperitoneum is a marked anechoic peritoneal fluid, with viscera and mesentery floating on ultrasonographic examination, as observed in this case. The most common cause of uroperitoneum in foals is dorsal cystorrhexis.1 Nevertheless, an intact bladder wall was observed on ultrasonographic examination in this case (Figure 1), indicating that the cause of the uroperitoneum originated from another site of the urinary tract such as a ureter, urachal or urethral defect. Uroperitoneum due to ureteral defects may develop slower than bladder defects due to smaller urine leakage as described in an 11-day-old foal with bilateral ureteral congenital defects diagnosed by exploratory laparotomy.2 Urachal defects are causative in approximately 20% of cases,3,4 to which all of them were diagnosed by ultrasonographic examination in 1 study.4 In this case, the urachal defect could be observed by ultrasonographic examination (Figure 1).

Several complications can occur with foals treated surgically for uroperitoneum. In addition to general anesthesia risks, reported surgical complications include re-occurrence of uroperitoneum due to suture failure, peritonitis, incisional infection, abdominal/intestinal adhesions, and postoperative myositis.3 There are limited reports on the medical management of uroperitoneum, as they are typically repaired surgically. A case report describes the conservative management of a urinary bladder defect in a neonatal foal.5 Conservative management was also elected in a case after cystorrhaphy failure, therefore the uroperitoneum was managed with an indwelling Foley urinary catheter for a duration of 3 to 7 days.3 The complications associated with conservative management could include treatment failure, catheter obstruction, and ascending urinary tract infection. Prophylactic systemic antimicrobial therapy is recommended for the prevention of ascending urinary tract infections.

The urachal defect closure was confirmed by cystography, a fluoroscopic diagnostic tool evaluating the integrity of the bladder by absence of contrast media spilling into the peritoneal cavity.

In summary, the conservative medical management of uroperitoneum caused by a urachal defect was achieved in this case using an indwelling urinary Foley catheter (open system). This treatment may be considered in foals with small urinary tract tears and financial constraints. One year after discharge, the foal was urinating normally, and no health concerns were reported after hospitalization.

Acknowledgments

None reported.

Disclosures

The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors have nothing to disclose.

References

  • 1.

    Schott HC II, Woodie JB. Bladder. In: Equine surgery. Elsevier; 2019:1129-1145. doi:10.1016/B978-0-323-48420-6.00066-1

  • 2.

    Jean D, Marcoux M, Louf CF. Congenital bilateral distal defect of the ureters in a foal. Equine Vet Educ. 1998;10(1):17-20. doi:10.1111/j.2042-3292.1998.tb00841.x

    • Search Google Scholar
    • Export Citation
  • 3.

    Ford MG, Nelson BB, Ford TS, Souza CRS, Easley JT, Hackett ES. Complications and comorbidities in foals undergoing surgical repair for uroperitoneum. J Equine Vet Sci. 2022;110:103852. doi:10.1016/j.jevs.2021.103852

    • Search Google Scholar
    • Export Citation
  • 4.

    Kablack KA, Embertson RM, Bernard WV, et al. Uroperitoneum in the hospitalised equine neonate: retrospective study of 31 cases, 1988-1997. Equine Vet J. 2000;32(6):505-508. doi:10.2746/042516400777584712

    • Search Google Scholar
    • Export Citation
  • 5.

    Lavoie JP, Harnagel SH. Nonsurgical management of ruptured urinary bladder in a critically ill foal. J Am Vet Med Assoc. 1988;192(11):1577-1580.

    • Search Google Scholar
    • Export Citation
All Time Past Year Past 30 Days
Abstract Views 2553 2553 0
Full Text Views 4860 4860 1483
PDF Downloads 334 334 32
Advertisement