BVSc-V [MASSEY] STUDENT CASE REPORT UROPERITONEUM AND CLOSTRIDIUM DIFFICILE INFECTION IN A THREE-DAY OLD COLT Anna Forbes annaforbes@hotmail.co.nz
INTRODUCTION Uroperitoneum is well documented in neonatal foals and numerous aetiologies have been described. Bladder rupture is the most reported cause of uroperitoneum in the equine neonate, with the majority of these cases resulting from trauma due to increased intra-abdominal pressure during parturition (Castagnetti et al. 2010; Hardy 1998; Love 2011). Various other causes have been recorded, including urachal and urethral defects, urinary tract infections, and sepsis (Butters 2008; Mendoza et al. 2010). While most of these cases report trauma as the cause of urinary tract rupture, congenital defects have also been reported (Chaney 2007; Hardy 1998). This report describes an interesting and relatively uncommon case of uroperitoneum caused by a congenital bladder defect, which was diagnosed and surgically repaired in a 3-dayold colt. The colt was subsequently confirmed to have a concurrent Clostridium difficile infection.
CLINICAL FINDINGS A three-day-old thoroughbred colt was presented to Massey University Veterinary Equine Clinic with an acute onset of lethargy, distended abdomen, and haemorrhagic diarrhoea. The stud farm was experiencing a neonatal outbreak of Clostridium perfringens at the time, so veterinary treatment was promptly sought with concern for C. perfringens infection. Parturition had been uneventful three days prior, and the foal had appeared healthy at birth and throughout the first two days of life. He had received an enema of warm soapy water the day before due to a meconium impaction and had reportedly experienced haemorrhagic diarrhoea since. The colt was able to stand and nurse on admission, with normal hydration. He had a heart rate of 110 bpm and a respiration rate of 40 brpm. Rectal temperature was 38.8⁰C. Auscultation of his abdomen revealed typical borborygmi present in all four quadrants. The abdomen was noted to be moderately distended. Haematologic results revealed mild leucocytopenia (4.3x109/L), with a mild left shift neutropenia (segmented neutrophils 3.1x109/L, band neutrophils 0.5x109/L), and mild lymphocytopenia (0.6 x109/L). Blood biochemical results [Table 1] showed hyponatraemia, hyperkalaemia, hypochloraemia,
markedly increased creatinine, and signs of metabolic acidosis: hyperlactataemia (4.48 mM/L), hypocapnia (22.5 mM/L), low pH (7.33), and low bicarbonate (22.8 mM/L). Abdominal ultrasonography revealed a large volume of hypoechogenic fluid (Figure 1), as well as a collapsed urinary bladder (Figure 2). Table 1. Serum biochemical values obtained on this case [Epoc analysis system]. Time point
Potassium (mM/L)
Sodium (mM/L)
Chloride (mM/L)
Creatinine (µM/L)
Admission
6.3
121
91
710
Initial stabilisation
4.4
127
92
371
Immediately post-surgery
4.3
129
94
314
1.9 - 4.1
128 - 142
100 - 111
35 - 195
Reference ranges
Uroperitoneum resulting from a ruptured bladder was diagnosed, and the decision was made to stabilise the colt and then proceed to surgery. An over-the-wire catheter was placed in the left jugular vein and he was administered 2L of 0.9% NaCl (Sodium Chloride 0.9%, Baxter) IV, with 30mL 50% glucose solution (Glucose 50%, Baxter) added per 1L bag. The colt was also given 5mg/kg ceftiofur (Calefur, Dechra) IV 30 minutes prior to the start of surgery.
SURGERY The colt was anaesthetised and positioned in dorsal recumbency and a urinary catheter was placed through the urethra and secured in the bladder. A fusiform shaped incision was made around the external umbilicus and this was removed via sharp dissection. A 10cm long ventral midline abdominal incision was made. The free fluid in the abdominal cavity was diluted with warm 0.9% sodium chloride and then suctioned out. Stay sutures were placed in the urachus to allow retroflexion of the bladder and exposure of the dorsal surface. A 4cm long rent was noted on the dorsal surface of the bladder [Figure 3]. The defect had smooth edges with no evidence of haemorrhage, indicating that this was likely of congenital origin rather than traumatic. This defect was repaired with a double layer of 3-0 monocryl suture using a Cushing pattern. The umbilical and urachal remnants were removed via sharp dissection and the site was closed with 0
Eq Vet Pract 2021 September; 46 (3) 41