Uroperitoneum and C. difficile infection in a 3-day-old colt Anna Forbes

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)

Admission 6.3

Sodium (mM/L)

121

Chloride (mM/L) 91

Creatinine (µM/L) 710

Initial stabilisation 4.4 127 92 371

Immediately post-surgery 4.3 129 94 314

Reference ranges

1.9 - 4.1 128 - 142 100 - 111 35 - 195

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

Figure 1. The colon surrounded by hypoechogenic free fluid (star).

Figure 2. The empty urinary bladder with surrounding free fluid and umbilical arteries visible on either side (arrows).

Figure 3. Defect in the dorsal bladder wall (arrow) at time of surgery.

monocryl suture in a double layer with Lembert and Cushing patterns. The bladder was then fully distended with sterile saline via the urethral catheter to confirm secure surgical closure. The abdomen was lavaged with 5L of 0.9% NaCl which was then suctioned out followed by placement of 500mL carboxymethylcellulose (Belly Jelly, Sigma-Aldrich) into the abdomen. The linea alba was closed with 2-0 PDS in a simple continuous pattern, the subcutaneous tissue closed with 2-0 Monocryl™ (Ethicon) in the same pattern, and the skin with 2-0 ethylon in a simple interrupted pattern. The site was bandaged with a primapore dressing and the colt was recovered from the two hour-long uncomplicated anaesthesia. Post-surgery, the colt was given ceftiofur at 5mg/kg IV QI D for four days, and flunixin meglumine (Flunixin, Norbrook) at 0.5mg/kg IV BID for six days, then once daily as needed following discharge. One-hour post-surgery he was administered a 2L bolus of 0.9% NaCl IV, followed by additional 1L boluses approximately four hourly for five days. The foal started urinating an hour after surgery and was then ambulatory and nursing from the mare with progressive normalisation of blood biochemical parameters [Table 1]. One day post-surgery the colt developed watery yellow diarrhoea which was treated with continued fluid support and Bio-Sponge® (Platinum Performance). A faecal sample was PCR positive for Clostridium difficile and negative for Clostridium perfringens, following which metronidazole antibiotic was administered. Other than the diarrhoea and some resulting mild dehydration, the colt recovered well from the surgery and had no further issues while in hospital. He was discharged six days postsurgery with continuing marbofloxacin and metronidazole. The diarrhoea resolved following discharge and the colt recovered fully.

DISCUSSION

The presentation and management of uroperitoneum in this case was typical of similar reported cases (Butters 2008; Castagnetti et al. 2010; Hardy 1998). Uroperitoneum is a commonly documented occurrence in neonatal foals, with traumatic bladder rupture during parturition being the most common aetiology (Castagnetti et al. 2010; Landro 2011; Mendoza et al. 2010). Bladder rupture should therefore always be a prominent differential when neonatal foals present with indicative clinical signs. Foals typically appear healthy at birth, but deteriorate over the first 24-72 hours of life, with a distended abdomen, lethargy, and stranguria or anuria becoming apparent. Recumbency, tachycardia, tachypnoea, reduced peripheral circulation, and diarrhoea have also been reported (Butters 2008; Mendoza et al. 2010; Pelt 1994). The colt in this case presented with acute onset of lethargy, abdominal distension, and haemorrhagic diarrhoea, although the diarrhoea was likely due to concurrent infection with C. difficile. He was still able to stand and nurse at the time of admission, indicating that electrolyte imbalances were not yet advanced enough to cause a more severe clinical manifestation. Biochemical parameters associated most with uroperitoneum are hyperkalaemia, high creatinine, hyponatraemia, and hypochloraemia, all of which were present in this case (Butters 2008; Dunkel et al. 2005; Mendoza et al. 2010).

These abnormalities are seen due to the high concentrations of potassium and creatinine, and low concentrations of sodium and chloride in urine, which rapidly equilibrate with blood across the peritoneum (Love 2011). Diagnostically, abdominal ultrasonography was equally conclusive in this case. Large areas of hypoechogenic fluid within the abdominal cavity and a collapsed urinary bladder strongly indicated uroperitoneum caused by a defect in the urinary bladder (McAuliffe 2004). Due to most bladder defects in neonates regarded as being caused by traumatic rupture, trauma during parturition was the top differential for the bladder rent. Intraoperatively, there was very little evidence of recent trauma to the bladder, which might be more indicative of a congenital developmental defect in closure of the bladder wall. Regardless of the precise aetiology, the treatment and surgical plan would have been the same, so this was not a clinical issue. The bladder defect in this case made anaesthesia a necessary risk, but uroperitoneum causes a multitude of biochemical changes including hyperkalaemia, hyponatraemia, hypochloraemia, azotaemia, and metabolic acidosis, that have the potential to react poorly with anaesthetic drugs (Hardy 1998; Love 2011; Butters 2008; Love 2011). Hyperkalaemia is perhaps the most important of these changes, as it has the potential to cause severe bradycardia and ventricular fibrillation, while hyponatraemia and acidaemia may worsen these cardiovascular effects (Love 2011). These serum abnormalities carry a significant risk on their own but combined with anaesthetic drugs that depress the cardiovascular system, may quickly become life threatening. Thus stabilisation prior to surgery is essential, the goal being to bring these biochemical parameters quickly but safely to as close to normal ranges as possible before surgery. This foal was given 0.9% NaCl IV with added glucose to lower potassium and creatinine concentrations, while increasing sodium and chloride [Table 1]. Administration of glucose stimulates insulin release, which promotes the insulinmediated movement of glucose intracellularly. Potassium is also affected by this mechanism and is similarly transported intracellularly, thus reducing blood potassium concentration (Shingarev and Allon 2010). The concurrent administration of insulin along with glucose has been shown to be effective in more severe cases, although was likely not called for in this case as no clinical effects of the hyperkalaemia were apparent. Calcium gluconate can also be administered to minimise the cardiac effects of hyperkalaemia by restoring the transmembrane electrical gradient of the cardiac myocytes (Shingarev and Allon 2010). Dunkel et al. (2005) reviewed 32 cases of uroperitoneum in foals and found that most patients presenting with uroperitoneum had a leucocytosis and mature neutrophilia. In this case however, haematology on admission revealed a mild neutropenia with a mild left shift. These leukocyte changes were indicative of a more severe degree of acute inflammation than a bladder rupture would have accounted for alone. The subsequent confirmation of C. difficile infection by faecal PCR likely explained this discrepancy (East et al. 1998; Uzal et al. 2012). Clostridium difficile is an endospore-forming, anaerobic, grampositive bacillus, widely reported as a cause of diarrhoea in neonatal foals (Arroyo et al. 2004; Båverud 2004; Uzal et al. 2012). A range of clinical signs and severities have been documented, from mild softening of faeces and abdominal discomfort, to watery, haemorrhagic diarrhoea, extreme lethargy, dehydration, and death (Arroyo et al. 2004; East et al. 1998; Uzal et al. 2012). A link between severity of disease in foals and failure of maternal antibody transfer has been suggested, with adequate serum immunoglobulin G (IgG) concentrations (>8g/L) associated with milder clinical signs and improved recovery rates (Arroyo et al. 2004). Had the foal not also had the bladder defect and resulting uroperitoneum, it is probable that the C. difficile infection would have resulted in veterinary attention regardless when clinical signs progressed. It is likely that the colt’s early admission to hospital and subsequent supportive care minimised the effects that the clostridial infection may have otherwise had. C. difficile is not only highly infectious to other horses, it also poses a significant zoonotic risk to humans (Båverud 2004; Diab et al. 2013; Kelly and LaMont 2008). In humans, C. difficile infections have been shown to cause colitis resulting in a range of clinical signs from mild diarrhoea to severe abdominal pain, haemorrhagic diarrhoea, and death (Kelly and LaMont 2008). Infection can occur via direct contact with an infected patient, or via fomites (Båverud 2004). To reduce risk of infection in both humans and other horses, it is therefore imperative that strict infection control measures as used herein are adhered to. The farm involved in this case was already aware of a C. perfringens outbreak in their foals, so had some control measures in place to reduce infection with both organisms between foals. It is essential that these control measures are strictly adhered to for the duration of the clostridial outbreak. It is also important that any handlers are aware of the zoonotic risk that this disease presents and are educated on how to reduce the risk of infection.

ACKNOWLEDGEMENTS

Massey Equine Veterinary Clinicians involved with this case referred by EquiVets/SRVS were Emma Gordon, Ellison Aldrich and Ella Chappaz, and Stuart Gordon helped with editing.

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Sun TC et al. Ketofol: A ketamine-propofol admixture for induction of anaesthesia in two foals. Vet Rec Case Rpt, 2021; e136. DOI 10.1002/vrc2.136

Two foals undergoing surgery for angular limb deformities were anaesthetised using ketamine:propofol admixture (ketofol). Ketamine was used at 2 and 1 mg/kg, and propofol at 2 and 1.5 mg/kg in cases 1 and 2, respectively. Induction of general anaesthesia was smooth and occurred within 30 s after ketofol administration. No apnoea, nystagmus and paddling were noted. In case 1, anaesthesia was maintained with additional boluses of propofol (0.4 mg/kg) and flow-by oxygen delivered via face mask, and in case 2 with isoflurane delivered in oxygen. The anaesthetic time was 20 and 55 min in cases 1 and 2, respectively. Before recovery, xylazine (0.2 mg/kg) was administered IV in case 2. Both foals stood at the first attempt approximately 10 min later with mild ataxia. NOTE: Lots of uncontrolled variables here. So, as recommended in human emergency medicine, structured clinical trials comparing ketofol, each drug separately, and other combinations such as ketamine/benzodiazepine are required before this combination can be promoted. See https://www.aliem.com/ketofol-game-changer-procedural-sedation/