An unusual case of urinary retention and ulcerative cystitis in a horse, sequelae of pelvic abscessation, and adhesions

Abstract

A 21-year-old Quarter horse gelding was presented with stranguria and incontinence of 10 days duration. Despite catheterization and antibiotic therapy, the horse was euthanized. Necropsy revealed posterior abdominal and pelvic abscessation with adhesions of the urinary bladder and severe ulcerative cystitis.

Urinary dysfunction in the horse can be a diagnostic challenge as it may involve various body systems and musculoskeletal pain can cause signs of dysuria due to difficulties in posturing, particularly in males (1). Owners can further complicate diagnosis as they may misinterpret signs of dysuria, stranguria, pollakiuria, or polyuria.

Urinary incontinence can result from primary lower urinary tract disease, such as developmental anomalies, cystolithiasis, or a complication of dystocia, as well as neurologic dysfunction (1,2). Treatment of affected horses depends on the underlying cause and prognosis will vary with etiology. Prognosis for repair of congenital abnormalities is generally good, while for neurological or traumatic causes it depends greatly on correction of the underlying disorder and how quickly detrusor and sphincter functions are restored. Long-standing bladder paralysis generally carries a poor prognosis due to significant detrusor myopathy from chronic stretching, urinary tract infection, and sabulous accumulations (1).

The present case describes a 21-year-old Quarter horse gelding with a history of stranguria and urinary incontinence of 10 days duration. The horse was unresponsive to therapy and was euthanized. Gross postmortem examination revealed caudal abdominal adhesions involving the urinary bladder, the small colon, a 60-cm loop of jejunum, and a large abscess at the pelvic inlet. The underlying cause of the abscessation and adhesions could not be determined. Although adhesion of the urinary bladder is not well-documented in the horse, this should be considered as a potential cause of lower urinary tract dysfunction.

Case description

A 21-year-old Quarter horse gelding was attended on the farm with a complaint of stranguria and incontinence of 10 days duration. The gelding had been vaccinated against tetanus and West Nile virus within the last year. On physical examination, the horse had a body condition score of 6/9, was depressed, had a heart rate of 80 beats per min, body temperature of 38°C and normal findings on thoracic and abdominal auscultation. During neurological examination, no cranial nerve deficits, proprioceptive deficits, anal or tail tone deficits were detected. Although the horse was lethargic, he responded with normal mentation when handled. Blood was collected for a complete blood (cell) count (CBC) and serum biochemistry prior to sedation with xylazine (Rompun; Bayer, Toronto, Ontario) at 0.22 mg/kg body weight (BW), IV, 25 mg acepromazine (Acevet 25 injectable; Vétoquinol, Lavaltrie, Quebec), 0.05 mg/kg BW, IV and butorphanol (Torbugesic; Wyeth, New York, New York, USA), 0.02 mg/kg BW, IV. A urinary catheter was inserted without resistance, and reddish-grey urine was collected and submitted for urinalysis. Abdominal palpation per rectum revealed a distended urinary bladder that was easily expressed manually without eliciting signs of pain. Following examination, flunixin meglumine (Banamine; Intervet/Merck Animal Health, Summit, New Jersey, USA), 1 mg/kg BW, IV and trimethoprim/ sulfadiazine (Tribrissen; Intervet/Shering Plough Animal Health, Millsboro, Delaware, USA), 24 mg/kg BW, IV, were administered. The horse was discharged with instructions to administer 1 g of phenylbutazone powder (Buzone; Vétoquinol), PO, q24h and trimethoprim/sulfamethoxazole (Novo-Trimel DS; Novopharm, Toronto, Ontario) 25 mg/kg BW, PO, q12h.

The CBC revealed a leukocytosis [20.3 × 10⁹/L; reference range (RR): 4.2 to 11.0 × 10⁹/L], neutrophilia with slight toxic change (16.6 × 10⁹/L; RR: 1.8 to 7.5 × 10⁹/L), and monocytosis (1.4 × 10⁹/L; RR: 0.0 to 0.4 × 10⁹/L). Hemoconcentration was indicated by an elevated hematocrit (0.56; RR: 0.30 to 0.48). Total protein and fibrinogen levels were high normal at 67 g/L (RR: 37 to 70 g/L) and 4.0 g/L (RR: 0.5 to 4.0 g/L), respectively. Serum biochemistry showed a stress hyperglycemia and azotemia of probable post-renal origin. Urinalysis identified the presence of 40 to 60 red blood cells and 20 to 40 white blood cells per high power field, indicative of hematuria and infection. The owner declined further diagnostics and treatment; euthanasia was elected 2 wk following the initial farm visit due to the horse’s deteriorating condition.

On gross pathological examination, the small colon and a 60-cm loop of jejunum were adherent to the cranial aspect of a 30 × 25 cm, well-encapsulated mass that occupied the right caudal abdominal and cranial pelvic wall. Once incised, the mass was found to be a multiloculated, non-communicating abscess filled with tan yellow to pinkish grey purulent material. The mass was adherent to the right lateral aspect of the urinary bladder. The ventral aspect of the urinary bladder was also firmly adhered to the underlying ventral abdominal body wall. The urinary bladder was markedly distended with thickened walls measuring 2 to 3 cm. The mucosal surface of the bladder exhibited irregular, well-demarcated, raised yellow tan areas intermixed with depressed hemorrhagic areas. The bladder contained turbid pinkish grey urine with sabulous material. The urethra exhibited mucosal congestion but was patent. A small amount of sabulous material was present within the renal pelvices and the ureters were normal.

Histopathological examination of the urinary bladder mucosa showed areas of overt ulceration intermixed with large foci of adherent neutrophils, fibrin, and necrotic cellular debris. Mixed inflammation extended from the submucosa to the serosal surface of the bladder with marked congestion and irregular replacement of the tunica muscularis by fibrous connective tissue. Based on the degree and character of the fibrosis involving the urinary bladder wall, the lesion was estimated to have been present for at least 4 wk. The encapsulated abdominal/pelvic mass had widespread neutrophilic infiltration and coagulation necrosis of adipose and connective tissue with large numbers of coccobacillary bacteria.

Bacteriological culture of the urinary bladder mucosa, urine, and abdominal mass produced a light growth of non-hemolytic Escherichia coli and heavy growth of Enterococcus sp. A light growth of non-hemolytic E. coli was also isolated from the lung, liver, and kidney. The E. coli was resistant to sulfamethoxazole/ trimethroprim, ampicillin–sulbactam, and tetracycline.

Discussion

Urinary bladder adhesions resulting in urinary dysfunction in the horse have been reported twice previously. A 10-year-old Quarter horse mare exhibited focal ulceration and abscessation of the wall of the colonic pelvic flexure with adhesion to the cranial aspect of the urinary bladder. The mare had signs of fever, tachycardia, depression, anorexia, dysuria, stranguria, and colic and the bladder was not palpable per rectum due to its small size (3). Although there was an area of urinary bladder mucosal folding, edema, and congestion, cystitis was absent in that case and it was concluded that the intestinal adhesion to the urinary bladder resulted in the abnormal urination due to external pressure (3). In contrast, the horse described herein had adhesion of the ventral aspect of the urinary bladder to the ventral body wall and to the abdominal mass causing physical impairment of bladder contraction and inability to void. The other case report involved an ovarian granulosa cell tumor documented as a cause of mild pollakiuria due to adhesion to the left lateral ligament of the bladder in a mare (4). Clinical signs resolved with removal of the tumor and breakdown of the abdominal adhesions; cystitis was not reported (4).

In the present case, the cause of the abdominal/pelvic abscess could not be determined. Although there was no history of a prior colic episode, an intestinal perforating injury or rectal tear could have occurred, leading to bacterial contamination and abscessation of the intestinal wall, as is reported in horses with perirectal abscesses (5). The isolation of enteric bacteria from the abscess lends support to this explanation. There was no intestinal ulceration, similar to a previous case of urinary bladder adhesion in 1 horse (3). Other suggested etiologies of pelvic abscessation include poorly contained lymphadenitis associated with inflammation of the rectum with spread to pelvic connective tissue (6), and gravitation of a gluteal abscess to the pelvic cavity following intramuscular injection (5). Other predisposing factors for intestinal adhesion in horses include primary and secondary peritonitis, intestinal surgery, small intestinal distension, ischemia, and prolonged ileus (7–9). Adhesions of the small intestine and urinary bladder to a fracture callus within the pelvic canal have also been documented in dogs (10).

Cystitis is not common in the horse and usually occurs secondary to conditions which alter urine flow such as obstructive abnormalities (urolithiasis, urethral sphincter dysfunction, neoplasia), and neurologic deficits (equine protozoal myeloencephalitis, cervical spinal cord compression, cauda equine syndrome, equine degenerative myelopathy, neurological herpes virus, parasitism, trauma, spinal neoplasia) (7). Iatrogenic etiologies include urinary catheterization and endoscopsy (11). Sudan grass and Johnson grass consumption can cause bladder paralysis associated with ataxia as a result of demyelination of the lower spinal cord (1,2,11,12). In the present case, the ulcerative cystitis was most likely secondary to adhesion of the bladder to the ventral abdominal wall and the adjacent abscess. These adhesions led to inadequate bladder contraction and emptying, predisposing to ascending infection from the urethera and the clinical signs of overflow incontinence. There was no clinical or pathological evidence for a neurogenic etiology and uroliths were not found, although sabulous accumulations were present. Primary ulcerative cystitis has been documented in horses receiving long-term phenylbutazone therapy, possibly as a result of decreased prostanoid synthesis leading to dysfunction of the mucosal glycosaminoglycan layers (13). In the present case, phenylbutazone therapy was short-lived and was thus not likely to have contributed to the cystitis.

If further diagnostic workup had been possible, ultrasound may have been useful in diagnosing the abdominal abscessation and perhaps the bladder adhesion, as in a similar case (3). Cystoscopic examination would have been useful to rule out urolithiasis and to visually diagnose the severe ulcerative cystitis. However, prognosis for surgical correction would have been poor due to the infection, damage to the muscle wall, and multiple adhesions. Earlier diagnosis would likely have improved the prognosis by minimizing chronic stretching, inflammation, and fibrosis of the bladder wall. Laparoscopic adhesiolysis has proven useful for persistent postoperative colic due to intestinal adhesions (8). Laparoscopic examination, particularly of the urinary bladder, should also be considered in horses that are presented for signs of urinary dysfunction when risk factors for adhesions exist.

In summary, this first report describes a gelding with ulcerative cystitis and urinary retention associated with urinary bladder adhesions. Intestinal-urinary bladder adhesions are not a well-documented cause of urinary dysfunction; however, they should be considered when predisposing conditions for their development exist.