Felipedia

Acute ureteral obstruction in cats

Acute ureteral obstruction (AUO) is an emerging feline disease process that can result rapidly in life-threatening electrolyte and metabolic derangements. All ages and breeds of cats seem susceptible, and AUO has been documented in previously nonazotaemic cats and cats with pre-existing azotaemia or with nonazotaemic urinary disease (e.g. urolithiasis). AUO currently is the most common cause of presentation of cats for hemodialysis. Successful short-term and long-term management of AUO depend on rapid diagnosis, proactive medical and/or surgical care, thorough client education, and meticulous patient follow-up and management. Maintaining a high index of suspicion for AUO in an acutely uremic cat is critical to identification of this patient population and institution of appropriate care in a timely fashion.

Aetiology

Feline AUO results from intraluminal stones but also can occur secondary to nonmineralised intraluminal substances, ureteral stricture, surgical ligation or trauma, mural or retroperitoneal neoplasia and retroperitoneal fibrosis, among other less common causes.

1. Mineralised obstructions

The most common cause of feline AUO is ureterourolithiasis and by far the most common urolith type identified in the feline upper urinary tract is calcium oxalate. Calcium oxalate is an insoluble mineral, and its prevalence in uroliths recovered from the canine and feline urinary tract has been increasing over the last decade. Currently, calcium oxalate is the chief component of more than 90% of canine and feline nephroliths and ureteroliths. These stones form in the kidney and sometimes pass into the ureter. Stones may be propelled successfully via ureteral peristalsis into the urinary bladder or may become lodged in the ureter along the way. Obstruction of the ureter increases ipsilateral ureteral peristaltic activity significantly, which can result in severe pain (ureteral colic).

2. Nonmineralised obstructions

AUO resulting from hardened clots of blood also has been documented in cats. This type of obstruction can occur unilaterally or bilaterally and may consist of a single larger stone-like clot or many small ones. Causes of the blood accumulations are unknown, but prognosis and clinical course for these cats do not appear to be different from those of cats with mineralised obstructions. Ureteral trauma (e.g. trauma induced by stone passage) can cause a fibrinohemorrhagic exudate that may result in ureteral obstruction. Sloughed tissue and other debris from pyelonephritis also can collect in the renal pelvis and proximal ureter and obstruct urine flow.

Ureters may be ligated inadvertently during ovariohysterectomy or other caudal abdominal surgery, or compressed, entrapped, or crushed by closure of a cystotomy incision located near the trigone. Surgical damage to the ureters often is not noted before development of severe uraemia and hyperkalemia, and surgical revision is required for resolution. The normal feline ureteral lumen has an internal diameter of approximately 0.4 mm; therefore its patency can be disrupted easily by inflammation or fibrosis from any cause. Surgical manipulation of the ureters must be performed in a fashion that minimises the effect of this inevitable post-surgical swelling and the ensuing fibrosis associated with healing, lest the surgery itself result in ureteral obstruction.

Primary ureteral neoplasia is rare; more often, ureteral obstruction resulting from neoplasia occurs secondary to trigonal tumours. Bladder cancers are rarer in cats than in dogs, but primary trigonal tumours, most often transitional cell carcinoma, smooth muscle tumour, or lymphoma, do occur in cats and can cause bilateral ureteral obstruction and an acutely uremic presentation.

Epidemiology

In a recent review, the median age of cats with AUO managed with hemodialysis was 6 years, with a range of 8 months to 16 years. No sex predilection was identified, but Siamese cats appeared overrepresented. Cats were markedly azotemic and many were hyperkalemic. Obstruction of one or both ureters initiates a complex cascade of events, which eventually can result in permanent loss of function in the associated kidney(s). The exact course of events varies depending on age, species, degree of obstruction, and whether one or both ureters are obstructed.

Complete unilateral ureteral obstruction (CUUO) (as with ureteral ligation or ureterolithiasis) causes an increase in ureteral pressure, which results in a nearly immediate increase in proximal tubular pressure. Renal blood flow and ureteral pressure increases initially. A concurrent increase in glomerular capillary hydrostatic pressure occurs, but not in proportion to the increase in tubular pressure. Because of this change, the net hydrostatic pressure gradient across the glomerular capillaries decreases, resulting in a decline in filtration (decreased glomerular filtration rate). After 5-6 hours, intratubular pressure starts to decline (and are back at preobstruction levels by 24 hrs), but glomerular capillary pressures decline faster , so GFR stays significantly decreased or absent. After 24 hrs of obstruction, the decreased GFR in the obstructed kidney induces a compensatory increase in GFR in the contralateral normal kidney.

Prostaglandin release causes renal blood flow to increase transiently to the cortex (and decrease to the medulla), but then afferent arteriolar resistance begins to increase, resulting in decreased GFR. In a study examining normal, conscious dogs subjected to CUUO via ligation, GFR in the obstructed kidney decreased to 50% of controls at 24 hrs, 30% after 6 days, 20% after 2 weeks, and 12% after 8 weeks of obstruction. Events that lead to long-term development of interstitial fibrosis are initiated promptly after obstruction. In rabbit models of complete ureteral obstruction, increased presence of renal interstitial collagen fibres is detectable by 7 days post-obstruction, and organised interstitial fibrosis and tubular basement membrane thickening are detectable microscopically by 16 days post-obstruction.

The degree of permanent renal damage resulting from ureteral obstruction depends on the completeness and duration of obstruction, Irreversible damage actually occurs more rapidly, and recovery of function is slower when a normal contralateral kidney is present than when bilateral obstruction occurs. Prospective studies in cats have not been performed.

Pathogenesis

Clinical AUO often is a situation of sequential bilateral ureteral obstruction, with one ureter chronically obstructed and one ureter acutely obstructed. Initial unilateral ureteral obstruction rarely results in clinically apparent disease. The obstructed kidney enlarges at first because of hydronephrosis and interstitial oedema but then begins to fibrose and atrophy with chronicity of obstruction; simultaneously, the contralateral kidney hypertrophies to compensate for the decrease in GFR. The disease remains clinically silent until the ureter associated with the hypertrophied kidney becomes obstructed, at which point uraemia, often severe, occurs. A similar scenario is encountered in cats with a sole or primary functioning kidney that becomes obstructed.

Clinical signs

The most dramatic clinical signs associated with AUO usually are the signs related to uraemia, including anorexia or inappetence, lethargy, weight loss, fetid breath, and sometimes vomiting. Owners may suspect abdominal discomfort or detect decreased or absent urination. The severe, acute 'renal colic' associated classically with unilateral ureteral obstruction and ureteral spasm in humans is appreciated only rarely in cats. On physical examination, most cats presented for AUO do exhibit abdominal pain, however, localised to the obstructed kidney(s). The most likely source of discomfort is distension and stretching of the richly innervated renal capsule by pelvic distension and renal parenchymal oedema.

Cats with AUO may be polyuric, olgioanuric or produce normal urine volumes depending on the degree of obstruction. In cases with sequential obstruction, the ureter associated with the end-stage kidney often is at least partially patent. This kidney may produce surprisingly large amounts of poor-quality urine that does little to mitigate azotaemia but provides enough excretory function to prevent hyperkalemia and volume overload.

Differential diagnosis

Differential diagnosis for AUO include most other causes of feline acute uraemia, including acute pyelonephritis, nephrotoxicoses (e.g. lily, ethylene glycol, nonsteroidal antiinflammatory medications), and renal lymphoma. Moderate to marked (>4mm) renal pelvic and/or ureteral dilation, with or without renal asymmetry, renders AUO the most likely diagnosis.

Diagnosis

The mental status and general appearance of cats presented with AUO ranges from bright and active to moribund; indeed, even some extremely azotemic cats (BUN >300 mg/dl) appear remarkably normal at first presentation. Most severely azotemic (BUN >100 mg/dl) cats are hypothermic (rectal temp <37.8 C). A rectal temperature higher than 37.8C in a cat with severe azotemia should be considered suspicious and should alert the clinician to the potential presence of concurrent infectious or inflammatory disease.

Careful initial assessment of hydration is critical, particularly if fluid therapy has been instituted already, because many AUO cats are oligoanuric and easily become over-hydrated. Because uremic toxins can cause xerostomia, dry mucous membranes alone should not be taken as an indication of dehydration. Skin turgor correlates more reliably with hydration status in uremic patients. The breath odour often has a characteristic 'uremic' quality (fishy, metallic or ammoniacal) and also may smell necrotic if oral ulceration is present. A fundic examination should be performed with the cat's eyes properly dilated to detect retinal haemorrhages or detachments, particularly if hypertension is documented. Altered pupillary light reflexes or menace reflexes may reflect cerebral damage from hypertension or uraemia.

Significant renal asymmetry is common in cats with AUO and, if present, should raise suspicion of ureteral obstruction substantially. In some cats, the chronically obstructed kidney is so small that it cannot be found on abdominal palpation. The smaller kidney often is very firm and irregular. Most cats presented with AUO have some degree of palpable unilateral or, less commonly, bilateral renomegaly, and the enlarged kidneys usually are painful and have a resilient, turgid feel. Overhydration may result in peritoneal effusion, but effusion volumes usually are small.

No cardiopulmonary changes are specific for AUO; associated abnormalities are referable to severe uraemia (e.g. pneumonitis, tachypnoea), hyperkalemia (e.g. cardiac arrhythmias), volume overload (e.g. pulmonary oedema, pleural effusion, gallop rhythm), and anaemia (e.g. tachycardia, cardiac murmur).

Severe uraemia and hyperkalemia can cause neurological abnormalities ranging from hyperreactivity to slight obtundation to seizure and coma. Additionally, many cats with AUO are hypertensive and have some degree of uraemic platelet dysfunction, which can lead to significant cerebral haemorrhage. Again, these signs are sequelae to the uremic syndrome in general and not specific to AUO.

Imaging studies will help reveal irregularities in the renal parenchyma but visualisation of ureteral obstructions and ureteroliths may be difficult without specialist referral

Treatment

Medical management

Initial medical therapy for AUO centres on judicious diuresis (crystalloids, with or without furosemide and/or mannitol) and routine management of the sequelae of uraemia (with gastric protectants, antiemetics, antihypertensives, erythropoietic agents/blood products, chlorhexidine oral rinses and so forth). If hyperkalemia and volume overload are not present (or if dialytic therapy is available to mitigate these problems), medical management for 3-5 days may permit spontaneous resolution of obstruction. Clinical evidence suggests that resolution occurs in approximately 20% of affected cats. Diuresis must be undertaken with foresight, caution, and rigorous monitoring, however. Even in cats producing urine, intractable volume overload can occur rapidly and become life threatening swiftly. Oligoanuric cats that have not responded to medical therapy within 24 hrs probably are better served by early surgical intervention (if stable), or by dialytic management followed by surgery if necessary.

Glucagon has been used as an adjunctive therapy for AUO in human beings and cats and decreases ureteral peristalsis markedly and increases renal blood flow. The single retrospective study done in cats with AUO given glucagon did not demonstrate any improvement in overall outcome with its use, although it was associated with conversion from oligoanuric in several cats and did seem subjectively to be an effective analgesic. In another study with 20 cats treated with naturally occurring urethral obstruction with oral amitriptyline (1 mg/kg PO q24hrs) achieved 100% passage of the urethral obstruction, presumably because of the urethral smooth muscle relaxation. This drug also has potent, lasting, reversible relaxant effects on ureteral ring segments.

Lithotripsy

Extracorporeal shock wave lithotripsy (ESWL) is available at a few veterinary teaching hospitals, and a limited but growing number of clinical cases of feline ureteral obstruction have been managed successfully with this non-invasive modality

Surgical management

The majority of cats with AUO require surgical management for successful outcome. In a recent study, 65% of the cats required surgical correction of the obstruction. Obstruction in the proximal one third of the ureter generally is managed with ureterotomy or pyeloureterotomy. This approach has the advantage of surgical manipulation of an anatomically larger area. (i.e. the renal pelvis and dilated proximal ureter), compared with operation on a nondilated ureter and thus should result in decreased risk of postoperative ureteral obstruction from swelling or stricture. Gentle attempts should be made to milk palpable stones lodged in a nondilated or less dilated region of ureter to a proximal area of greater dilation for removal.

Ureteral obstruction in the distal two thirds of the ureter most of is managed with ureteroneocystostomy, particularly when the regional ureter is relatively nondilated. Ureteroneocystostomy entails transection of the ureter just proximal to the obstruction, with subsequent reimplantation of the proximal ureter into the bladder apex. The remnant distal ureteral segment is resected. This type of reconstruction carries less risk of postoperative obstruction because of stricture or swelling than does ureteral resection and anastomosis or ureterotomy on the nondilated feline ureter. Extravesicular and intravesicular techniques for ureteroneocystostomy have been well described; in feline patients, particularly those with minimal ureteral dilation, the modified Lich-Gregoir extravesicular technique often is preferred because it results in less postsurgical swelling and consequently a reduced occurrence of postsurgical ureteral obstruction. The intravesicular mucosal apposition technique also has been used successfully in cats with AUO.

Significant postoperative complications occur in 30% of cats surgically managed for AUO; the most common major postoperative complications being ureteral obstruction and urine leakage into the abdomen.