20.1 Urethral calculi visible on preputial hairs.
Acute urethral obstruction is commonly associated with acute colic symptoms such as bruxism, repeated stretching, treading of feet, and kicking of the abdomen in bulls and steers. In addition to the previously mentioned clinical signs, palpation of the preputial orifice and preputial hairs is dry, indicating no urine passage. Upon rectal palpation, affected individuals will have an enlarged urinary bladder and palpable urethral pulsations. Individuals with a partial urethral obstruction show signs of discomfort as well as dribbling of urine, stranguria, and hematuria. If a complete obstruction is left untreated for 48 hours or longer, a urethral rupture or bladder rupture will occur and signs of colic typically cease. If a urethral rupture occurs, subcutaneous edema develops along the ventral abdomen that can extend from the scrotum to the sternum, but especially in the preputial region (Figure 20.2). Severe necrosis and sloughing of these tissues can occur if left untreated. With bladder rupture, bilaterally symmetric ventral abdominal distention will occur (“waterbelly”). With bladder rupture, a palpable fluid wave will also be present. Upon rectal palpation, free abdominal fluid will be appreciable and a small partially filled urinary bladder. Bulls with uroabdomen may also develop a hydrocele. Owners typically report the colic associated with a complete urethral obstruction, then improvement for 24–48 hours, after which they notice the abdominal distention and worsening depression again. Dehydration is also severe (≥10%) with bladder rupture, due to osmotic pull of fluid from the vascular space into the abdomen. Individuals afflicted with ureteroliths and nephroliths will experience similar clinical signs as those listed above. A ureterolith and hydroureter may be palpable per rectum, but often definitive diagnosis of ureteroliths and nephroliths does not occur antemortem.
Figure 20.2 Subcutaneous peripenile swelling typically extends from the base of the scrotum cranially and involves the entire ventrum.
Diagnosis
Urolithiasis can typically be diagnosed utilizing historical data and clinical signs. Additionally, rectal palpation and careful palpation of the penis can typically locate the site of obstruction and the presence or absence of a urethral or bladder rupture. For feedlot steers or economically constrained cases, treatment is implemented based on physical examination. However, for valuable individuals a complete diagnostic picture includes a complete blood count (CBC), biochemistry profile, and ultrasound.
The abnormalities observed with a CBC will typically coincide with the severity and duration of disease. Typical findings include a neutrophilia and possible hemoconcentration depending on the degree of dehydration. Cases with urethral rupture may have increased fibrinogen with excessive subcutaneous tissue necrosis. Common biochemical abnormalities include azotemia, hyponatremia, and hypochloremia. In ruminants, potassium can be normal or elevated in individuals with obstructive urolithiasis. When hyperkalemia is present, the degree of elevation is typically mild. One study experimentally induced uroabdomen and demonstrated increased salivary potassium excretion, possibly explaining the less severe hyperkalemia observed in ruminants with urolithiasis [11]. In small ruminants, Ewoldt et al. found individuals with no free abdominal fluid and a serum potassium less than 5.2 meq/l more likely to survive [12]. Individuals with urolithiasis may have a metabolic alkalosis, acidosis, or normal blood pH. When acidosis occurs, individuals are often severely dehydrated and suffering from lactic acidosis [13]. With prolonged obstructions, hyperphosphatemia and hypomagnesemia can occur and concerns of secondary renal failure should be considered. One study stated the best prognostic indicator was excessive serum phosphate being associated with increased likelihood of death [14]. In absence of hydronephrosis, 48 hours of fluid diuresis should be administered before diagnosing an individual in secondary renal failure. In individuals with uroabdomen, the degree of azotemia, hyponatremia, hypochloremia, and hyperkalemia can be severe due to the osmotic gradient across the abdominal wall pulling sodium and chloride into the abdomen, potassium and blood urea nitrogen intravascularly, with creatinine staying mostly intra‐abdominally, since it diffuses at a slower rate being a larger molecule.
If available, ultrasound can be used to assist with assessment of the urinary tract. Ultrasonography can be used transcutaneously or transrectally to assess the integrity and location of uroliths. Additionally, ultrasonography can assist with diagnosing the presence of cystoliths, ureteroliths, or nephroliths. Cystoliths usually have a sandy debris appearance that is hyperechoic with a rough, irregular surface that casts acoustic shadows [15]. Ureteroliths and nephroliths are often difficult to diagnose antemortem, but are hyperechoic half‐moon‐shaped or round calculi that cast acoustic shadows through deeper tissues [15]. Ureteroliths may also be diagnosed via rectal examination if hydroureter is associated with the condition. Prior to surgical intervention, presence of hydronephrosis and/or hydroureter should be investigated. The right kidney extends from the 13th rib to the third lumbar vertebrae with the cranial pole in the renal impression of the liver in the 12tth intercostal space [15]. The left kidney can be imaged from the right paralumbar fossa caudal and is found slightly ventral to the right kidney from the 2nd to 5th lumbar vertebrae [15]. The left kidney can also be evaluated with transrectal ultrasound. If severe hydronephrosis is present, humane euthanasia is recommended (Figure 20.3). Presence of peripenile subcutaneous edema is suggestive of a urethral rupture and poor prognosis for returning to breeding soundness. Significant diffuse hypoechoic free fluid in the abdominal area is generally suggestive of uroabdomen. However, definitive diagnosis of uroabdomen is done by performing an abdominocentesis in either the flank fold of the abdomen or at the location of the fluid found ultrasonographically with an 18‐gauge, 3.8‐cm (1.5‐inch) needle after surgical prep. An abdominal fluid creatinine to serum creatinine ratio of 2 : 1 or greater confirms the diagnosis of uroabdomen [11, 16].
Figure 20.3 Severe hydronephrosis in a mature bull.
A baseline urinalysis can be performed. Common abnormalities include hematuria, proteinuria, and alkalinuria. Diagnosis of bacteriuria is beneficial to ensure a primary urinary tract infection is not the etiology of the urolithiasis. Baseline pH knowledge is important if urinary acidification is implemented. Ideally, if uroliths are obtained during surgery, the uroliths should analyzed to determine type. This information will help determine the best prevention strategy for the individual and herd. If urolith analysis is not feasible or delayed, a urolith can be placed in an acidifying solution to determine if urinary acidification would be a useful adjunct therapy. If available, urethroscopy can be utilized to assess location of the obstruction, extent of urothelial damage, and presence of strictures, or provide possible avenues for utilization of a laser or basket retrieval method.
Treatment
Immediate Care
Prior to initiating treatment for urolithiasis, the intended use of the animal, economics, site of obstruction, and integrity of the urinary tract should be considered. For acute cases, medical management can be attempted or immediate slaughter if uremia is not present. Most cases of urolithiasis will require surgical intervention. For breeding bulls, maintaining a patent urethra is paramount for successful outcome and breeding career. Surgical procedures utilized in breeding individuals include tube cystostomy, cystotomy, ischial urethrostomy, and urethrotomy. Surgical procedures utilized in salvage bulls and steers include ischial urethrostomy, perineal urethrostomy, and urethrotomy.
Before sedation or anesthesia, any severe electrolyte derangement should be corrected. For severe hyperkalemia, a bolus of 50% dextrose can be