Obstructive Uropathy and Nephropathy

Chapter 11 Obstructive Uropathy and Nephropathy



Introduction




A. Obstructive nephropathy refers to the functional and anatomical effects of obstruction on the kidney.

B. Obstructive uropathy refers to local effects on the urinary tract at the site of obstruction as well as to effects on sites proximal to the obstruction, including the kidneys.
1. Urothelial damage.

2. Hemorrhage.

3. Inflammation.

4. Necrosis.

5. Erosion.

6. Perforation.

7. Rupture under pressure proximal to the obstruction.

C. Total obstruction of one kidney eventually results in the total destruction of the renal parenchyma.

D. Partial obstruction, or complete short-term obstruction, results in decreased renal function that may be reversible if adequate urine flow can be re-established promptly.

E. Total obstruction of both kidneys is not compatible with life, and death occurs in experimental animals with complete obstruction after 3 to 5 days.

F. A predictable sequential loss of renal function occurs during progressive obstruction.
1. Decreased concentrating ability.

2. Decreased acidifying ability.

3. Decreased glomerular filtration rate (GFR).

4. Decreased renal blood flow (RBF).

G. Types of obstructions.
1. Unilateral (affecting one kidney).

2. Bilateral (affecting both kidneys).

3. Partial.

4. Complete.

5. Acute.

6. Chronic.

7. Combinations of the above.

H. Location of obstruction.
1. Renal pelvis.

2. Ureters.

3. Urinary bladder.

4. Urethra (most common site of obstruction).



Etiology of Obstruction




A. Urolithiasis (most common in dogs).

B. Urethral plugs (common in cats).

C. Idiopathic urethral (most common in cats).

D. Functional (increased urethral tone).
1. Neurologic.

2. Idiopathic.

E. Neoplasia (intraluminal or extraluminal).

F. Strictures.
1. Posttraumatic (including after indwelling urinary catheterization).

2. Postsurgical.

3. Idiopathic.

4. Congenital.

G. Accidental placement of ligature around a ureter during ovariohysterectomy.

H. Suture granuloma.

I. Severe ureteritis or cystitis.

J. Proliferative (granulomatous) urethritis.

K. Prostatic enlargement (severe).

L. Perineal hernia entrapment.

M. Congenital anomaly (e.g., ectopic ureter, urethral abnormalities).

N. Dioctophyma renale (renal pelvic worm).


Lower Urinary Tract Obstruction




A. Obstruction within the urethra is the most common cause (Figure 11-1).
1. Urethral calculi in dogs.
a. Males more commonly are obstructed due to their long narrow urethra as compared with females.

b. Obstructing calculi often are trapped behind the os penis of male dogs.

2. Idiopathic urethritis or urethral plugs in cats.

3. Urethral or trigonal neoplasia in older animals.

B. Obstruction of urine outflow also can occur from masses in the trigone region of the bladder.

C. Clinical and laboratory abnormalities depend on the extent and duration of obstruction.
1. Signs of lower urinary tract distress (e.g., stranguria, pollakiuria).

2. Paradoxical (overflow) incontinence.

3. Oliguria or anuria.

4. Azotemia (acute postrenal failure and uremic syndrome).

5. Postobstructive diuresis.

6. Bladder atony.

7. Azotemia (chronic postrenal failure and uremic syndrome).

8. Polyuria without azotemia as a result of impaired urinary concentrating ability.

D. Bladder overdistension decreases blood supply to the bladder wall (Figure 11-2).
1. Ischemia contributes to bladder injury when the bladder is distended and subject to increased hydrostatic pressure.

2. Referred to as detrusor atony (bladder atony) or hyporeflexia.

3. Bladder overdistension disrupts the continuity of detrusor smooth muscle fibers.
a. Tight junctions between cells are separated.

b. Loss of detrusor reflex usually is temporary.

4. Urine retention results because the patient cannot urinate, despite relief of obstruction.

image

FIGURE 11-1 Underlying causes and mechanisms of urethral obstruction.


image

FIGURE 11-2 Overdistended bladder–urethral obstruction. A, Lateral radiograph. B, Necropsy specimen.



Urethral Obstruction (UO) in Male Cats



Causes and Associations





1. Idiopathic urethritis/cystitis, urethral plugs, and uroliths are the most common causes of UO in male cats. Urethral plugs and idiopathic urethritis/cystitis are responsible for obstruction in more than half of affected cats (Table 11-1).


TABLE 11-1 Frequency of Occurrence for Causes Associated With Urethral Obstruction in Male Cats

image


Urethral Plugs (Figure 11-3)






a. According to conventional wisdom, UO in cats usually is associated with urethral plugs.

b. Recent studies, however, show that only 18% of UO episodes were associated with urethral plugs. This is consistent with findings from an unpublished pilot study at The Ohio State University using urethroscopy at the time of initial evaluation.


image

FIGURE 11-3 Urethral plug. A, Salubrious mucoid plug cm marker. B, Plug with mostly mineral component. (No stain, ×400) Dissecting scope.



image Urethral plugs are less commonly associated with urethral obstruction in cats than has previously been assumed.





c. Urethral plugs have minimal intrinsic cohesive structure but often are cylinder-shaped after extrusion from the urethra.

d. Urethral plugs are fundamentally different from calculi that lodge within the urethra (i.e., urethroliths).
(1) Uroliths have an organized internal structure with much less matrix and are not easily compressed or distorted.

(2) Urethral plugs consist largely of matrix mucoprotein with embedded minerals.

(3) The predominant mineral composition in most plugs is magnesium ammonium phosphate hexahydrate (i.e., struvite). This is true despite the fact that cats form calcium oxalate and struvite uroliths with nearly equal frequency.

(4) Secondary components can contribute to plug formation, including inflammatory exudate (i.e., white cells, proteins), red cells, cellular debris, sloughed tissue (i.e., epithelial cells), struvite crystals, and combinations of these (Figure 11-4).

(5) Virus-like particles resembling calicivirus and bacteria also have been observed in urethral plugs examined by transmission electron microscopy.
(a) Finding virus-like particles within urethral plugs does not prove that viruses create the plug or are contributory to the obstructive process.

(b) Virus particles can be shed into urine during periods of stress and after recent vaccination.

e. Most plugs are assumed to lodge within the penile urethra, but obstructions also can occur at more proximal sites (Figure 11-5).

f. Definitive diagnosis of a urethral plug requires retrieval of the plug. Supportive evidence for the presence of a urethral plug can be seen on radiographs in some cats with UO (Figure 11-6).
(1) Many veterinarians assume that a urethral plug has been dislodged during hydropulsion and attempts to pass a urethral catheter when the catheter suddenly advances.

(2) This could indicate movement of a plug into the bladder or it could indicate that resistance caused by urethral spasm has been overcome.

(3) Retrieval of a plug or retropulsion of the plug into the bladder does not always result in restoration of normal urine flow (several other factors initiate or maintain the obstructing process).

g. Previously, the crystalline-matrix hypothesis proposed that plugs that then became embedded in a matrix formed secondary to precipitation of struvite crystals in the urine. According to this hypothesis, plugs created UO and urethritis.

h. It is now hypothesized that plugs form as a consequence of underlying idiopathic urethritis and cystitis (i.e., inflammation occurs first, followed by plug formation).
(1) Urine pH increases as plasma exudes into urine and the alkaline pH favors struvite precipitation.

(2) Urethral spasm and edema favor urine retention and struvite precipitation.

(3) Primary inflammatory changes (i.e., exudate, blood, edema) or changes within the urethral wall secondary to the presence of lodged intraluminal urethral plugs may contribute to the obstructive process.

image

FIGURE 11-4 Possible urethral plug composition. RBC, red blood cells; WBC, white blood cells.


image

FIGURE 11-5 Possible locations for obstruction in male cats.


(Drawn by Tim Vojt.)


image

FIGURE 11-6 Mineralized “sand” within the bladder and proximal urethra. A, Lateral radiograph mineralized material in a dependent location within the bladder. B, Mineralized debris within the urethra (arrow).


(Courtesy of Dr. Edward Cooper, Columbus, Ohio.)



image Urethral plugs develop secondary to underlying idiopathic urethritis and cystitis rather than as a primary event arising from crystalluria.



Urethral Calculi (Figure 11-7)



Idiopathic







a. Most common association in cats with UO.

b. This process is an extension of idiopathic/interstitial cystitis (see Chapter 10, Nonobstructive Idiopathic or Interstitial Cystitis in Cats).

image

FIGURE 11-7 Radiopaque urethral stones in a male cat with urethral obstruction.



image Most male cats with urethral obstruction have no identifiable cause (i.e., idiopathic).







(1) Some cats have signs of nonobstructive idiopathic/interstitial cystitis before UO.

(2) Many cats have signs of idiopathic/interstitial cystitis after relief of UO.

c. Obstruction is secondary to functional urethral spasm in addition to swelling of the urethra due to edema and hemorrhage.
(1) Refers to pathologic or neurogenic processes that cause contraction of the circular smooth or skeletal muscle of the urethra or both.

(2) Part of urethral tone maintained by the skeletal muscle (so-called rhabdosphincter) is influenced by sympathetic innervation.

(3) Stimulation of adrenoreceptors (particularly α-1) within the urethra increases urethral tone in normal cats. Pain and stress after UO increase sympathetic outflow from the central nervous system, leading to additional urethral spasm.

d. Bacterial urinary tract infection (UTI) is very uncommon before urethral catheterization. UTI deserves more consideration in cats with recurrent UO that have undergone urinary instrumentation.

e. Urethral stricture may occur (Figure 11-8).
(1) Especially in cats that have had previous indwelling urinary catheters.

(2) Severe recurrent episodes of nonobstructive idiopathic/interstitial cystitis.

f. Neoplasia of the urethra or bladder neck is rare.

g. Phimosis is rare.

h. Catheter fragment foreign body in urethra or bladder is rare.

image

FIGURE 11-8 Urethral stricture demonstrated on positive contrast urethrogram.


(Courtesy of Dr. Jordan Jaeger, Carolina Veterinary Specialists Medical Center, Charlotte, N.C.)



Signalment and History





A. The majority of cats with UO are relatively stable; approximately 10% are critically ill. Increased client awareness that male cats can have a life-threatening emergency associated with “urinary blockage” likely is responsible for these percentages.

B. Approximately 75% of cats presented with UO are experiencing their first episode.

C. The median age is 4 to 5 years old, but any age can be affected (0.5 to 16 years).

D. Most affected cats in the United States are neutered males. Intact males comprise 10% of cats with UO.

E. In the United States, more than 80% of affected cats are housed exclusively indoors.

F. Median duration of clinical signs before initial presentation was 3 days in a study of 223 cats. Signs include those of cystitis and partial obstruction before development of complete obstruction.


image Most cats presented with UO are experiencing their first episode.




G. Clinical signs depend on the completeness of the obstruction and its duration. Cats with long-standing obstruction display signs of uremia (e.g., vomiting, lethargy, dehydration) in addition to signs referable to the lower urinary tract (e.g., stranguria, pollakiuria, hematuria, pain, overflow incontinence).

H. The time required to develop clinical signs of uremia after UO varies widely.


image Some cats with UO continue to urinate small volumes. Urine overflow from a large bladder with total or partial obstruction may occur.





1. Cats with experimental UO do not demonstrate signs of uremia until after 24 to 48 hours of complete obstruction (Figure 11-9).

2. By 48 hours, lethargy and vomiting are noted.

3. After 48 hours, clinical signs become severe.

4. By 72 hours, many cats are moribund and some die. Some cats can survive periods of UO up to 98 hours, however.

5. Azotemia develops at a variable rate among individuals with the same degree of obstruction based on:
a. Rate of urine formation at the time of obstruction.

b. Distensibility of urinary tract proximal to the obstruction.

c. Integrity of the urothelium at the time of obstruction. Cats with damaged urothelium develop azotemia more quickly as waste products traverse the bladder wall. This may explain why cats that immediately re-obstruct become sick and azotemic very quickly.

image

FIGURE 11-9 Potential syndromes associated with urethral obstruction. BUN, blood urea nitrogen.


(Drawn by Tim Vojt.)



Physical Examination




A. A readily palpable bladder at a time when the cat is straining to urinate defines UO.

B. Urine is not readily expressible from an enlarged bladder (only gentle pressure should be applied). Failure to express urine, however, is not diagnostic for UO.


image Do not rely on inability to express urine to diagnose UO.



C. A large, turgid bladder if obstruction has been long-standing.

D. The penis may be reddened and self-traumatized from licking.

E. A urethral plug may be seen protruding from the tip of the penis.

F. Already extruded plug material may be adhered to perineal hair.

G. Signs of dehydration as a consequence of anorexia and vomiting.

H. Bradycardia from the effects of hyperkalemia.
1. Median heart rate, 187 beats per minute (bpm); range, 40-296 bpm (Lee and Drobatz, 2003).

2. Severe bradycardia: <100 bpm in 5% of cases.

3. Moderate bradycardia: 100 to 140 bpm in 6% of cases.

4. Mild: 140 to 160 bpm in 12% of cases.

5. Most cats without hyperkalemia that are presented with severe illness and stress are expected to have heart rates of >160 bpm.

I. Arrhythmia was detected in 11%.

J. Hypothermia.
1. Normothermia (100° F-102.5° F) in 50%.

2. Hypothermia (<100° F) in 39%.

3. Hyperthermia (>102.5° F) in 11%.

K. Tachypnea (median, 36 breaths per minute). As respiratory rate increases, there is less likelihood of severe hyperkalemia.

L. Rectal temperature of <95° F-96.6° F heart rate of <120 bpm was the most accurate predictor of severe hyperkalemia. A combination of hypothermia and bradycardia was 98% to 100% predictive for severe hyperkalemia (> 8.0 mEq/L).

M. Twitching or seizures are very uncommon (0.5%) and related to ionized hypocalcemia.


image The combination of hypothermia and bradycardia is a good predictor of severe hyperkalemia.



N. Systemic blood pressure most often is normal.
1. Median systolic blood pressure was 135 mm Hg, median mean arterial pressure was 120 mm Hg, and median diastolic blood pressure was 108 mm Hg in a study of 28 affected cats (Malouin, Milligan and Drobatz, 2007).

2. No cat was hypotensive, 71% were normotensive, and 29% were hypertensive.

3. Less seriously affected cats tended to be hypertensive.

4. Pain, stress, and anxiety likely increased blood pressure.

5. Normal blood pressure at initial presentation may be misleading because of combinations of major stress, hypovolemia, and bradycardia.

6. Mean arterial pressure correlated inversely with serum potassium and directly with total serum calcium concentrations.

7. Major abnormalities on physical examination and serum biochemistry were encountered despite normal blood pressure.


image Normal systemic blood pressure does not preclude abnormal physical examination or biochemical findings.



Diagnostics



Serum Biochemistry





1. Severity of abnormalities varies depending on duration and extent (partial or complete) of obstruction.

2. Blood urea nitrogen (BUN): Median, 25 mg/dL; range, 8 to 257 mg/dL; 33% were above the reference range (Lee, Drobatz, 2003). We have observed BUN concentrations of >300 mg/dL.

3. Serum creatinine concentration: Median, 1.5 mg/dL; range, 0.8 to 7.7 mg/dL; 29% were above the reference range. We have observed serum creatinine concentrations of >20 mg/dL.


image Initial magnitude of BUN, serum creatinine, and serum phosphorus concentrations do not predict survival or failure to regain normal renal function. They may predict the severity of postobstructive diuresis.




4. Serum phosphorus concentration: Median, 5.0 mg/dL; range, 2.8 to 20 mg/dL; 25% were above the reference range and 6% were below the reference range. We have observed serum phosphorus concentrations between 20 and 30 mg/dL.

5. Serum potassium concentrations ranged from 3.4 to 10.5 mEq/L in 199 cats.
a. Six percent were below the reference range, 41% were above the reference range, and 53% were in the reference range.

b. Serum potassium concentration was:
(1) <6.0 mEq/L in 66% of cases.

(2) >6.0 but <8.0 mEq/L in 12% of cases.

(3) >8.0 but <10.0 mEq/L in 12% of cases.

(4) >10.0 mEq/L in <1% of cases.


image It is important to measure serum potassium concentration because some cats with severe hyperkalemia do not have classic ECG or physical examination findings.





c. Hyperkalemia most often was encountered with acidosis (pH <7.2 in 74% of cases) and low serum ionized calcium concentration (<1.0 mmol/L in 75% of cases).


image Hyperkalemia does not occur in isolation and often is accompanied by acidosis and low serum ionized calcium concentration.





6. Blood gases.
a. Median venous pH was 7.29 in 198 cats (range, 7.02 to 7.45); 40% were below the reference range and 4.5% were above the reference range.
(1) pH of >7.35 in 25% of cases.

(2) pH >7.2 but <7.35 in 60% of cases.

(3) pH >7.1 but <7.2 in 9% of cases.

(4) pH less than 7.10 in 6% of cases.

b. Median venous pCO2 was 40.2 mm Hg (range, 26.6 to 74.2 mm Hg); 13% were below the reference range and 30% were above the reference range.

c. Median venous bicarbonate concentration was 19.2 mEq/L (range, 7 to 27.8 mEq/L); 30% were below the reference range and 7% were above the reference range.

7. Serum ionized calcium concentration.
a. Median serum ionized calcium concentration was 1.10 mmol/L (range, 0.57 to 1.60 mmol/L) in 199 cats (median, 4.40 mg/dL; range, 2.28 to 6.44 mg/dL).

b. Normal serum ionized calcium concentration for cats is 1.10 to 1.22 mmol/L or 4.40 to 4.88 mg/dL.

c. Serum ionized calcium concentration was below the reference range in 34%, above the reference range in 19%, and in the reference range in 47% of cases.


image Approximately 33% of cats with UO are expected to have clinically relevant hypocalcemia based on serum ionized calcium concentration.





d. Serum ionized calcium concentration was:
(1) 1.2 mmol/L (> 4.8 mg/dL) in 23%.

(2) 1.0 but <1.2 mmol/L (>4.0 but <4.7 mg/dL) in 57%.

(3) 0.8 but <1.0 mmol/L (>3.2 but <4.0 mg/dL) in 14%.

(4) ≤0.8 mmol/L (≤3.2 mg/dL) in 6%.

e. Serum total calcium concentration in 51 cats was below the reference range in 39%, above the reference range in 0%, and within the reference range in 61%.

f. Serum ionized calcium concentration was negatively correlated with BUN, serum creatinine, serum phosphorus, and serum potassium concentrations.

g. Serum ionized calcium concentration was positively correlated with venous pH in contrast to the expected decrease in ionized calcium concentration associated with increasing pH under normal circumstances.

h. Cats with low serum total calcium concentrations had moderate to severely decreased serum ionized calcium concentrations (Drobatz, Hughes, 1997.). In one study, more cats were found to have hypocalcemia when defined by measurement of serum ionized calcium concentration (75%) than when defined by serum total calcium concentration (27%).

i. Serum parathyroid hormone (PTH) concentration was increased in 63% of cats with UO in one study, including 8 cats with low and 4 cats with normal serum ionized calcium concentrations (Drobatz, Ward, Graham, et al., 2005). Serum PTH concentration was much higher in cats with hypocalcemia as compared with those with normocalcemia. Serum 25-hydroxycholecalciferol status was not correlated to serum ionized calcium concentration.

j. Low serum ionized calcium concentration is not a consequence of deficient secretion of PTH, nor does it appear related to serum concentrations of 25-hydroxycholecalciferol. Rather, it likely is a consequence of increased serum phosphorus concentration. The potential role of decreased serum calcitriol concentration has not been studied.


Urinalysis





1. Urine specific gravity (USG) is unpredictable. USG can be >1.040 when evaluated early during UO. In more advanced cases, submaximal urine concentration can occur due to the effects of obstruction on renal tubular function.

2. Red blood cells (RBCs): Hematuria is almost always observed because of the presence of underlying idiopathic urethritis/cystitis and the effects of overdistension of the bladder wall with resultant hemorrhage.

3. White blood cells (WBCs): A mild increase can be observed, but numbers of WBCs in the sediment may be normal.

4. Epithelial cells: A mild increase can be seen; occasionally rafts of epithelial cells are observed in the urine sediment.

5. Bacteria usually are not present, but often are described as present because particulate matter in the urine sediment may resemble bacteria and be erroneously interpreted as such.

6. Crystals: Struvite crystals may be observed, especially if urine pH is alkaline. Crystals are more likely to be secondary to urine stasis or alkaline urine pH than a primary cause of obstruction.

7. Proteinuria usually is present due to hemorrhage.

8. pH often is neutral to alkaline due to anorexia and plasma protein exudation into urine from bleeding.

9. Glucosuria: Positive glucose oxidase dipstrip reactions are sometimes observed.
a. Detected in 74% of cats with severe UO in one study (Burrows, Bovee, 1978). Detected in 40% of cats with less severe UO (Loeb, 1971).

b. Thought to be a consequence of stress hyperglycemia. Moderate hyperglycemia occurs in many cats with UO, but frequently not above the renal threshold for glucose.

c. Transient renal glucosuria may occur.

d. 40% of cats with glucosuria actually had pseudo-glucosuria due to presence of a non-glucose, oxidizing substance that acts directly with the chromogen in the dipstrip pad; 60% had true glucosuria (Loeb, 1971).


Urine Culture





1. Nearly all cats with UO have sterile urine on original presentation for obstruction.

2. Bacterial culture at the time of urinary catheter removal is more likely to identify pathogenic bacteria.

3. Isolation of bacteria from cats with a previous history of UO is more likely than isolation from cats suffering an initial episode of obstruction.


image Expect no growth from urine culture in cats presented during their first episode of urethral obstruction.



Abdominal and Urinary Tract Imaging



Radiography




image All cats with UO should have radiography to determine if urolithiasis is contributing to obstruction.





a. Abdominal radiographs should be obtained in all cats with UO to rule out the presence of radiopaque calculi in the bladder or urethra. It is very important to include the perineal region in the radiographs to identify urethral calculi.

b. Evaluation of the kidneys and ureters to be sure nephroliths or ureteroliths are not part of the overall process is important because upper urinary tract involvement can markedly affect the overall prognosis.

c. Free fluid resulting in a loss of abdominal detail can be seen in some cats with severely distended urinary bladders.

d. Free fluid has been observed at surgery and necropsy in some UO cats in which no tear in the bladder or urethral wall could be demonstrated. This fluid likely arises from transmural movement across an inflamed and highly permeable bladder wall (i.e., underlying idiopathic cystitis) subjected to increased hydrostatic pressure from UO.


Contrast Radiographic Studies






a. Useful for cats with recurrent UO, especially after recent instrumentation of the urethra.

b. Positive contrast urethrography is helpful to rule out urethral stricture. It also is useful to document the presence of urethral rupture after urethral catheterization.

c. Double contrast cystography is useful to demonstrate small urinary calculi and blood clots.


Abdominal Ultrasonography






a. A small amount of free abdominal fluid sometimes is observed (more often on ultrasonography than on radiography).

b. Evaluation of bladder for blood clots and evaluation of bladder wall thickness are best accomplished by ultrasonography.

c. Small cystic calculi can be identified.

d. Urethral calculi are not reliably identified; only those in the proximal urethra can be seen.


image A small amount of free abdominal fluid may be identified at initial presentation and may be more easily detected on ultrasonography when a large bladder has been emptied.



Urethroscopy





1. A small number of cats have what appears on endoscopy to be plugs.

2. Many cats have urethral erosions and submucosal hemorrhage.

3. Some cats have increased urethral vascularity.

4. Some cats have crystalline material adherent to denuded areas of the urethra.

5. Cystoscopy at the time of obstruction usually is not rewarding due to the presence of hemorrhage and the need to use very small diameter flexible endoscopes.


Treatment of Urethral Obstruction




A. Diagnostic testing and treatment of UO are performed simultaneously (Figure 11-10).

B. The severity of clinical signs from uremia, electrocardiographic (ECG) findings, and magnitude of bladder distension dictate how quickly and in what order treatments must be performed.

C. Cats in uremic crisis and those with very large turgid bladders are in need of prompt attention (Figure 11-11).

D. The causes of collapse and hypotension are multifactorial.
1. Hyperkalemia leads to venous dilatation and pooling of blood.

2. Bradycardia leads to decreased cardiac output.

3. Acidosis decreases vascular sensitivity to catecholamines.

4. Ionized hypocalcemia decreases myocardial contractility and causes peripheral vasodilatation.

5. Acute uremia contributes to myocardial depression and decreased cardiac output.

6. Hypothermia contributes to decreased mean arterial pressure, cardiac contractility, and cardiac output.

E. Stabilize the patient and treat the adverse effects of uremia, if present, before administering any anesthetic agents. Hypovolemia, hyperkalemia, metabolic acidosis, and hypocalcemia must be treated first.
1. Intravenous (IV) administration of fluids is needed for seriously ill cats with UO. Ten of 13 cats died after relief of advanced UO when not treated with IV fluids (Finco, Cornelius, 1977).
a. IV fluid therapy at 10 to 20 mL/kg/hr is started and the rate adjusted as the animal becomes more stable.

b. 0.9% NaCl often is recommended as the fluid of choice because it contains no potassium.

c. 0.9% NaCl corrects chloride deficits faster than more balanced electrolyte solutions (e.g., lactated Ringer’s solution) due to the relatively high chloride concentration (154 mEq/L) (Drobatz, 2008), but the high chloride concentration of 0.9% NaCl also makes it an acidifying solution.

d. No difference in the rate of decline in serum potassium concentration was seen in a randomized study of 68 cats with UO (22 with hyperkalemia and 31 with metabolic acidosis) treated with 0.9% NaCl compared with a more balanced polyelectrolyte solution containing 5 mEq/L of potassium as well as the base precursors acetate and gluconate (i.e., Normosol-R, Abbott Laboratories, North Chicago, Ill.).

e. More rapid correction of acidosis was accomplished within 12 hours of treatment with the more balanced polyelectrolyte solution compared with 0.9% NaCl.

f. From a practical point of view, both fluid types are acceptable for treatment of most cats with UO.

g. Severely affected cats with metabolic acidosis may benefit more from an alkalinizing polyelectrolyte solution (e.g., lactated Ringer’s solution, Normosol-R).

2. Management of hyperkalemia will be needed in the approximately 12% of cats that have severe hyperkalemia and may be warranted in another 12% that have moderate hyperkalemia. No specific treatment is needed for cats with mild hyperkalemia.
a. Restoration of normal renal function after relief of obstruction results in kaliuresis and a rapid decrease in serum potassium concentration.

b. Calcium gluconate is the treatment of choice for cats with severe hyperkalemia (>8.0 mEq/L), heart rate of >140 bpm, and especially in cats with ECG abnormalities.


image

FIGURE 11-10 A decision-making algorithm for management of urethral obstruction due to a urethral plugs in male cats.


image

FIGURE 11-11 Overview of the approach to the moribund cat with advanced urethral obstruction. ECG, electrocardiogram.



image Serum potassium concentration decreases soon after relief of urethral obstruction and often is normal by the time substantial decreases in BUN and serum creatinine concentrations are observed.






(1) Conversion to a more normal ECG tracing is very rapid (minutes).

(2) This treatment stabilizes the heart, but does nothing to change the severity of the hyperkalemia.

(3) 50 to 100 mg/kg of calcium gluconate (0.5 to 1.0 mL/kg of 10% calcium gluconate) is given over 2 to 3 minutes with continuous ECG monitoring.

(4) The beneficial effects are short-lived (about 20-30 minutes), and other methods to lower serum potassium concentration are needed.

c. IV dextrose is helpful for longer term control of hyperkalemia, especially if serum potassium concentration initially is >8.0 mEq/L.
(1) 0.5 g/kg dextrose bolus (1 mL/kg of a 50% dextrose solution).

(2) Dextrose should be diluted to a final concentration of 10% to 20% before IV injection.

(3) The goal is to create hyperglycemia that stimulates endogenous insulin release with subsequent translocation of potassium into cells.

d. Some clinicians also give one unit regular insulin IV to further stimulate the transcellular shift of potassium. Insulin should always be given with a bolus injection of dextrose with or without a constant rate infusion of dextrose to prevent hypoglycemia.

e. Sodium bicarbonate may be administered IV in cats with serum potassium concentration >10.0 mEq/L.
(1) 1 mEq/kg (1 mL/kg of an 8.4% sodium bicarbonate solution) is the standard dosage of sodium bicarbonate.

(2) 4 mEq/kg (4 mL/kg of an 8.4% sodium bicarbonate solution) is the maximal dosage of sodium bicarbonate.

(3) A potentially serious disadvantage to this treatment is development of ionized hypocalcemia due to increased binding of calcium to albumin and intracellular translocation.

3. Management of acidosis will be needed in approximately 6% of cats with severe acidosis and may be warranted in another 9% with moderate acidosis. No specific treatment is needed for cats with mild acidosis.
a. Restoration of normal renal function after relief of obstruction allows for rapid correction of metabolic acidosis, especially when an alkalinizing polyelectrolyte crystalloid solution (e.g., lactated Ringer’s solution, Normosol-R) is used for IV fluid therapy.

b. In cats with severe metabolic acidosis, 1 mEq/kg of sodium bicarbonate is given by IV infusion and then acid-base status is checked after 15 to 30 minutes to see if more sodium bicarbonate should be given. A partial increase in blood pH back toward normal is the goal rather than full restoration of normal blood pH.

4. Management of hypocalcemia.
a. Specific treatment rarely is needed.

b. Relief of obstruction usually results in rapid correction of serum calcium concentration as serum phosphorus concentration decreases toward normal.

c. An IV infusion of calcium gluconate is administered until the desired effect is achieved in cats that have muscular twitching or seizures.

d. Stop any infusion of NaHCO3 because alkalinization will exacerbate ionized hypocalcemia.

F. Sedation and analgesia for relief of obstruction due to urethral plugs, idiopathic urethritis/cystitis, or urethral stones (Table 11-2).
1. An IV catheter is placed before sedation, analgesia, and anesthesia in unstable cats.

2. An IV catheter can be placed after sedation and analgesia in stable cats.

3. Nearly all cats benefit from preanesthetic analgesics to decrease pain and anxiety; these usually are given before decompressive cystocentesis and before anesthesia to pass a urinary catheter.

4. Urethral relaxation while the cat is sedated or under anesthesia may increase the likelihood of urethral plug dislodgment or facilitate urethral relaxation.

5. Little or no sedation is indicated for cats with severe uremia.

6. Many different sedation protocols are available, depending on the cat’s condition and the clinician’s comfort and familiarity with their use (Figure 11-12).
a. Buprenorphine.

b. Acepromazine.

c. Hydromorphone or oxymorphone.

d. Fentanyl.

e. Diazepam or midazolam.


TABLE 11-2 Drugs Useful During the Management of Cats With Urethral Obstruction

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FIGURE 11-12 A, B, and C, Examples of sedation/analgesia protocols for use in cats with urethral obstruction. CRI, Constant rate of infusion; KUBU, kidney, ureter, bladder, urethra.



Decompressive (Therapeutic) Cystocentesis





1. Cystocentesis to empty the bladder should be performed as soon as possible in cats with very enlarged bladders to prevent rupture of the bladder and to allow renal excretory function to resume.

2. Cystocentesis allows for rapid reduction of urinary tract pressure and resumption of GFR compared with catheterization, which can take considerable time. Decompressive cystocentesis may stabilize the cat before anesthesia for urinary catheter placement.

3. Relief of bladder pressure before urethral catheterization also may facilitate efforts to dislodge urethral plugs, and allows collection of a superior urine sample for analysis before manipulation of the urinary tract and contamination by irrigation solutions.
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Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Obstructive Uropathy and Nephropathy

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