Urinary tract emergencies

36 Urinary tract emergencies



Urethral Obstruction



Feline



Theory refresher


Clinical signs associated with the lower urinary tract – in particular dysuria, stranguria, pollakiuria and haematuria – are a common reason for cats to be presented both as routine and emergency patients. Lower urinary tract disorders include urolithiasis, feline idiopathic cystitis, urinary tract infection, anatomical defects, behavioural disorders and neoplasia. An increased risk of lower urinary tract disease has been reported for example in cats confined indoors and those restricted to dry food diets with inadequate fluid intake, and signs are most commonly seen in 2- to 6-year-old cats.


Depending on the underlying disorder, complete urethral obstruction may or may not occur and this clearly has significant implications from an emergency perspective. Complete urethral obstruction almost exclusively occurs in male cats and is a potentially fatal condition (see below). Cats presenting with lower urinary tract signs but without obstruction usually have a small or empty bladder and require symptomatic medical therapy, analgesia in particular. Many of these cats will have idiopathic cystitis and will improve within 3–5 days. All these cats require appropriate analgesia but antibiosis should only be used in cases in which bacterial infection is documented by microbiology.



Clinical Tip



• Lower urinary tract signs typically suggest a degree of inflammation of the lower urinary tract with associated irritation and discomfort. However, it must be remembered that only a small proportion of cats with lower urinary tract signs have either a primary or a secondary infectious process and the empirical use of antibiosis is strongly discouraged. Antibiosis should ideally be administered only on the basis of confirmed infection and the choice of agent should be directed by sensitivity testing.


Nursing Aspect


On an emergency basis, nurses are often the first members of staff to speak to owners ringing about cats with lower urinary tract signs. In the author’s opinion, emergency consultation should be recommended for all cats showing dysuria, stranguria, pollakiuria or haematuria. Male cats in particular may have urethral obstruction which can be rapidly fatal. Both unobstructed male and female cats require analgesia as a minimum as these clinical signs are typically associated with varying degrees of pain.


In some cases of urethral obstruction owners report that their cat is straining nonproductively but are unable to distinguish stranguria from constipation. It is also noteworthy that not all cats with urethral obstruction show consistent urinary signs, at least earlier on. In some cases, owners ring to report an abnormal pelvic limb gait that is often presumed to be the result of trauma; alternatively, the cat may be showing nonspecific vocalization or apparent discomfort, especially when picked up. There is therefore perhaps an argument to examine all male cats with potentially compatible signs of obstruction. As a minimum, the author would strongly recommend examining all male cats with potential signs of obstruction that either have a history of lower urinary tract disease or that are confined indoors (at increased risk of urethral obstruction).


Mechanical urethral obstruction is much more common in male cats due to the narrow diameter of the penile urethra; it occurs very infrequently in females. Urethral plugs are the most common cause in male cats but uroliths may also cause obstruction, potentially in combination with a plug. Urethral strictures and rarely tumours are other possible causes. Urethral plugs are often made up of struvite material in a proteinaceous matrix. The most common uroliths in cats are made of struvite or calcium oxalate. Unlike in dogs, struvite urolithiasis in cats is not typically associated with urease-producing bacterial infection.


Prolonged urethral obstruction results in hypovolaemia and systemic hypoperfusion that may occur for a number of reasons, including the effect of hyperkalaenia and acidaemia on the cardiovascular system, and dehydration where this is a factor. In addition to azotaemia, urethral obstruction can result in profound electrolyte and acid–base disturbances including metabolic acidosis, hyperphosphataemia and hypocalcaemia. Hyperkalaemia occurs mainly due to impaired urinary excretion of potassium. The clinical manifestations of hyperkalaemia reflect alterations in cell membrane excitability and of greatest concern are the potentially life-threatening effects on cardiac conduction (Box 36.1).



BOX 36.1 Electrocardiographic findings associated with hyperkalaemia



• Sinus bradycardia (Figure 36.1)

• Prolongation of the PR interval

• Widening and bizarre appearance of the QRS complex, including sinoventricular rhythm

• Decreased amplitude, widening or complete absence (atrial standstill) of the P wave (Figures 36.2 and 36.3)

• Peaked/tall T waves (Figures 36.2 and 36.3)

image

Figure 36.1 Sinus bradycardia in a cat.


(Courtesy of Virginia Luis Fuentes)


image

Figure 36.2 Atrial standstill in a cat with hyperkalaemia showing absence of P waves; peaked T waves are also present.


(From Darke PGG, Bonagura JD, Kelly DK 1996 Color atlas of veterinary cardiology. Mosby-Wolfe, London, with permission.)


image image

Figure 36.3 Electrocardiogram from a cat with severe hyperkalaemia (a) before and (b) shortly after administration of calcium gluconate. The pre-treatment strip shows atrial standstill with absence of P waves, as well as peaked T waves and ventricular premature complexes (VPCs). P waves are visible and there are no VPCs in the post-treatment strip.



Clinical Tip



• The severity of clinical signs resulting from hyperkalaemia does not necessarily correlate with the absolute increase in serum potassium concentration. The treatment required is therefore dependent not only on the cat’s serum potassium level but also, very importantly, on whether the hyperkalaemia is assessed to be clinically significant.

• If treatment is deemed necessary, it should be performed before urethral catheterization is attempted; treatment is directed at improving the cat’s clinical status and not at the serum potassium concentration per se. In some cases, intravenous fluid therapy and restoring urine production and drainage is all that is necessary for hyperkalaemia to resolve. However additional therapy is required in cases in which hyperkalaemia is assessed to be having clinically significant effects on the cardiovascular system. Further treatment options for hyperkalaemia are summarized in Table 36.1.

• If serum electrolytes cannot be measured but clinically significant hyperkalaemia is suspected on the basis of electrocardiography or perhaps physical examination alone, the author firmly believes that empirical use of calcium gluconate, and potentially insulin with glucose, is appropriate. This treatment can be life-saving and is unlikely to cause any significant harm if not required.

Table 36.1 Treatment of clinically significant hyperkalaemia























Agent Dose/route Comments
10% calcium gluconate 0.5–1.0 ml/kg i.v. bolus over 30–60 s
Rapid onset of action (can be a few seconds) and first line choice in a crisis

Short duration of action (often 10–15 minutes)

Monitor ECG during administration

Does not lower serum potassium concentration but restores normal cell membrane excitability

Will also address possible ionized hypocalcaemia

Bolus can be repeated while other measures are used to reduce hyperkalaemia directly
Neutral (regular, soluble) insulin 0.1–0.5 IU/kg i.v. Slower onset of action (can be more than 15 minutes)
Glucose solution 0.25–0.5 g/kg i.v.
Lowers serum potassium concentration by moving potassium into cells

Intravenous glucose supplementation typically required for several hours (monitor and adjust accordingly)
Sodium bicarbonate 1–2 mmol/kg slow i.v. (repeat if necessary)
Also lowers serum potassium concentration by moving potassium into cells

Effect can persist for several hours

Access to on-site acid–base analyser much preferred

ECG, electrocardiogram; IU, international units; i.v., intravenous.


Cats with urethral obstruction present with a spectrum of clinical compromise and, as always, the management provided should be appropriate to the individual case. With rational intensive management, even the most moribund of patients has an excellent prognosis for full short-term recovery. Long-term prognosis clearly depends on the underlying urinary tract disorder.



Case example 1




Presenting Signs and Case History


A 4-year-old male neutered domestic short hair cat presented collapsed. The owner reported that the cat may have been lethargic 24 hours prior to presentation and was inappetent on the morning of presentation. The owner was at work during the day and had returned to find the cat collapsed, at which point she contacted the practice for an emergency consultation. The cat had outdoor access and the owner had not noticed any clinical signs of lower urinary tract disease. No other significant preceding history was reported.



Major body system examination


On presentation the cat was obtunded. Cardiovascular examination revealed a heart rate of 60 beats per minute with no obvious murmur. Femoral pulses could not be palpated and mucous membranes were very pale without a discernible capillary refill. Respiratory rate was 36 breaths per minute and lung auscultation was unremarkable. Abdominal palpation revealed a moderate to large rigid bladder, and rectal temperature was markedly lowered (33.0°C).



Clinical Tip



• Although rare, urinary bladder rupture may occur due to urethral obstruction and therefore the absence of a palpable bladder does not exclude this condition. Cats with urethral obstruction and bladder rupture are very likely to be moribund and severely azotaemic.


Assessment


The cat was assessed as being severely hypovolaemic. While severely hypovolaemic cats are very often bradycardic and hypothermic, the degree of bradycardia in this case was inappropriately severe. Bladder palpation was suggestive of urethral obstruction and the severity of bradycardia was therefore suspected to be partly due to hyperkalaemia.



Emergency database


An intravenous catheter was placed in a cephalic vein and blood obtained via the catheter for an emergency database. The most significant findings of this were severe hyperkalaemia (10.1 mmol/l, reference range 3.6–4.6 mmol/l) and severe azotaemia (blood urea nitrogen 80.0 mmol/l, reference range 3.0–10.0 mmol/l; creatinine 1950 µmol/l, reference range 50–140 µmol/l). Facilities were not available to measure blood pH or ionized calcium.


Continuous electrocardiography was commenced that demonstrated atrial standstill with a wide-complex sinoventricular rhythm.



Clinical Tip



• Urethral obstruction is a major cause of postrenal azotaemia that frequently is (very) severe. However, in most cases the azotaemia fully resolves, often within 24 hours, if the obstruction is relieved so diuresis can occur and adequate fluid therapy is provided.

• Very occasionally, prolonged urethral obstruction and back pressure on the kidneys may result in sufficient renal injury as to cause a degree of renal azotaemia that may therefore persist long-term. However, in the author’s experience this is rare in cats with feline urethral obstruction that are presented for treatment.

• The degree of azotaemia at presentation should not be used as a prognostic indicator and renal insufficiency must not be assumed until full treatment for urethral obstruction has been provided.


Case management


The cat was started on a 20 ml/kg bolus of 0.9% sodium chloride (normal, physiological saline) and treated immediately thereafter with 10% calcium gluconate (see Table 36.1) to which there was a rapid response with respect to heart rate and rhythm (see Figure 36.3). Neutral (regular, soluble) insulin and glucose were administered intravenously at this time. No warming measures were performed initially in order not to worsen hypoperfusion (see Ch. 17) but the cat was given a low dose of methadone (0.1 mg/kg i.v.). Another dose of calcium gluconate was also given, prompted by deterioration of the heart rhythm.


The cat was monitored very closely and continuously reassessed. Perfusion showed some improvement following the initial bolus, after which the cat was assessed to be mildly to moderately hypovolaemic. A further smaller bolus (10 ml/kg) of saline was administered. Serum potassium concentration was rechecked approximately 30 minutes after the initial emergency database and was improving in keeping with clinical progress.



Clinical Tip



• All cats with urethral obstruction will benefit from intravenous fluid therapy prior to catheterization. An isotonic replacement crystalloid is the fluid of choice to restore perfusion and enhance urinary potassium excretion. Normal saline (0.9% sodium chloride) has traditionally been recommended due to its lack of potassium. However, this fluid may contribute to existing metabolic acidosis and there is no clinically significant difference between the use of 0.9% sodium chloride solution and Hartmann’s (buffered lactated Ringer’s solution) which contains a small amount of potassium. The priority is very much to start the cat on one or other of these solutions at a rate that is appropriate for the degree of hypovolaemia (see Ch. 2).

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Sep 3, 2016 | Posted by in SMALL ANIMAL | Comments Off on Urinary tract emergencies

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