Page 778 - Small Animal Clinical Nutrition 5th Edition

806 Small Animal Clinical Nutrition

total protein, sodium and chloride concentrations), anemia (i.e., low hematocrit with dehydration), metabolic acidosis (i.e.,
decreased TCO ) and hypokalemia, the cat was diagnosed with chronic kidney disease (CKD).
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VetBooks.ir Assess the Food and Feeding Method

The cat was fed a mixture of commercial semi-moist and dry foods. These foods and water were always available.

Questions
1. What is the cause of this cat’s generalized weakness and cervical ventriflexion?
2. What is the likely cause of the hypokalemia?
3. Outline a treatment and feeding plan for this cat.
4. What parameters should be monitored to assess response to treatment?
5. How would you classify the stage of CKD in this cat using the International Renal Interest Society staging scheme
(Table 37-1)?
Answers and Discussion
1. Potassium depletion results in morphologic and functional changes in muscle and kidney, alterations in carbohydrate metabolism
and protein synthesis and disturbances in acid-base balance. Muscle weakness develops when the serum potassium concentra-
tion falls below 3.0 mEq (mmol)/l and frank rhabdomyolysis or life-threatening respiratory muscle paralysis may occur when the
serum potassium concentration is less than 2.0 mEq/l.
Clinical signs of hypokalemic polymyopathy include appendicular muscle weakness, reluctance to walk or a stiff stilted gait with
forelimb hypermetria and a broad-based hind-limb stance and apparent pain on palpation of muscles. The most dramatic myo-
pathic finding is a characteristic cervical ventriflexion due to weakness of the extensor muscles of the neck. Similar ventriflexion
has been observed in cats with thiamin deficiency and myasthenia gravis. Other neuromuscular signs may be observed in some
cats, including bilateral mydriasis, disorientation, staggering and falling.
2. In retrospective studies, hypokalemia was found in approximately 20% of cats with CKD and CKD was the most common asso-
ciated disorder in cats with hypokalemia. The hypokalemia observed in cats with CKD presumably is caused by a combination
of inappetence, weight loss with muscle wasting and polyuria. A clinically distinct syndrome of polymyopathy and nephropathy
characterized by hypokalemia, azotemia, impaired renal concentrating ability and lymphoplasmacytic tubulointerstitial nephritis
has been documented to occur in cats fed a food low in potassium and high in acid content; however, the role of hypokalemia as
a cause of CKD is uncertain.
3. The initial management of cats with clinically apparent potassium-depletion requires diligent potassium supplementation by oral
and intravenous routes. Potassium chloride usually is added to parenteral fluids for intravenous administration. Infusion of potas-
sium-containing fluids initially may be associated with a further decrease in serum potassium concentration as a result of dilu-
tion, increased distal renal tubular flow and cellular uptake of potassium, especially if the fluid contains glucose. Selecting a fluid
that does not contain glucose, administering fluids at an appropriate rate and beginning oral potassium supplementation as soon
as possible can minimize this complication.
Potassium gluconate is recommended for oral supplementation of hypokalemic cats because potassium chloride and potassi-
um bicarbonate are often unpalatable.The recommended initial oral dosage of potassium gluconate is 2 to 6 mEq potassium glu-
conate/day divided into two or three doses; the dose should be adjusted based on clinical response and serial analyses of serum
potassium concentration. Clinical improvement is usually seen after one to three days of treatment. Feeding a commercial veteri-
nary therapeutic renal food, which contains increased amounts of potassium, may be all that is need to maintain normokalemia.
However, oral supplementation with potassium gluconate should be considered if food alone does not maintain serum potassi-
um concentration above 4.0 mEq/l. Additional studies are needed to determine whether routine potassium supplementation is
indicated in all cats with CKD, regardless of serum potassium concentration.
4. It is difficult to estimate the amount of potassium required to reestablish normal potassium balance in a given patient. Thus, the
amount of potassium required must be determined by judicious supplementation and serial measurement of serum potassium
concentrations during treatment and recovery. Treatment usually results in resolution of muscle weakness within one to two
weeks, weight gain and an improved coat. During recovery, renal function (i.e., urea nitrogen and creatinine concentrations) and
anemia (i.e., hematocrit values and red blood cell count) may stabilize and improve in some cats. Persistent CKD is managed
using conservative medical and nutritional management.
5. Staging of CKD should be performed on the basis of stable serum creatinine concentrations (at least two measurements approx-
imately two weeks apart) obtained while the patient is well hydrated. Because the initial serum biochemistry profile was obtained
while the cat was clinically dehydrated, the serum creatinine may be higher because of an additional prerenal component of the
azotemia.Therefore staging should be determined after rehydration and measurement of stable serum creatinine concentrations.
The cat was eventually classified as having stage 2 CKD (Table 1).