Managing the Complicated Senior Cat

Old age is not a disease. Both veterinarians and owners must resist the temptation to ascribe signs of illness to aging. Some signs of illness such as chronic pain, dehydration or hypokalemia may lead to clinical signs that owners scribe to “slowing down” with old age. Many problems of senior cats are chronic and progressive so that early diagnosis and treatment is important for pain management and quality of life. It can also be tempting to find a “diagnosis” and treat for that without continually evaluating the “whole” cat. The focus on a single diagnosis and treatment plan can neglect common comorbid conditions that can dramatically affect quality of life. A hyperthyroid cat, for example, may suffer from other conditions more common in older cats; overgrown nails, decreased olfactory sensing, which can impact appetite, muscle atrophy and osteoarthritis or periodontal disease.

For these reasons and a host of others, comprehensive wellness examinations, history assessment and a minimum database are recommended every 6 months for seniors. Health status may change rapidly in this group and early detection and treatment is important to preserve quality of life. Signs of illness in cats are often quite subtle and easy for owners to overlook. The minimum database includes a compete blood count (CBC), a full serum chemistry panel with electrolytes, a full urinalysis and total T4. Early detection of a decline in renal function will be found in declining urine specific gravity before BUN and Creatinine are beyond the normal range, making the urinalysis a critical part of information gathering. Depending upon risk factors, fecal examination and retrovirus testing may also be indicated. Blood pressure measurement should also be included in any cat with known risk factors.

Because senior cats’ response to vaccination is largely unknown and immune function may be affected by both aging and the presence of chronic disease, vaccinations should be given according to the AAFP Feline Vaccine Advisory Panel for all cats.

The home environment is critical to wellness. Staff members should be trained to educate owners about enrichment, stress identification and modification for aging changes. Senior cats may benefit by an additional heat source such as a heated bed or one placed close to a heat source. Resting or hiding areas that are inaccessible to other pets, quiet and easily accessible for the senior may help with stress reduction. Litterboxes should be large and shallow with low sides and placed in quiet locations. If the home has multiple stories, boxes should be placed on each. Night-lights may be helpful with declining vision. Multiple fresh water sources can encourage moisture consumption in cats that may be prone to dehydration because of reduced urine concentrating ability.

In senior cats, cognitive dysfunction (CD) is now recognized as an important problem. Formal diagnostic criteria have yet to be established. It is a diagnosis of exclusion. The most common signs are disorientation in time and space, altered learning, house soiling, altered interactions (e.g. attention seeking, anxiety, irritability) changes in activity (wandering or pacing) changes in sleep patterns, decreased appetite, decreased grooming and increased vocalization. Medical problems such as hyperthyroidism, hypertension, pain of osteoarthritis, or chronic kidney disease can mimic many of these signs and so must be excluded before presuming CD.

Published studies are lacking on the efficacy of treatment. Therapies extrapolated from studies in humans and dogs include anti-oxidant enriched diets, supplements phosphatidyserine, omega-3 fatty acids, Vitamins E and C, L-carnitine. One ingredient found in supplements for dogs, alpha-lipoic acid, is toxic in cats. SAMe improved activity and awareness in dogs and is commonly used in cats with hepatic disease. No trials with these supplements have been published for cats with CD. Therapies for cats with CD are anecdotal.

There is evidence of cholinergic decline in senior cats so drugs with anticholinergic activity (e.g. some SSRIs such as paroxetine and TCAs) should be avoided. Selegiline ( Anipryl), which has been anecdotally reported to be useful in cats and proven beneficial in dogs for CD, should not be combined with SSRIs or TCAs. Environmental enrichment and Feliway have often been recommended but no studies in cats show benefit. In fact, in cats with CD modifications to the environment may be detrimental. Regular and predictable routines are most desirable. Any changes should take place slowly.

Hyperthyroidism and Chronic Kidney Disease (CKD)

Recent literature suggests that treatment of FHT while avoiding hypothyroidism is desirable in cats with renal insufficiency . The new Hyperthyroid guidelines recommends treatment of hyperthyroid patients regardless of concurrent disease. This includes cats with pre-existing CKD and those that develop azotemia after initiation of FHT treatment. These patients will require careful monitoring in order to achieve and maintain a euthyroid state while at the same time preventing hypothyroidism or mild hyperthyroidism.

Treatment recommendations differ depending on the degree of underlying renal disease. Therefore, it is important to fully determine the renal status of the patient prior to initiating FHT treatment. The new guidelines recommend using the staging guidelines set out by the International Renal Interest Society (IRIS), including determination of blood pressure and urine protein quantification. Note that cachexia will affect the serum urea nitrogen level (elevated due to increased protein turnover) and creatinine level (decreased due to loss of muscle mass) Recording a body condition score and muscle condition score at each physical exam will help to document progressive changes. Cats that are identified as hyperthyroid with concurrent renal azotemia fall into the should be monitored accordingly. Comorbidity of azotemia with FHT is common.

The guidelines recommends treating FHT in cats with pre-existing CKD. Treat both diseases concurrently. Manage IRIS stage 1 and 2 cases as though they are nonazotemic. If the patient responds favorably and renal function is stable using a reversible treatment, then consider an irreversible FHT treatment. IRIS stage 3 and 4 patients warrant a more prudent approach for example, using lower doses of methimazole and more aggressive management of CKD. If a permanent treatment for FHT is pursued, careful monitoring and aggressive kidney support may be required during the period of regeneration of previously suppressed normal thyroid tissue.

Typically the thyroxine nadir occurs 2 weeks after radioiodine treatment, with T4 normalization occurring around 4 weeks after treatment. Supplementation with during this period will resolve iatrogenic hypothyroidism and may be necessary in clinically hypothyroid patients. However, this treatment will also suppress pituitary TSH, which is needed to stimulate regeneration of atrophied thyroid tissue. In such cases, it is imperative to establish euthyroidism in order to avoid renal hypertension and further glomerular damage, while at the same time avoiding iatrogenic hypothyroidism. Just as in those cats that develop azotemia after treatment of FHT, the evaluation of serial concomitant creatinine, T4 and TSH tests may help to determine whether T4 supplementation is necessary. The Panel generally recommends testing post-surgical and post- radioiodine patients at 30, 60, 90 and 180 days after treatment.

Heart Failure and Chronic Kidney Disease (Cardiorenal Syndrome or CRS)

In the cat, the incidence of chronic abnormalities in cardiac function (e.g. congestive heart failure) causing progressive and permanent chronic kidney disease is unknown. A study of 102 cats with hypertrophic cardiomyopathy reported 59% prevalence for azotemia as compared to 20% for age-matched controls.

CRS occurs when worsening renal function limits diuresis despite clinical volume overload associated with heart failure. In cats being treated for chronic heart failure, declining renal function should be anticipated. The diagnostic marker for CKD, isosthenuria, cannot be relied upon in cats being treated with diuretics. Monitoring of Creatinine especially should be used to discern trends in renal function. A progressive rise even within the normal range should alert the practitioner, along with clinical signs: PU/PD, hyporexia, anorexia, weight loss and vomiting.

A minimum database should include abdominal ultrasound to assess for typical changes in renal architecture and to identify underlying causes that may have specific treatments, such as neoplasia, pyelonephritis, and nephrolithiasis. Blood pressure monitoring should be included as well as hypotension from therapy can decrease renal perfusion. The usual diagnostic imaging; echocardiogram, thoracic radiographs are important for type of cardiac disease, risk assessment, and treatment planning.

Goals of treatment are to recognize CRS, reverse it as much as possible and deal with the renal consequences of heart failure and the complex relationship between heart failure and renal injury. The difficult balance is to “dry out” the heart failure and hydrate the kidneys. Different therapeutic strategies are based upon the degree of compromise of each organ.

Ace inhibitors are the mainstay of therapy for CRS especially in the presence of hypertension or proteinuria. Cats with CRS should be hydrated before starting therapy. Low dose benazepril or enalapril 0.25mg/kg Q 24 hours can be increased to proved better control for heart failure. Benazepril is metabolized in the liver, Enalapril in the kidneys. Therefore, cats with CRS may need a lower dose of enalapril than benazepril. Initiation of therapy may show a transient increase in BUN/Creatinine concentrations. If persistent, lowering the dose is usually sufficient.

If azotemia is becoming a concern, the first step is to lower the dose of diuretics. The goal is to find the lowest effective dose that controls heart failure. The dose must be continuously reassessed. The ideal dose for an individual patient achieves the threshold rate of drug excretion. An individual HF patient that is not responsive to 5mg of furosemide per 24 hour for example will need 10 mg per 24 hours, not 5mg every 12 hours. Adequate natriuresis can be grossly assessed by observation of increased urine volume and decreased specific gravity. Periodic drainage of pleural fluid or ascites can be used to avoid excessive diuretic use.

In the event that diuretic resistance occurs, several options are available to correct fluid balance. A CRI of furosemide (0.3-0.6mg/kg/hour IV inhibits sodium resorbtion more effectively than oral or IV Boluses. Once the volume overload has resolved, most cats will again respond to oral therapy. Another loop diuretic, torsemide has superior diuretic action and long half-life. (0.3mg/kg PO Q 24 hours) It appears to be 10 times more potent than furosemide. Dual-diuretic therapy can be considered when furosemide dose needs to be decrease. Spironolactone (1-2 mg/kg Q 12 hours) may cause severe facial pruritus and must be used with caution. Aldosterone sometimes causes significant hyperkalemia. Each work at different sites within the nephron and if tolerated may be helpful.

Systemic hypertension is common in CKD and by increasing afterload increases the cardiac workload. Hypertension worsens both CKD and heart failure. If present, amlodipine (0.625 mg/cat PO Q 24 hours) should be added. Blood pressure monitoring is critical to avoid the effects of iatrogenic hypotension.

In advanced CRS, a positive inotrope (pimobendan) may improve azotemia, demeanor and appetite and allow reduction in diuretic dose.

Dietary modification should consider both conditions. Sodium restriction is sometimes needed and the extent to which it is required will vary. Distilled or low sodium water may be offered for drinking if more sodium restriction is needed than can be provide with diet. Clients should be cautioned not to feed high sodium treats. Lower phosphorus diets may be helpful in managing kidney disease but may result in the loss of lean body condition. High quality protein should be given to the level that it does not worsen azotemia. Omega -3 polyunsaturated fatty acids have been shown to be beneficial in both cardiac and renal conditions. Many renal diets are supplemented or if given separately EPA 40mg/kg/day, DHA 25mg/kg/day.

Fluid administration is a balance between improving renal blood flow without precipitating congestive heart failure. Fluids should be given slowly to correct azotemia, tailored to the individual’s ability to tolerate. Abrupt changes in weight, a new gallop heart sound and/or heart rate may indicate impending congestive event and justify fluid rate reduction. Sometimes a low-dose CRI of furosemide will be indicated concurrently in cats with end-stage CRS. SQ fluids may be less likely to trigger a congestive event and can be given every 24 -48 hours via a balanced electrolyte solution and adjusted to the individual patient’s ability to tolerate. In fragile patients, a smaller volume of fluids, as little as 30mls every 48 hours may be necessary, titrating slowly upward if the expected effect on uremia is not evident. Electrolytes should be monitored closely, especially potassium, as hypokalemia can trigger arrhythmia. Correction can take place through fluid therapy or oral means.

Although renal function may remain stable for a period of time in cats with heart failure, when CRS occurs it leads to frequent hospitalization, difficulty maintaining good quality of life and eventually euthanasia. The therapy described here is directed at improving quality of life for cats with CRS. Whether they contribute to prolonged survival is unknown.

Sarcopenia and Cachexia

In both people and companion animals, cachexia and sarcopenia are 2 important syndromes that occur in a variety of chronic diseases and aging, respectively. Although cachexia has been recognized in people for over 2,000 years, only recently has it become acknowledged as a common and detrimental finding that is associated with increased morbidity and mortality, and with this observation has come rapidly expanding interest and research. Both of these syndromes are becoming increasingly important in human and veterinary medicine because of their high prevalence and adverse clinical effects, and a better understanding of the mechanisms underlying these syndromes is critical for optimal patient care, whether human or veterinary.

Cachexia is defined as loss of weight and muscle mass secondary to chronic inflammation or disease. Sarcopenia, “poverty of flesh”, is an age-related loss of lean body mass. Sarcopenia is not caused by disease, is a gradual process and progresses with age. Loss of muscle can occur without fat loss or a decrease in Body Condition Score (BCS). Individual cats, particularly those with long coats or a history of obesity may appear to have a high BCS and yet be under muscled.

One of the keys to the management of cachexia and sarcopenia in cats is recognizing it in its earliest stages. To achieve this, BCS and Muscle Condition Score (MCS) must be consistently assessed. The goal for BCS in a healthy cat is 4–5 on a 9-point BCS scale. However, in certain diseases (eg, CHF, CKD), a slightly higher BCS may be desirable (ie, a BCS of 6–7/9), although further research is required to make specific recommendations. Even in animals with these diseases, obesity (BCS > 7/9) should be avoided.

The MCS differs from the BCS in that it specifically evaluates muscle mass. Evaluation of muscle mass includes visual examination and palpation of the head, scapulae, epaxial muscles over the thoracic and lumbar vertebrae, and pelvic bones.

In people, the loss of LBM has direct and deleterious effects on strength, immune function, wound healing, and survival. In fact, cachexia is an independent predictor of survival in people. The specific deleterious effects of muscle loss have not been as well studied in cats although there are studies associating thin body condition with decreased survival.

The weight loss that occurs in cachexia is unlike that seen in a healthy animal that loses weight. In a healthy animal that is receiving insufficient calories to meet requirements, metabolic adaptations allow fat to be used as the primary fuel source, thus preserving LBM. Conversely, acute and chronic diseases alter concentrations of a variety of mediators (eg, inflammatory cytokines, catecholamines, cortisol, insulin, glucagon), which then decrease the ability to make metabolic adaptations required to switch to fat utilization, and amino acids continue to be used as a primary source of energy. Therefore, muscle and LBM quickly are catabolized.

Numerous other factors can contribute to muscle and weight loss. Maintenance energy requirements vary with age, genetics, health status and gender (intact or altered). In presence of some disease states, maintenance energy requirements increase significantly. Decreased nutrient absorption is another possible mechanism for muscle loss in cachexia and sarcopenia. Studies in cats have shown decreased digestive ability. One investigator showed a reduced ability to digest protein in 20% of geriatric cats with about 33% having a significant reduction in ability to digest dietary fat. Micronutrient absorption, potassium, phosphorus, sodium, choline, B vitamins and Vitamin E, is also decreased.

Cats derive most of their energy requirements from protein and are metabolically less able to handle decreased amounts of protein and increased amounts of carbohydrates to maintain their energy requirements. Omnivores adapt to lower dietary protein by down regulation of their protein metabolism (protein sparing) but cats have been proven to be unable to make this physiologic adaptation. This preferential use of protein for energy can have clinical effects when cats are ill or anorectic as protein malnourishment can occur.

An important problem in cardiac and other forms of cachexia is a decreased calorie intake. The anorexia may be secondary to fatigue, dyspnea, or may be because of medication toxicity or alterations in appetite that often accompany CHF, cancer, and CKD in cats. Absolute food intake may decrease in animals with these diseases, but there also may be altered food preferences, cyclical appetite, and other issues that negatively affect overall food intake. Anorexia, for example, is present in 34–84% of dogs and cats with heart disease.

Increased energy requirements, alterations in nutrient absorption, and decreased energy intake all likely play important roles in the pathogenesis of cachexia by causing a net calorie deficit. However, a healthy animal that has a calorie deficit, either as a consequence of decreased food intake or increased energy requirements, would primarily lose fat. Therefore, these factors are not sufficient to explain the muscle and LBM loss and relative sparing of fat that are the hallmarks of cachexia and sarcopenia. This discrepancy suggests that metabolic alterations also are present.

Because of the important implications of cachexia and sarcopenia on morbidity and mortality in people, there is now extensive research into the prevention, diagnosis, and treatment of these syndromes. There are exciting opportunities for new and effective targets to decrease energy requirements, enhance energy intake, improve nutrient absorption, and modify metabolic alterations to prevent and even reverse the effects of both cachexia and sarcopenia.

A 2008 study on longevity in aging cats studied in a controlled environment for 5 years showed that all cats lost weight over time. However, cats supplemented with dietary antioxidants, prebiotic chicory root and a blend of Omega 3 and 6 fatty acids had a beneficial effect over a commercially fed diet alone or one supplemented only with antioxidants (Vitamin E and beta carotene). Cats in the fully supplemented group lost less weight, lived longer, had better LBM scores, improved fecal flora and fewer diseases.

In many cases, practical methods to help owners manage their animal’s appetite are critical to success. This is particularly important because anorexia is one of the most common contributing causes to an owner’s decision to euthanize his or her pet.

Any issues that potentially can affect food intake should be addressed, whether physical or environmental. Dental disease, for example, can substantially impair food intake in an otherwise healthy or sick animal. Pain (eg, back or joint) can decrease an animal’s mobility and make it more difficult to secure adequate food intake. Environmental issues also can negatively impact food intake. Multipet households may impede the ability of an individual animal to gain access to food (eg, a more frail or timid animal may be crowded out from the food bowl). Stress often can increase for animals after diagnosis of any illness because of lifestyle changes (eg, medication administration, new foods), as well as increased stress on the part of the owner, which may be detected by the animal.

Once environmental issues are ruled out as a cause of weight loss, a nutritional screening is crucial. Older cats may need 5-6 g of protein/kg to prevent protein catabolism. Reduced digestive ability indicate that a high energy, highly digestible diet may be needed. Some kitten formulas may be more appropriate. Folate and cobalamin supplementation may be useful. Commercial cat foods vary quite widely in caloric density. Specific formulas should be investigated for adequacy.

Cachexia should be anticipated in animals with chronic diseases such as CHF, CKD, cancer, and others. Consistently evaluating MCS in all patients will help identify muscle loss at an early, mild stage in aging or ill animals, rather than waiting until muscle loss is moderate or severe, when it may be more difficult to successfully manage. Similarly, as animals age, muscle loss is likely to occur, even in healthy individuals. Therefore, muscle mass should be thoroughly evaluated in geriatric cats and dogs.

References

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