Download GERIATRICS William Fortney DVM Kansas State University

GERIATRICS
William Fortney DVM
Kansas State University
Manhattan, KS
785-532-4605
[email protected]
Aging Process: Why pets age and How we can influence the process
In the last AVMA pet owner survey, more than 39 % of the owned pet population were
7 years of age or older and these percentages continue to grow. This change in pet
population demographics is in part due to advances in the control of infectious disease,
improvements in nutrition, newer surgical techniques, newer medications for
controlling chronic disease, plus more comprehensive understanding of the aging
process. Changing owner attitudes toward elderly pets (human animal bond /
humanization of pets), has also contributed to potential increases in life expectancy.
An animal’s life can be divided into four stages; pediatric, adult, senior, and
geriatric. The senior years represents the transition period between the adult and the
traditional geriatric period. Although the exact time of each stage could be argued,
everyone would agree that smaller breeds live longer than that the giant breeds and
each life stage would have a corresponding chronological difference. Human / Pet Age
analogy charts reinforce this concept and are excellent client education and marketing
tools. The chart also emphasizes the idea of comparable “time compression” in pets as
it relates to disease progression, wellness testing intervals, and chronic drug
monitoring. (See the age analogy chart on the last page).
Aging is a complex subject influenced by numerous interrelated causative factors.
The current causes / theories of aging can be broken down into four general categories;
1. Accumulations of toxic substances or compounds within cells; 2. Cumulative cell
damage from ionizing irradiation, oxygen derived free-radical-mediated damage,
and/or environmental pollutants; 3. Immune mediated or immune compromised
processes; and 4. Genetically preprogrammed cell death initiated by a portion of the
gene responsible for the cell’s lifespan. Every cell is genetically preprogrammed for a
specified number of divisions and will die at a predetermined point in time dictated by
a specific cellular gene.
"Old age" is not a disease but represents the effects of time upon the physical,
mental, and internal organs, but bears no absolute relationship to actual chronological
age. Unfortunately each internal organ system will age at a different rate. While it is
appropriate to use age as a benchmark of organ decline, any assessment of a patient
health should be based on a complete health screening of mental and organ function
because the organs degenerate at different rates.
The generalized changes associated with aging changes include dryness of all
tissues, progressive degeneration of organ function, tissue hypoxia, cellular membrane
alterations, decreased enzyme systems, decreased immune competence, and definite
personality alterations. These progressive changes represent the complex interactions
aging has on bodily functions however considerable individual variation exists even
with litter mates. Three reference books one should consider owning when dealing with
the older patients include Geriatrics and Gerontology of the Dog and Cat by Dr.
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Hoskins, the Veterinary Clinics of North America, 2005 Geriatrics edition, and
Veterinary Drug Handbook by Plumb.
Gradual changes in the overall body condition are not easily detected by the owner.
Regular weight monitoring combined with body condition scoring allows the
veterinarian to better assess minor or earlier changes in overall weight status especially
in multi-doctor practices. Based on ideal weight, older patients can be placed in three
classifications; pets within the normal weight range, animals that are too thin, and
patients that are overweight or obese. Decreases in activity and basal metabolic rates
without a corresponding decrease in caloric intake produces the overweight pet.
Several studies have shown that geriatric pets are often too thin. The issue is whether
this low body condition score is the result of some underlying disease state or just
“normal’ aging seen in dogs, cats and humans. Common age-related causes of insidious
weight loss include metabolic diseases, cardiac failure, cancer, and maldigestion.
Decreases in muscle mass and partial age-related inappetance can be “normal”.
Despite the category, a decreased or picky appetite needs to be investigated. Pathologic
etiologies associated with a decreased appetite include dental disease, metabolic
dysfunctions, a gastrointestinal disorder or cancer. In addition to the normal loss of
olfactory neurons, normal loss of taste buds, masticatory muscle atrophy, a lack of
sufficient saliva to swallowing dry food, or “senility” can also contribute to deceased
appetite in the “healthy” older pet. Feline food aversion is often associated with
environmental changes, palatability issues, nausea from IBD, chronic pain, stress,
and/or medication administration with food.
Following a thorough physical examination and medical evaluation attempting to
rule out cancer cachexia or various metabolic disease, this author advocates one or
more of the following non-medical options for encouraging the pet to eat; more
frequent meals; hand feeding the pet; adding water to the dry food; feeding canned
food; warming the food; adding commercial flavor enhancers; and mild exercise prior
to mealtime. Bowls used for feeding elderly cats should be wide and shallow so that the
sides do not touch the cat’s whiskers. Dietary fat helps make foods more palatable, an
important consideration in older animals that may have a diminished sense of smell or
taste. Benzodiazepine derivatives are commonly used to stimulate appetite and are
effective in up to 50% of patients. Unfortunately, there uses have been associated with
drug related hepatopathies especially in cats. Diazepam may be used in dogs or cats
and is most effective when administered intravenously. Fresh, palatable food should be
offered immediately following administration (0.2-0.5 mg/kg administered
intravenously, a maximum dose of 5 mg per patient). Feeding usually starts within one
minute and may continue for up to 20 minutes. Longer lasting oral benzodiazepam
derivatives such as Oxazepam produce results within 20 minutes following oral dosing
(2.5 mg per cat administered orally). Cyproheptadine (Periactin) 2-6 mg/dog PO BID
and 1-2 mg/cat PO BID has been used as an effective appetite stimulant but may take
several days before the desired effect. In cats and humans weekly B complex injections
has also been shown to be effective in increasing appetite in some cases.
Effective thermoregulation is deceased in the aging dog. Their decreased ability to
pant and decreased cardiac output make them more prone to heat stroke. Age-related
cold intolerance is often attributed to less Sub Q fat, decreased basal metabolic rate,
decreased cardiac output and decreases in peripheral vaso-constriction. Cold
intolerance can also be a sign of hypothyroidism. The resulting response to cool
ambient temperatures may manifest as behavioral problems including reclusiveness,
trembling, and reluctance to go outside for eliminations, and/or sleep cycle
disturbances. In addition to suggested environmental changes and thyroid evaluation,
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warm bedding and outdoor garments may help alleviate some of the abnormal
behavior.
The integument changes are the most obvious to the owner. The skin and hair
undergoes some degree of pigment loss (graying), hyperkeratosis, follicular atrophy,
and decreased sebum production. The nails become longer and more brittle. The
dryness of the skin and coat can be helped with increased grooming, less bathing, postbathing conditioners, topical emollient (oils) or humectants (moisture) sprays, and
essential fatty acid nutritional supplements. As a result of decreases in cell mediated
immunity, older patients especially dogs are more prone to infectious skin diseases ie
pyoderma and yeast infections.
Progressive loss of muscle mass is a normal finding in the older pet especially the
geriatric patient. This change is related to a combination of inactivity combined with a
decrease in muscle cell numbers due to fibrosis, atrophies of existing muscle cells, and
decrease sensitivity to ATP. Additional muscle atrophy can also be attributed to
decreased dietary protein when using a “low protein” prescription diets. When dietary
protein is sufficiently restricted, the patient is forced to catabolize their skeletal muscle
as a protein source. Unfortunately this muscle wasting may be responsible for or
exaggerate hind limb weakness. The resulting difficulty climbing stairs or jumping can
be confused with the symptoms of arthritis and disuse atrophy. In dogs systemic or oral
anabolic steroids combined with increased dietary protein and a sensible exercise
program has been advocated in management of the generalized muscle weakness and
muscle wasting conditions. The use of creatine / phosphocreatine nutritional
supplements is also indicated.
Decreases in hearing and vision are common age-related changes that may have
associated changes in behavior patterns. Unfortunately these sensory dysfunctions may
not be recognized as such and are often mis-diagnosed or mis-interpreted as senility or
Cognitive Dysfunction Syndrome as the symptoms are often similar. Hearing loss
associated with decreased sound wave conduction from the external ear to the cochlea
(conduction deafness) can be helped with amplification. However specific loss of nerve
function (neurogenic deafness) is the most common cause of deafness in older dogs.
The use of a high frequency dog whistle is a temporary solution until the higher
frequency recognition is finally lost. The normal aging changes in the lens called
nucleus or lenticular sclerosis should be always differentiated from opacities of the
lens/capsule called cataracts. All cataracts should be staged (immature, mature or hyper
mature) to better assess the cataracts impact on vision and the appropriateness of lens
extraction. Neither nuclear sclerosis nor an immature cataract should affect a pet’s
vision.
Progressive functional renal nephron loss may impact drug and anesthetic selections.
Advancing progressive renal nephron loss can be easily determined by urine specific
gravity, BUN/ Creatinine, and perhaps persistent micro-albuminuira. Once more than
66% of renal function is lost, the patient losses the ability to concentrate their urine.
The bun/creatinine start to rise after more than 75% real function is lost. With the
remarkable adaptation of nephron in slowly progressive renal disease, the patient can
survive and a very small percentage of kidney tissue. This baseline testing is also
helpful in trending, the concept of repeated monitoring / charting of a biological
parameter that is helpful in “predicting” the patient’s future health status. The
significance of microscopic renal proteinuria is still being debated. Persistent renal
proteinuria (persistent microabuminuira or overt proteinuria) can be the first laboratory
finding with chronic progressive real disease. A complete urinalysis with specific
gravity, dip Stix, and sediment examination is an essential part of a senior care
program. Microabuminuira using ELISA based technology is a very sensitive test but
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not very specific. Conversely a urine protein/creatinine ratio while not as sensitive a
test, is much more specific. Both Heska and IDEXX have proteinuria algorhythms
charts available that include step by step workup and management options.
Liver function maybe altered by fatty infiltration and/or hepatocyte damage as
indicated by elevated alkaline phosphates. Mild elevations (2-3X high normal) in ALP
could be considered normal in the older dog. The implications are at what point should
the “healthy” patient with an elevated ALP be worked up or just periodically monitored
(trended)?
Decreases in both cellular and humeral immunity are associated with the aging
process and explain the increase prevalence of tumor growth and infection rates in the
senior and geriatric patients. That said, what should the vaccination schedule be for the
older pets…. none, more, less or the same?
The four most common causes of death in older dogs, based on a 1993 study funded
by the Morris Animal Foundation for Animals, re cancer, cardiovascular disease, renal
failure, with epilepsy & hepatic diseases tied for 4th. In cats, the top four fatal diseases
in order include cancer, renal failure, cardiovascular disease, and diabetes mellitus.
These facts are important when educating your clients and staff on the early warning
signs of serious life shortening common diseases in the elderly pet and in determining
what tests should be included in a geriatric health screening. Considerable research in
the area of interrupting the aging process is ongoing. Technologies such as gene
splicing may someday allow each of us to live longer. Until then, exercise, senior diets
and antioxidant supplements are generally recognized as valuable anti-aging strategies.
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Managing Common Behavioral Changes in Older Pets
Definite personality changes and behavioral problems can be extremely challenging to
the practitioner and extremely frustrating to the client. Some problems are mild and
acceptable, while others are major concerns initiating euthanasia discussions. Referral
resources for complex behavioral problems include American College of Veterinary
Behaviorist 409/845-3195; Animal Behavior Society 781/891-4200; and American
Society of Animal Behavior 630/983-7749.
General behavioral changes are elderly patient’s desire more attention, are more
jealous, are more irritable, are less mentally alert, and have altered sleep cycles. 60% of
pets sleep in the owner’s bed or in the bedroom according to an AAHA sponsored
study. Altered sleep patterns are common geriatric "behavioral" dilemmas especially in
those situations where both the patient and owner are affected. The owners report one
or more of the following complaints; pacing at night, periods of panting, awaking the
owners to go outside for no obvious reason, inability to get comfortable or constantly
"fluffing" their bed. Various causes include an underling painful condition such as
osteoarthritis, spondylosis or a chronic IVD; sleeping on a hard surface; an altered
biological clock where they sleep all day then can't get to sleep at night; cold from poor
circulation or a basal metabolic rate or a poor thermoregulation; or a phobia of the dark.
This complaint can also be linked with Canine Cognitive Disorder. The author would
advocate the following options; a warm soft bed, a night light, a radio playing softly, a
brief walk before bedtime, hydroxyzine 1-3 mg/kg prior to bedtime, melatonin 1-3 mg,
and/or a 2 week trial of a short term pain management program.
COGNITIVE DYSFUNCTION SYNDROME
Many of these common “old dog or old cat” behaviors are often grouped into a
syndrome called Cognitive Dysfunction Syndrome (CDS). CDS is a progressive
disease syndrome of older dogs and cats associated with some brain pathology that
result in commonly recognized group of behavioral changes. The clinical signs in older
patients are related to impaired mental function commonly referred to as "senility,
dementia, or doggy Alzheimer’s disease". Impairments in memory, learning, perception
and/or awareness are common. CDS is a progressive disease of the brain in older
dogs and cats associated with changes in behavior.
The pathogenesis of CDS is complex and is associated with four categories of
pathology each resulting in altered behavior; hypoxia, free radical damage, beta
amyloid accumulation, neuro-transmitter anomalies. Initially any one of the following
agents will initiate varying degrees of neuronal dysfunction that can be reversible if
treated early. Except with alterations in neurotransmitters levels, with time the
damaged neurons will eventually die leading to permanent abnormal behavior. This
explains why some treatments may be not be beneficial at all or become less effective
with time.
One cause of CDS is the accumulation of metabolic waste products in the neurons. The
primary offender in humans, dogs and cats is Beta amyloid that exhibits characteristic
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plaques when viewed on histopathology sections. Initially any behavioral changes
associated with Beta amyloid can be attributed to neuronal dysfunction but eventually
the affected cells will die. Another category of causative agent is hypoxia. Decreased
oxygen to neurons will result in neuronal dysfunction and eventually neuron death. The
hypoxia can result from decreased cardiac output, chronic pulmonary disease or
vascular compromise from arterial constriction or sclerosis. Another area of current
CDS research focuses on the age-related decreases in various CNS neuro-transmitter
levels i.e. ACH, GABA, dopamine, nor-epinephrine, or serotonin. The confirmatory
diagnosis of a specific neurotransmitter deficiency is based on the patient’s behavioral
response to any replacement therapy. The last category of a cause for CDS involves the
deleterious affect of oxygen derived free radical on brain neuronal function. There has
been considerable research into the effects of positive effects of anti-oxidants on brain
function in patients with CDS. Antioxidant packages are becoming common place in
most quality senior diets and are currently being investigated as possible preventatives
for many age-related diseases.
The common clinical signs of Canine Cognitive Dysfunction in dogs fall into four
distinct categories found in the acronym DISH. The D= disorientation / confusion: the I
= decreased interactions with family or housemates; the S= Sleep cycle disturbances;
and the H= house soiling. It is important to note that most cases of CDS have
symptoms in only one or two of the four categories. In the feline, the common clinical
signs of CDS include one or more of the following; aggression, inappropriate
elimination, increased vocalization, sleep cycle disturbances, excessive grooming,
and/or disorientation/ confusion.
Since certain metabolic diseases, endocrinopathy, sensory dysfunction, or brain tumors
can also present with similar if not identical symptoms, the patient should undergo a
complete work up prior to initiation of any therapy. The minimum data base for CCD
should include a behavioral history, a complete physical examination, neurological
examination, CBC, chemistry profile, UA, and thyroid evaluation. CSF tap, and brain
imaging is also recommended to run out other causes of organic brain disease.
The therapy depends on the underlying pathological cause. One of the management
strategies of CDS involves increasing the oxygen to the brain by increasing cerebral
blood flow. A product approved for use in Europe called propentofylline (Vivitonin)
increases the blood flow to the brain and therefore the oxygen supply without
increasing the brain’s glucose demand. Another European product Nicergolin (Fitergol)
is a competitive antagonist to norepinephrin at the alpha-adrenergic receptors. This
drug effectively increases the cerebral blood flow via decreasing the vasoconstriction
associated with excessive norepinephrin production.
Numerous other products are advocated as effective neuroprotectants agents (those
nutritional supplements that protect the neurons from the effects of oxygen derived free
radicals) including nutritional supplements vitamins E, C and zinc; other antioxidant
compounds; anabolic steroids; and selegilline. Specific agents such as selegilline,
Nicergolin, Cholodin® & Dyna-load® alter specific neurotransmitter levels often
associated with CDS.
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Until the advent of selegilline, the management of CDS was extremely frustrating. In a
1985 report, Dr. Sheffy advocated mild exercise in older dogs to increase their mental
acuity. He reported that mild forced exercise was conducive to increased alertness, plus
improved the dog’s spirit and enthusiasm in response to human socialization. Dr.
Mosier reported positive clinical cognitive benefits in dogs using oxygen therapy on a
weekly schedule. In addition the lay press was filled with testimonials of the benefits of
nutritional supplements (vitamins, antioxidants, and Cholodin).
Selegilline also known as L deprenyl is a specific B monoamine oxidase inhibitor
(MOA-B). The animal form of Selegilline is marketed as Anipryl by Pfizer Animal
Health. In some dogs and cats with signs of CDS, prolonged Selegilline therapy
resulted in significant clinical improvements in greeting behavior, client / patient
interactions, inappropriate urination and defecation, activity levels,
confusion/disorientation, and/or sleep cycle disturbances. These positive behavioral
effects are usually attributed to restoration of depleted Dopamine levels via MOA
activity and/or the facilitation of Dopaminergic transmission by some other related
mechanism. However, another suggested mechanism of action includes the CNS
stimulatory action of two of the metabolites, L-amphetamine and L-methamphetamine.
Selegilline has some neuro-protecting properties against amyloid deposition and
oxygen derived free radicals.
Regardless of the exact mechanism(s) of action, Selegilline can be beneficial in
managing certain age-related behavioral problems in dogs. The initial dosage of
Anipryl for use in Cognitive Dysfunction Syndrome is 1.0 mg/kg PO SID each
morning for at least a 60-day trial. Adverse reactions including restlessness, vomiting,
diarrhea, diminished hearing, pruritis, shivering/shaking/trembling and disorientation
can occur at the lower dosage but are much more commonly reported at the 2.0 mg/kg
PO SID range or when given at bedtime. The contraindications of Anipryl therapy
include concurrent use with meperidine (and other Apodes), tramadol, or use in
combination with other MOA inhibitors. Expense will become a major issue with the
life long administration.
Recently several studies have validated the use of dietary “anti-oxidants” and essential
fatty acids (hills b/d) to be effective in the managing some clinical aspects of CDS
especially when used in combination with environmental enrichment activities. These
nutritional supplements can be alone or as a prescription diet.
Osteoarthritis; Management Strategies for the Arthritis Pet
Osteoarthritis (OA) is a chronic, non-infectious, progressive disorder of any synovial
joint. OA is characterized by deterioration of the articular cartilage, synovitis, with
secondary bony changes. Osteoarthritis is classified as being primary or secondary in
nature. Primary arthritis (age-related) results from abnormalities within the cartilage
(abnormal quality) and is considered an intrinsic problem with the cartilage
homeostasis associated with aging. In this form of OA, normal joint forces impact
abnormal cartilage. The affected cartilage has limited ability to regenerate and maintain
itself in the face of the cumulative effects of ongoing trauma and/or inflammation.
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Primary osteoarthritis has a slow progressive course, generally involves one or more
joints, and is most common in geriatric patients.
Secondary arthritis is a more common cause of clinical lameness in the younger dog. It
is the consequence of some external event or force affecting the articular cartilage
adversely. In this form there are abnormal forces affecting normal cartilage. Examples
would include overt trauma, joint incongruity (instability), and joint malalignment.
Secondary arthritis can be seen in any age animal and usually involves a single joint. In
order to prevent, halt or minimize the degeneration process, the underlying joint
incongruity must be eliminated.
The pathophysiology of primary arthritis involves a series of steps that eventually
becomes a progressive self-perpetuating process. The mediators of the inflammation,
pain, and joint destruction include prostaglandins, cytokines, leukotriens, and kinnins.
The variation in clinical response of the each pharmacological agent used in treating
OA reflects the specific effect on each of these specific inflammatory mediators or
pathways. Articular cartilage is a very complex and dynamic structure. The cartilage
matrix is composed of proteogycan macromolecules (hyaluronic acid and GAGs), type
1 collagen, and 80% water. The matrix is synthesized and maintained primarily by the
chondrocytes. In primary arthritis, there is a shift in the cartilage homeostasis towards
catabolism. Initially there is decreased production of proteogycan by the chondrocytes,
a loss of chondroitin sulfates and water from the matrix. The resultant articular
cartilage is less elastic with less shock absorption. Any minor trauma produces
cartilage fissures and chondrocytes damage. Surface cracks produce "flaking" exposing
the collagen fibers to wear and tear. Some cracks extend into the deeper layers and
bone produce fibrillation. Degrading enzymes are released which further break down
cartilage matrix and collagen. These enzymes include serines, collagenase, cathepsins,
metalloproteinase’s, hyaluronidases, stromelysins, plus the cartilage breakdown
products, initiate a mild synovitis The resulting inflamed synovial membrane releases
primary inflammatory mediators IL 1, IL 6, tissue necrosis factor, proteases, and
prostaglandins that further increasing cartilage destruction and inhibiting new matrix
production. The further decreased resiliency of the cartilage results in sclerosis of the
subchondral bone and osteophyte development in the periarticular margins in advanced
cases.
The clinical signs of osteoarthritis are similar regardless of whether the disorder is
primary or secondary. The onset is often insidious but progressive. Early in the course
of the disease, the animal may sporadically be reluctant to perform previous tasks or
activities, i.e., jumping into the car. In the next stage, a lameness or stiffness occurs
following periods of excess activity or overexertion. These signs often disappear after
several days of rest. As the degeneration progresses, the stiffness and lameness may be
most pronounced following periods of rest. The pet typically "warms out" of the signs
with activity. Any cold or damp weather will increase the severity and duration of the
symptoms. Continuous stiffness, lameness and chronic pain typify the final stage
producing an irritable, reclusive and restless pet. In a recent study, 90% cats > 12 years
had radiographic evidence of osteoarthritis (Hardie, E., JAVMA 2002). The most
common location in cats was the spine followed by the elbow and the hip. Common
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feline symptoms include grooming difficulties, inappropriate eliminations, less
jumping, aggressive when handled, and lameness.
There is no cure for arthritis, only control. The goals in the treatment should be to
alleviate patient discomfort, minimize further degenerative changes, and to restore the
affected joints to as near normal and pain-free as function possible. The management of
arthritis involves the following strategies and should be tailored to best meet the patient
and clients needs; 1. Client education on the progressive nature of the disease is
critical; 2. Set realistic outcome goals (expectations); 3. Adequate rest periods; 4.
Sensible exercise program; 5. Weight assessment and reduction if necessary;
6.Analgesics and anti-inflammatory therapy for rapid results; and/or 6.
Chondroprotective agents; 7.Anti-oxidant nutritional therapy (dietary); 8.
Complementary therapies, i.e. message therapy, physical therapy, acupuncture,
chiropractic, etc.
When choosing between NSAIDs and Chondroprotective agents we initially select the
NSAIDS because NSAIDS have a more consistent, predictable and faster response our
client expects. In addition NSAIDS have more research backing the products and
generally the product quality control is much better. Unfortunately there are potentially
serious side effects that must be communicated and assessed. Conversely the
chondroprotective are less reliable in there effect, slower to work, but are much less
toxic. NSAIDS have a variable combination of anti-inflammatory, antipyretic, and
analgesic effects. The variation in clinical response of the each pharmacological
NSAID agent used in treating arthritis reflects the specific effect on various mediators
of the inflammation via selective inhibition of pyrogens, COX1, COX2, and pain
mediators. While all NSAIDS have some common toxicity, each has unique
pharmacological and dosing advantages and should never be considered identical or
interchangeable. In fact when switching NSAIDs, I always recommend a “WASH
OUT” period of at least 7 days. Managing feline osteoarthritis involves the judicious
use of chondroprotective agents, steroids and/or a non-approved long term NSAIDs
such as metacam.
NSAIDS toxicity ranks at the very top of the geriatric adverse drug reaction list.
Primarily this is because of their wide spread usage and potential life threatening side
effects. Adverse Drug Events (toxicity) are usually associated with over dosages,
misuse by owners, combined therapy with steroids, failure to “wash-out” a NSAID
before switching to another one, concomitant disease, and the lack of pharmacovigilance on the veterinarians part. During washout the drug tramadol at 2-5mg/kg
q12h can be used in dogs. It stimulates the opiate, adrenergic, and serotonin receptors.
This pain reliever is compatible with all the COX inhibiting NSAIDS drugs but NOT
with serotonin reuptake inhibitors, tricyclic antidepressants, or monoamine oxidase
inhibitors such as Anipryl. The induced enzyme Cyclooxygenase 1 (COX1) is
responsible for maintaining the gastrointestinal mucosa health, renal and hepatic blood
flow. Nonselective inhibition of COX1 can result in gastrointestinal damage, decreased
renal blood flow and/or hepatopathies. The resultant toxicity(s) includes gastroduodenal hemorrhage, gastro-duodenal ulcerations, bleeding dyscrasias, and analgesic
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nephropathy/hepatopathies. Most toxicity associated with the administration of
NSAIDS results from Prostaglandin E inhibition by blocking the COX1. This is often
dose-related adverse drug event. Prostaglandin E is gastric cyto-protective by inhibiting
gastric acid secretion, maintaining mucosa blood flow, stimulating epithelial cell
renewal /restitution, increasing gastric bicarbonate and mucus secretion. Cytoprotective strategies are aimed at eliminating or reducing the possible side effects with
prolonged NASAID administration. Using more selective COX2 inhibitors (COX1
sparing), accurate dosing, administering NSAIDs with a meal, the use of concomitant
antacids, the use of H2 receptor blockers can all aid in prevent most of the untoward
side effects of nonsteroidal anti-inflammatory medication. Misoprostal, a synthetic
PGE1 replacement, was first advocated to combat the side effects of NSAIDS. The
dosage is 2-5 ug/kg PO TID and is contraindicated in pregnancy.
Glucocorticoids are very effective at decreasing the inflammation associated with
arthritis however they should only be used in those advanced cases that are
unresponsive to NSAIDS since steroids hasten the cartilage degeneration via
chondromalacia. PU/PD, GI bleeding and ulceration are common adverse reactions
which are amplified when used concomitantly with NSAIDs.
Chondroprotective Agents: Chondroprotective agents are a group of compounds that
directly benefit and/or support the cartilage matrix. As a group, these compounds act to
decrease the breakdown of articular cartilage and/or provide the building blocks to up
regulate cartilage synthesis. Some actually decrease inflammation and increase
beneficial synovial fluid secretion. Therefore chondroprotective agents may not only
relieve some symptoms but they may also decrease the degenerative process thereby
may actually “reverse” the degeneration. Although chondroprotective agents are not
considered analgesics, recent studies indicate they may have a direct anti-inflammatory
effect on the synovial membrane. Principle components of chondroprotective agents
include one or more of the following; PSGAG’s, glucosamine, and chondroitin sulfate.
Unfortunately clinical failures with chondroprotective therapies are common and could
be attributed to minimal cartilage remaining (bone to bone), unresponsive
inflammation, time /dose dependant responses, and the lack of analgesia. The low daily
dosage of chondroprotective in some diets, there efficacy in treating arthritis is
questionable. While more expensive, the injectable PSGAG’s give a faster and longer
lasting response than the oral forms. Although more expensive, the combination of
NSAIDs plus chondroprotective is attractive to many owners, especially if the
chondroprotective agent decreases the NSAID dosage and frequency of usage.
Of recent interest is the use of nutrition as part of an overall arthritis management
strategy. Dietary glucosamine (IAMS senior) and/or dietary n-3 fatty acids, especially
DHA and EPA, can reduce production of the pro-inflammatory factors and result in
clinical improvement is some arthritic patients (Purina L, Hills j/d, and IAMS).
A wide variety of other drugs have been used in the management of DJD in small
animals including Vitamin C, crysotherapy (gold injections), free radical scavengers
orgotein (Palosein), MSN, and hyaluronate sodium. In most cases the exact
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mechanisms of action is poorly understood and little scientific data exists to determine
any efficacy.
Complementary therapies continue to gain favor among the veterinary community and
pet owning public in managing arthritis. At Kansas State University we have a faculty
member Board Certified in acupuncture, chiropractic, and holistic medicine that I
common refer patients to for complimentary therapy when western medicine has failed,
is too toxic, or the owner wants to take another approach.
Common Dermatological Problems in Older Pets
To the owner, integument changes are the most obvious sign of aging. Aging of the
skin and adenexa is a complex subject influenced by a combination of interrelated
causative factors including wear and tear, cumulative cell damage from ionizing
irradiation, and genetically preprogrammed cell changes.
The decrease in the number of active hairs and the follicular atrophy results in a thinner
hair coat. Graying of the hairs especially on the muzzle results from the decrease in
melanocyte replication. The nails become longer, malformed and more brittle. There is
a progressive hyperkeratosis of the skin and hair follicles. This is especially obvious on
the patient’s foot pads and nose. The application of keratolytic agents or softeners is
usually helpful in managing this problem.
The altered sebum production and cystic dilation of the apocrine glands results in a dry,
lack luster hair coat and dry skin. The dryness of the skin and coat can be helped with
increased grooming, less bathing, post bathing conditioners, topical emollient (oils)
and/or humectants (moisture) sprays, and essential fatty acid nutritional supplements.
Use the same basic dermatology investigation principles for senior patients, however
the list of differentials and probability ranking differs significantly. In addition to
signalment, the following 6 vital Questions to ask are critical in making a presumptive
dermatological diagnosis;
1. Is it pruritic?
2. What are the lesions? (primary vs. secondary)
3. Location / Distribution Pattern?
4. Contagious?
5. Previous Rx and response?
6. Systemic signs?
Pruritis is a good discriminator of dermatological diseases. Unless some mild
secondary infection, endocrine, congenital follicular diseases and immune mediated
diseases should not be considered pruritic. The intensity of pruritis is also helpful in
ruling in or out specific itchy diseases. Basic lesion descriptions (ie pustules, papules,
bulla, plaques, ect.) are also very helpful assuming they can be distinguished from the
secondary lesion associated with self trauma. The location / distribution of lesions can
be a great aid in narrowing the list of differentials. Muco-cutaneous junctions /
junctional epithelium lesions are hallmarks for immune mediated and SND. Bilaterally
symmetrical lesion patterns are constant with auto immune, endocrinopathies, or
inherited skin diseases. Contagiousness to owners or housemates narrows the list of
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possibilities considerably. Often the historical assessment of previous treatments and
the response to that therapy can be of significant help. Since many systemic diseases of
older patients have some cutaneous manifestations, check for systemic signs/
symptoms can be helpful with many endocrine, SND, or immune mediated diseases.
Senior patients are to be more prone to food allergies, endocrine-related skin changes,
pressure point calluses, adult onset demodicosis, and cutaneous neoplasia. Sebaceous
gland tumors “senile warts” account for up to 35% of all canine skin tumors but are
rare in cats. They can be single but are usually multiple and occasionally ulcerate.
Rarely they do they become malignant. Clinical management options include surgical
excision, crysotherapy, electro surgery, laser surgery and topical chemotherapy agents
including 5 FU.
Infectious Diseases
Because of decreases in cellular immunity, except for fleas and ticks, infectious
diseases of the skin continue to be the most common skin disease of older pets.
Recurrent bacterial folliculitis, pyoderma, or otitis externa can be problematic in the
older pet. The use of antiseptic shampoos, antiseptic rinses, and long term / low dose
antibacterial therapy is often required to manage the problem. In older patients,
Demodicosis is not usually considered in the differential diagnosis of a skin problem,
but adult-onset demodex does occur and is often missed because of omitting a skin
scraping in the work up. Remember demodex is a great imposer and can look like a
pyoderma, an allergy, a dermatophytes infection, and even an auto-immune skin
disease. The decreased cell mediated immunity may also suppress the usual
inflammatory changes. With generalize adult-onset demodicosis cases, some
underlying immunosuppressive systemic disease such as hyperadrenalcorticism,
hypothyroidism, renal failure, diabetes mellitus, or neoplasia should be ruled out.
Adverse Skin Reactions to Food
Food allergy and food hypersensitivity are terms used to describe the immunological
mediated disease reaction induced by food ingestion. Conversely food intolerance is
the term used for an abnormal physiological response of foods or food additives that
does not have an immunological basis. In a clinical setting, food hypersensitivity and
food intolerance are rarely differentiated and refer to a non-seasonal pruritis skin
disorder associated with ingestion of a substance usually found in the diet.
Numerous dietary allergens exist including beef, pork, chicken, cows’ milk, horsemeat,
chicken egg, wheat, oats, fish, corn, and soy protein. Although any dietary protein is
capable of causing pruritis, beef, dairy products, wheat and soy proteins are the most
common cause of adverse cutaneous reactions. Dogs and cats can react to one or more
dietary allergens.
Non-seasonal pruritis is the most common clinical sign in dogs with food-related
dermatitis. In dogs the age of onset of food-related dermatitis is variable. Food-related
dermatitis should be considered a differential for pruritis in any age of dog and
especially senior dogs with no previous “allergic” history. Unfortunately, the onset of
food-related dermatitis is not usually associated with a recent change in diet. In one
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study 68% of dogs had been fed the offending diet for at least two years before onset
of clinical signs. Dogs with food-related dermatitis generally will not respond as well
to conventional anti-inflammatory doses of glucocorticoids, antihistamine therapy, or
essential fatty acid supplements as dogs with other allergic diseases. Therefore the lack
of response to these medications in a dog with mild to moderate pruritis would make
Atopic dermatitis less likely than food-related dermatitis.
The primary lesion of food-related hypersensitivities is erythema. A papular eruption,
urticaria, and angioedema have also been reported but are rare. The secondary lesions
associated with pruritis include alopecia, excoriations, hyperpigmentation, and
lichenification. The distribution is usually similar to that seen in Atopic dogs with
facial, ears (pinnas and external ear canals), feet, axilla, and ventral involvement. Some
patients with food related dermatitis will present with clinical tail head lesions which
are identical to those associated with flea allergy dermatitis.
In cats, food-related dermatitis is a major cause of pruritis and self-mutilation in young
to middle age cats. As in dogs, non-seasonal pruritis is the most common clinical sign
in cats. The pruritis tends to be localized to the head and neck. Only half of the cases
are considered “steroid responsive”. The often intense pruritis and self-trauma results in
erythema, alopecia, erosions, ulcerations, and crusty lesions. GI signs are present in 1030% of confirmed cases. Some of the cases of feline milliary dermatitis, esosinophilic
granuloma complex, and a symmetrical alopecia caused by excessive grooming, have
also been associated with food hypersensitivity.
In dogs and cats the histopathology is consistent with a non-specific hypersensitivity
plus often demonstrates the pathology of a secondary pyoderma or Malassesia
infection. Since intraderamal skin testing and serologic testing are considered
marginally diagnostic, the best way to confirm a diagnosis of food-related dermatitis is
evaluating the clinical response to a single novel protein test diet or a diet containing
protein hydrolysates, then a subsequent challenge with the patient’s original diet. A
single novel protein ingredient dietary trial involves feeding a diet that contains a
single protein and a single carbohydrate source based on the dietary history that has not
been previously fed to the patient. The single protein limited ingredient diet should be
fed for at least six to eight weeks before a decision is made regarding efficacy. If no
response is seen in 6 to 8 weeks, then it is unlikely that food is playing a major role in
the patient’s dermatitis and the diet is discontinued. However, if even a partial response
is noted then the diet should be continued for an additional four weeks since some cats
and dogs may take as long as 10 weeks for a maximum beneficial response. A follow
up challenge with the patient’s original diet is always recommended to be sure that the
improvement was not coincidental with other factors. A food allergic dog or cat will
typically break with pruritis and dermatitis within seven days of the challenge.
Dietary trials with protein hydrolysates are gaining favor with many veterinary
dermatologists. This process of protein hydroxylation involves cleavage of protein
peptide bonds into smaller units. The theory is that lower molecular weight “proteins”
will not elicit an immunologically mediated response. Avoidance is the most important
aspect of managing food allergies.
Superficial Necrolytic Dermatitis (SND) / Hepatocutaneous Syndrome (HS)
Superficial necrolytic dermatitis (SND), hepatocutaneous syndrome (HS), necrolytic
migratory erythema (NME), metabolic epidermal necrosis (MEN), diabetic
dermatopathy are terms used to describe a skin disease with a multifactorial underlying
etiologies. SND is the umbrella term for this condition and the diagnosis usually
attached with the skin histopathology report.
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This syndrome has been associated with diabetes mellitus, glucagon secreting tumors
of the pancreas. However the syndrome is most often seen with a variety of canine and
feline hepatopathies using the term hepatocutaneous syndrome (HS) for those
conditions.
Superficial necrolytic dermatitis is generally seen in middle-aged to older dogs with the
average being 10 years old. The history of skin lesions is weeks to months with a
typical waxing and waning but slowly worsening course. Skin lesions are usually noted
to first affect the feet and or foot pads. The lesions description includes
hyperkeratosis, interdigital erythema, some erosion with crusting and occasionally
intact bulla will be observed. The lesion pattern progresses to a more generalized
pattern include the face, hocks, genitals, interiginous zones, lower abdomen and/or
groin area. With the feet and muco-cutaneous junctions on the face the most common
sites.
Skin lesions may become mildly pruritis and usually painful. Systemic signs of illness
including lethargy, anorexia, and weight loss are reported in less that 20% of the cases.
Laboratory changes in dogs with hepatocutaneous syndrome (HS) include increased
liver enzymes especially serum alkaline phosphatase. Unfortunately many “normal”
older dogs have elevated liver enzymes.
Hepatic ultrasonography is often helpful diagnostically. With the hepatocutaneous
syndrome (HS) form of superficial necrolytic dermatitis the hepatic ultrasound
generally shows a characteristic "Swiss cheese" or “honeycomb” pattern that some feel
is pathognomonic for the syndrome. However in dogs with idiopathic hepatocellular
collapse as the cause for their liver disease, the liver has a nodular appearance with
variable sized hypoechoic regions of regeneration surrounded by an echogenic borders.
There is a lack of fibrosis and reduced liver size which is seen in cirrhosis. In cases
involving the glucagon secreting tumors of the pancreas, the ultrasound findings are
less consistent. The pancreas and liver maybe normal or a mass may be identified in
one or both organs. If a glucagonoma is suspected and ultrasonography is normal, a
glucagon assay should be performed. Plasma glucagon levels are characteristically 5-10
times above the normal range.
The differential diagnosis for the cutaneous lesions is extensive however they typically
have an immune mediated disease “look” and distribution pattern. However the rule
outs for the hyperkeratotic lesions on the feet and face would also include zinc
responsive dermatosis and generic dog food dermatosis.
Initial diagnostics tests should include skin surface cytology, cytology of vesicular
fluid if present. A complete blood count, a biochemical profile are indicated. Multiple
skin biopsies from several affected areas are essential. With H&E staining, the
epidermal parakeratotic hyperkeratosis is red, the epidermal edema as white and
hyperplasic basal laver is blue. This characteristic “red, white & blue” histopathologic
change is pathognomonic for superficial necrolytic dermatitis. However in older
lesions, this typical pattern may not be present, which may result in misdiagnosis or
failure to diagnose the condition.
Numerous treatments have been used in dogs with hepatocutaneous syndrome. A 10%
crystalline amino acid solution (Aminosyn, Abbott Labs) may be administered
intravenously at either 25 ml/g body weight or 500 mls total volume per dog slowly
over six to eight hours every 7 -10 days. The response has been variable. If minimal to
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no response is noted, the infusions are repeated every 7-10 days for four treatments. If
an individual dog does not respond by this time, they will generally not respond. For
those that respond, the amino acid infusion is repeated with each exacerbation of the
skin lesions. Dogs may go several months between amino acid infusions, but some
dogs will require monthly infusions to maintain remission. As the disease progresses,
the need for amino acid infusions will likely increase. This solution is hypertonic and
must be administered via a central vein such as the jugular vein to reduce the chance of
thrombophlebitis.
An oral amino acid supplementation (Promod, Ross Laboratories) has been noted to be
of some benefit, perhaps because of the specific amino acid profile provided. Another
choice for specific amino acids is a daily supplement of 3-6 egg yolks. The use of
human body builder protein supplements has been advocated by some authors. Oral
nutritional support with a high-quality protein diet such as Hill’s Prescription Diet a/d
or Eukanuba Recovery Formula is recommended if the dog is eating or via an enteral
route. Some dogs may benefit from daily supplementation with three to six egg yolks.
Zinc supplements (2 mg/kg daily of zinc methionine) and essential fatty acid
supplementation (high in omega 3 fatty acids) should also be used.
Temporary improvement of skin lesions and hyperkeratotic footpads may be seen with
topical and systemic glucocorticoids (prednisone starting at 1 mg/kg daily). However,
effects are usually transient and will eventually become refractory to these therapeutic
dosages plus steroids complicate the hyperglycemia.
The prognosis with Superficial Necrolytic Dermatitis is grave. The mean survival time
in one study was 1.6 months. The prognosis for dogs with idiopathic hepatocellular
collapse is generally poor. However, there have been reported cases which have been
medically managed for two to three years after diagnosis of the disease.
Common Endocrine Problems in Older Pets
Endocrine problems are common in the older pet. Unfortunately endocrinopathies are
both under-diagnosed and over-diagnosed in geriatric patients in part because the
effects of the excess or deficiency in circulating hormone(s) affects multiple body
systems. In addition the symptoms of hypothyroidism and naturally occurring
hyperadrenalcoritiscm usually have an insidious onset in older pets plus the fact that
the early symptoms can easily be attributed to “old age” by the owner who elects not to
seek veterinary care. Ad to this the confusion associated with testing. The lack of
testing specificity and lack of endocrinologists consensus on the which testing method
is the most appropriate to diagnose either hypothyroidism or hyperadrenalcoritiscm
compounds the diagnostic dilemma for the veterinary practitioner.
Canine Hyperadrenocorticism
Canine hyperadrenocorticism is an endocrine disease resulting in high circulating levels
of cortisol and is one of the more common endocrine diseases in older dogs however
the incidence is very rare in cats. Unfortunately some of the early symptoms associated
with Cushing’s especially with the insidious onset can appear like “normal” aging
changes in the older pet. There are three main etiologies of hyperadrenocorticism; 1.
Pituitary, 2. Adrenal, and 3. Iatrogenic. Pituitary hyperadrenocorticism (PDH) is
responsible for 85-90% of naturally occurring cases of hyperadrenocorticism in
canines. The pathogenesis usually involves a benign pituitary tumor that produces
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excessive ACTH that induces bilateral adrenal cortical hyperplasia and the production
of high circulating levels of cortisol. Adrenal hyperadrenocorticism (AT) is implicated
in only 10-15% of naturally occurring cases of canine hyperadrenocorticism. In this
form of hyperadrenocorticism, an adrenal tumor (~50% malignant) is responsible for
secreting high levels of cortisol. Iatrogenic hyperadrenocorticism occurs as a
consequence of the excessive and/or prolonged administration of exogenous steroids
(oral , topical or parenteral injections). Regardless of the pathogenic mechanism
responsible, the clinical symptoms are the result of the deleterious effects of the
elevated circulating endogenous or exogenous steroids on multiple organ systems.
PDH and AT induced hyperadrenocorticism usually occurs in the middle-aged to older
patients. There is no sex-predilection with PDH, however females are more prone to
AT. Although it has been reported in most breeds, Poodle, dachshund, Boston terrier,
boxer, and beagle are the most predisposed. As the condition is progressive, the clinical
picture can vary considerable with the levels of cortisol produced and course of
progression. Common findings include; PUPD, polyphagia, muscle weakness, muscle
atrophy, pendulous abdomen, hepatomegaly, lethargy, obesity, and panting. The skin
changes include thin skin, alopecia, hyperpigmentation, and occasionally calcinosis
cutis..
The common hematological findings are polycythemia (elevated hematocrit), and the
“stress leukogram findings (lymphopenia, neutrophilia, and eosinopenia). Common
laboratory findings include alkaline phosphatase (ALP) elevations in 80-95% of
Cushing’s patients, ALT elevations, hypercholesterolemia, and mild hyperglycemia.
On a complete urinalysis the urine specific gravity with be dilute (usually < 1.015) and
it is not uncommon for there to be evidence of a lower urinary tract infection. The
serum total T4 to be usually low from non-thyroidal illness.
Even the experts can not agree on which of the various diagnostic tests the most
accurate method to diagnose hyperadrenocorticism.
Urine Cortisol/Creatinine Ratio Test: The urine cortisol /creatinine ratio is considered
a screening test and thus cannot diagnose Cushing's, however and negative test can rule
it out. High cortisol in urine is suggestive of high serum cortisol. The urine cortisol
creatinine ratio appears to be a very sensitive test therefore any positive test must be
confirmed with either an ACTH stimulation, low dose dexamethasone suppression test
(LDDS), or plasma endogenous ACTH assay.
ACTH Stimulation Test: A dog with hyperadrenocorticism has overproducing set of
adrenals, the cortisol reserves are much greater, and the dog will be able to respond to
the ACTH with greatly elevated cortisol output. This test doesn't differentiate between
PDH and AT but is considered diagnostic 80-95% of the time. Half of adrenal tumors
will not respond on this test, and 15% of dogs with pituitary tumors will not respond.
Low Dose Dexamethasone Suppression Test (LDDS) : This is considered the best test
with an estimated 90-95% ability to diagnose hyperadrenocorticism disease. Blood
samples are taken 4 hours and 8 hours post. Cushingoid dogs will not suppress blood
cortisol in response to the dexamethasone injection, because their feedback
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mechanisms are not working properly. This test does not differentiate between PDH
and AT although it may be suggestive. Those dogs that suppress at 4 hours and then
rebound at 8 hours usually have pituitary tumors.
High Dose Dexamethasone Suppression Test (HDDS): Once a dog has been diagnosed
as having hyperadrenocorticism, this test can be used to differentiate between PDH and
AT. A dog with an adrenal tumor will not suppress at all. A dog with a pituitary tumor
(PDH) still has some limited ability to respond to feedback and thus should respond to
a high dose of dexamethasone with a suppressed cortisol level. Approximately 15%20% of dogs with pituitary tumors will not suppress on a HDDS; these dogs generally
have large macroadenomas.
Adrenal Imaging
In addition the adrenals can also be evaluated via adrenal ultrasonography (tumor or
mineralization).
While surgery can be beneficial and curative in some cases, medical management is the
most common approach.
Mitotane (Lysodren) is used to manage both PDH and AT. For PDH a loading dose of
40 – 50 mg/kg/day until both the pre & post ACTH stimulation cortisol levels are
normal, then 50mg.kg/week divided. (Maintain the p[re & post ACTH levels between 1
– 5ug/dl.
Side effects include lethargy, weakness, anorexia, vomiting , diarrhea, ataxia, and
iatrogenic hypoadrenalcortiscm. Most authors also recommend additional prednisone
(0.2 mg/kg/day) to prevent an Addisonian crisis.
Selegilline (L-deprenyl) at 1-2mg/kg/day has bee approved for use in dogs to control
many of the symptoms associated with PDH hyperadrenalcoritiscm. The proposed
mechanism of action of L-deprenyl is to decrease the ACTH pituitary secretions by
incr3easing the Dopaminergic tone to the hypothalamic-pituitary axis thus decreasing
the cortisol secretions by the adrenals.
Vetoryl (Modrenal, Trilostane) is a new British drug used to manage Cushing's disease.
The drug works by interfering with cortisol synthesis to prevent excess cortisol
production. Trilostane is an orally administered competitive inhibitor of 3ßhydroxysteroid-dehydrogenase. This enzyme system mediates the conversion of
pregnenolone to progesterone in the adrenal gland. Cortisol, aldosterone and
androstenedione are produced from progesterone via various biochemical pathways.
Trilostane inhibits the production of progesterone and therefore the synthesis of its end
products. It is not licensed in the United States at this time, but it can be obtained if one
gets an FDA waiver. There seem to be many favorable reports of its effectiveness and
safety. It is more expensive the Mitotane, but may be an alternative treatment for dogs
with adrenal tumors. As with Lysodren, the dog is reexamined repeatedly during the
initial phase of treatment, and ACTH stimulation tests are performed. In many cases,
after several months of therapy the dose needs to be increased.
Untreated cases have a poor prognosis and are euthanitized because of complications.
However cases of PDH treated with Mitotane have a much better outcome with the
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average survival time of 2 years post diagnosis with 10% of cases living 4 years or
longer (U of Penn. 2003)
Canine Hypothyroidism
Hypothyroism is the most commonly diagnosed endocrine disease in the geriatric
patients. This disorder can manifest in many different ways because of the multisystemic effects of the thyroid hormones on various body systems. Unfortunately the
condition is both over and under diagnosed. An accurate diagnosis of this disease is
based on a combination of clinical signs, diagnostic blood tests, and the response to
therapy. It is a disease characterized by low levels of circulating thyroid hormones
resulting in decreased cell metabolism in most tissues in the body. In dogs there are
two categories of hyperthyroidism based on the location along the hypothalamicpituitary-thyroid gland axis responsible for decreased thyroid hormone circulation.
Primary hypothyroidism (>95% of cases) is caused by thyroid destruction resulting in
thyroid dysfunction. In general, dogs with primary hypothyroidism will have
pathologic changes to the thyroid gland and be non-responsive to stimulation by TSH
and TRH. Secondary hypothyroidism is rare in dogs and is caused by decreased TSH
secretion by the pituitary gland. Dogs with secondary hypothyroidism have atrophied
thyroid glands but are responsive to TSH and TRH administration.
The most common etiologies of primary hypothyroidism in geriatric dogs are
lymphocytic thyroiditis and idiopathic thyroid atrophy. Both of these conditions result
in destruction of normal thyroid tissue and decreased circulation of thyroid hormones.
Lymphocytic thyroiditis is an immune mediated slowly progressive disease
characterized by infiltration of the thyroid gland by lymphocytes, plasma cells, and
macrophages. The auto antibodies to thyroid antigens, such as thyroglobulin, T4, T3,
and others result in the symptoms. This condition is believed to have a genetic link
plus recent evidence exists that repeated vaccination increases thyroglobulin antibodies.
Idiopathic thyroid atrophy is characterized by loss of normal thyroid tissue and
replacement with adipose tissue. Idiopathic thyroid atrophy is a diagnosis of exclusion
as there are no blood tests available to diagnose this condition.
It is reported that hypothyroidism is more common in Doberman Pinschers, Golden
Retrievers, Labrador Retrievers, Cocker Spaniels, German Shepards, Dachshunds,
Poodles, Rottweilers, Spaniels, Terriers, Boxers, and mixed breeds.
Owners of hypothyroid dogs many not be aware of the changes occurring in their dog
because of the slow progression of the disease and unfortunately the signs may be
erroneously attributing the changes to normal aging. Common histories include mental
dullness, lethargy, weakness, unwillingness to exercise, , “heat seeking” (cold
intolerance), and weight gain.
Abnormal physical findings include bilaterally symmetrical non-pruritic truncal
alopecia, dry and scaly coat, a “rat tail”, lichenification, hyperpigmentation,
myxedema, Malassezia dermatitis, recurrent pyoderma, otitis externa, and seborrhea.
Pruritis in hypothyroid dogs with dermatologic signs is often indicative of secondary
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bacterial or yeast infection. Neuromuscular signs associated with hypothyroidism can
include facial nerve paralysis, weakness, knuckling or dragging feet, vestibular signs,
seizures, ataxia, and circling. Cardiovascular abnormalities related to hypothyroidism
include bradycardia, arrhythmias, decreased myocardial contractility, and decreased
stroke volume.
The diagnosis of hypothyroidism is complex, and is often based on physical exam
findings, laboratory tests, and occasionally response to treatment. Diagnostic tests for
dogs suspected of being hypothyroid include CBC, biochemical panel, UA, and T4 (free
and total) and TSH levels.
If the serum total T4 or fT4 (T4 levels measured by equilibrium dialysis are highly
sensitive and specific) levels are well within the normal range, it indicates that the
animal is not hypothyroid. If one or both of these values are in the low normal or
below normal ranges the animal may be hypothyroid, but often further evaluation is
needed to eliminate the euthyroid sick syndrome. Unfortunately many diseases can
suppress circulating thyroid hormone levels through suppression of the hypothalamus
or pituitary resulting in depressed TSH secretion, decreased synthesis of T4, decreased
concentration or binding ability of circulating proteins, and inhibition of conversion to
T4 to T3. This condition is euthyroid sick syndrome. Serum TSH levels can be
normal or increased with euthyroid sick syndrome. Common drugs that can decrease T4
or T3 include diazepam, glucocorticoids, furosemide, penicillin, anticonvulsants, and
nonsteroidal anti-inflammatory drugs
The decision to treat a dog for hypothyroidism should be made based on the historical
information, physical examination findings, and laboratory data including T4 level.
This decision is less complicated when all results are compatible with a diagnosis of
hypothyroidism. However as is often the case that multiple test results are not
conclusive, a clinical trial response to thyroid supplementation should be evaluated. If
the animal responds and clinical signs improve it can be concluded that the animal had
hypothyroidism or at least thyroid responsive disease.
Thyroid replacement therapy is used to treat hypothyroidism animals with confirmed
hypothyroidism and as trial therapy in those animals suspected of being hypothyroid
with discordant diagnostic results. Oral synthetic levothyroxine (l-thyroxine) 0.02
mg/kg every 12 hours (a maximum dose of 0.8 mg.) is the initial dosage for the 6-8
weeks trial period before re-evaluation of the therapy. Although clinical signs resolve
at different rates, all are reversible. When signs of thyrotoxicosis (panting, nervousness,
aggression, PU/PD, polyphagia, and /overweight loss) are observed, a decrease in
either the dosage or daily administration schedule should be considered. Following the
6-8 weeks trial, serum T4 levels should be evaluated 4-6 hours after administration of
L-thyroxine when twice daily dosing is used, or just before administration and 4-6
hours after administration if once daily dosing is used.
The synthetic liothyronine (T3) therapy dosage is 4–6 µg/kg every 8 hours, and should
be considered in those patients with hypothyroidism when the appropriate therapeutic
L-thyroxine treatment has failed to improve the clinical signs. The most common
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reason for L-thyroxine failure is decreased intestinal absorption. Therapeutic
monitoring of serum T3 levels should be performed just before and 2-4 hours after
administration. T3 values should be in the normal range when the dog is receiving
appropriate treatment.
REFERENCES
1) Bruyette, D., Management of canine hyperadrenalcorticism with l-deprenyl. Vet
Clin North Am, 1997, ;27: 273-286.
2) Daminet S, Ferguson D. Influence of Drugs on Thyroid Function in Dogs. J Vet
Intern Med 2003;17[4]:463-472.
3) Feldman E, Nelson R. Canine and Feline Endocrinology and Reproduction, 3rd
edition. St. Louis: Saunders; 2004. p.155-6.
4) 25) Gaughan K, Bruyette D. Thyroid function testing in greyhounds. AJVR
2001;62(7):1130-1133.
5) Graham P, Nachreiner R, Refsal K, Provencher-Bolliger A. Lymphocytic thyroiditis.
Vet Clin North Am 2001;31(5):915-933.
IMPLEMENTING A SENIOR CARE PROGRAM:
A PRO-ACTIVE APPROACH TO SENIOR WELLNESS
A Senior Care Program provides a proactive comprehensive health care platform that
addresses the older patient’s special needs in a marketable package. This specialized
medical service is based on two premises; first there are fundamental differences in the
specific diseases, behavior problems, and the nutritional needs of the older pet;
secondly that prevention, early detection, and timely intervention of medical problems
can have a significant impact on the longevity and quality of life of an older pet.
Recently the AAHA came out with Senior Care guidelines. A copy can be found on
their website; aahanet.org
Senior Care changes the way veterinarians traditionally approach the senior pet. Senior
Care is a more inclusive health care program starting at seven years of age and
advocating twice-yearly evaluations. However, the major benefit of Senior Care is the
Industry support form companies like IDEXX, IAMS and recently Fort Dodge. IDEXX
‘s continued commitment to the program provides your practice with age related in
house and referral laboratory diagnostics plus all the marketing and implementation
tools necessary to make Senior Care successful in your practice. Tools for client
education, health data gathering and health reporting tools, patient diagnostic and
management charts plus program implementation tips are currently available.
Why build a Senior Care program in your practice? By advocating more
comprehensive histories, performing more complete physical examinations, and
recommending more diagnostic testing of older pets, you are providing higher quality
veterinary medicine for your senior patients. A great deal of professional satisfaction
for you and your staff comes from helping those long established senior patients live
longer healthier lives. Plus managing most age related disease in the early phases is far
more rewarding than the “end stage”. Senior Care can be a major profit center for your
practice. With over 39% of the pet population considered seniors, tremendous financial
opportunities exist.
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While the veterinary profession has been very successful at providing comprehensive
health care programs for the puppies and kittens, there are almost 2 1/4 times as many
senior pets as puppies and kittens and dogs are puppies for one year but are seniors for
four to ten years. By taking a more detailed history on the senior pet, performing a
more complete physical examinations, and submitting more diagnostic tests, not only
are you increasing the standard of care you provide your senior patients, but
approximately 40% of those patients will now require additional diagnostic testing,
medication or therapy. Ultimately a properly implemented Senior Care program can
represent 35% or more of your gross annual income.
A Senior Care program implies both a preventative and comprehensive therapeutic
approaches to management of acute and chronic conditions in aging dogs and cats. The
program emphasizes client education, prevention, early detection, and timely medical
intervention.
FOUR ESSENTIAL COMPONENTS of any Senior Care program should include; 1. A
comprehensive patient health assessment (discovery) 2. A formal 3. A review period
where all the findings are communicated to the owner and 4. A formulating specific
short & long term action plans A scheduled follow-up
I. HEALTH ASSESSMENT:
When implementing a Senior Care program, a critical decision each practice must
make is establishing the boundaries of the recommended health assessment. Exactly
how detailed the history should be? Which diagnostic tests should be included in the
health assessment? The ultimate programmatic decision is based on several interrelated
factors including patient age, presence or absence of disease, current medications, and
client resources. Most hospitals use a basic screening strategy however others employ a
more extensive comprehensive health evaluation approach.
Historical health assessment utilizing a medical, behavioral and dietary history is the
starting point of any program. Utilizing a waiting room questionnaire greatly expedites
time, ensures completeness plus can be a very useful in educating the client on the
warning signs of disease or behavioral problems. Pet owners can be invaluable sources
of information on the overall health of their pets. Observant owners can detect subtle
changes in their pet’s activity levels, alterations in elimination patterns, and behavior.
Often this critical information is unapparent to the veterinarian in an examination room
setting. Owner’s medication and monitoring skills are paramount for success in
managing certain chronic diseases. Therefore, our goal must be convince each owner to
become a much more active partner in the health care of their aging pet.
A complete age related physical examination is the second part of the health
assessment. In addition to a regular physical, the exam should also include a weight
assessment, gentle palpation of each joint and digital rectal examination. Extra time
should be taken for diligent palpation of the mammary glands, skin and subcutaneous
for any tumors. Each tumor identified should be accurately measured, mapped and
recorded in the medical record.
A minimum data base laboratory evaluation (MDBLE) should include a CBC,
chemistry profile, complete urinalysis, fecal and thyroid screening. Many Senior Care
programs also incorporate additional diagnostic testing such as a lead II ECG, thoracic
radiographs, abdominal imaging, blood pressure measurement, adrenal function testing,
and ocular pressure determination into the evaluation.
II. REVIEW PERIOD
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A formal review period is the time where all the normal and abnormal findings are
communicated to the owner. In addition to the important verbal communications of any
health concerns, I also suggest you provide a specific written evaluation, a health report
card, of their pet’s health. Sending home any appropriate client education materials
helps reinforce any health issues. To be optimally effective, this step must occur in a
timely fashion and not several days or weeks later.
III. SHORT AND LONG TERM ACTION PLANS
During the review period, you and the client need to formulate specific short and long
term plans of action for each problem identified. Specific recommendations for
medication, diet, exercise, and dental care should be explicitly communicated. Dietary
recommendation should be based on the health needs of the patient and not on cost
alone. Those factors influencing the diet selection includes quality of ingredients,
specific anti-oxidants shown to modify the aging process and a research based
formulation.
IV. FOLLOW-UP
Timely follow-up telephone calls and written reminders are essential components and
critical in the overall the success of any Senior Care Program.
MAKING THE PROGRAM SUCCESSFUL
Obviously any professional rewards are proportional to the success of the program.
While success is never guaranteed, the follow steps may help you reach your program
goals.
1. Convince yourself that a Senior Care Program will become a significant asset to
your practice before you invest the time, energy, training and resources necessary in
developing and maintaining the program. However, because of the commitment
necessary for success and growth, this program is not for every practice and may not
appeal to every client.
2. Convince your staff of the significant health benefits the program offers the senior
pet. Critical to the success or failure of a Senior Care program is the involvement
and buy –in of your staff. In fact, ownership of the program by every staff member
is essential. Staff incentive programs will also help the Senior Care program patient
base grow and maintain the program’s momentum.
3. Create a very specific and detailed program including age of onset, frequency of
visits, scheduling periods, fee structure, educational materials, and marketing
strategies. Decide exactly which tests are to be included in the routine program.
Finally ensure every member of the staff is “program proficient” in detailing the
specifics.
4. Now convince the owners of the significant health benefits the program offers their
aging pet. A percentage of clients will readily accept the program, but the rest will
need repeated convincing. Increased client knowledge usually equates to increased
client acceptance and compliance. Early and persistent owner education is a long
term investment in Senior Care.
5. A well designed market strategy correlates with success. Utilize newsletters,
reminder cards, invoices, yellow pages, and the media to educate your clients and
prospective clients on age-related problems. Many practices participate in various
Senior Month activities. Some practices celebrate a particular older pet as the Senior
of the Month. The pet’s picture and life story are placed on the waiting room bulletin
board. Client marketing efforts should emphasize all the State of the Art advances in
veterinary medicine including newer diagnostic testing, improved anesthetics and
anesthetic monitoring equipment, behavioral drugs, newer arthritis therapy options,
leading edge cancer chemotherapy, more effective cardiac medications, dental care
and nutritional advancements.
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6. Bundle the fee structure including a senior citizen discount. Charge one fee for both
visits or discount other preventative health care services/products
7. Start slow be patient and the program will grow. A Senior Care Program is a longterm hospital investment and actually begins when outlining a life long preventative
health care program to new puppy or kitten owner.
8. Periodic program review by your clients and staff is essential in maintaining the
consistent high standard of care you have established for your senior patients.
The goal of Senior Care Program should be to optimize the quality of life for the older
pet, using preventative health care combined with State of the art diagnostics and
therapies. Historically, veterinarians have only reacted to diseases / problems in the
elderly animals. Implementing Senior Care Program is a pro-active approach to elderly
health care and not waiting until overt disease is present. The program should
emphasize client education of age related disease, steps for prevention, programs for
early detection, and timely medical intervention using state of the art diagnostic and
treatment modalities.
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