Helping Animals Who Help People: ACVO Eye Exams for Service Animals
As veterinarians, we were drawn to our industry by a love for animals and a desire to help them. That’s why I and our other BluePearl ophthalmologists really enjoy participating in the ACVO National Service Animal Eye Exams during the month of May.
I’m sure most of you are already aware of this terrific event, which provides a valuable service to these remarkable animals. In a nutshell: Throughout the month of May, free eye exams are offered to eligible service animals including detection dogs, guide dogs, handicapped assistance dogs, police dogs, search and rescue dogs and therapy animals. In February, this wonderful program won the VMX Veterinary Innovation Council’s award, which recognizes people and organizations dedicated to innovation for the betterment of the animal health industry.
Registration is easy – owners or handlers simply have to fill out the appropriate forms at ACVOeyeexams.org between April 1 and April 30. ACVO will coordinate the exams at a hospital with a participating ophthalmologist.
To qualify, animals must be “active working animals” that were certified by a formal training program or organization or are currently enrolled in a formal training program.
We’ve treated some wonderful animals over the years (2018 marks the 11th time ACVO has held the annual event). From mobility dogs who open doors and pick up things for disabled owners, to therapy dogs who provide a soothing presence for children learning to read – each is special in his or her own way.
These animals provide essential services, so it’s easy to see why we should do everything we can to ensure they can do their jobs safely and properly. It’s also wonderful as veterinarians to give back to the community.
That’s why we’re asking for your help: join us in spreading the word about the exams. Be sure to mention it to your clients, and ask them to tell their friends or other members of their organizations. Together, we can provide a brighter – and healthier – future for these special patients.
DVM, MS, DACVO
Feline Osteoarthritis: A Comprehensive Review
Kendra Rushing, DVM
Dr. Rushing is one of our specialty interns. After completing her rotating internship, she joined SVS in Seattle as a surgery intern in anticipation of going into a follow-on residency. We’d like to thank her for putting together this comprehensive review of feline osteoarthritis.
Feline osteoarthritis (OA) is a common finding in patients, yet it remains underdiagnosed and undertreated. Studies have shown that almost 25% of cats are affected by osteoarthritis. In cats over 6 years, more than half have arthritis. Over the age of 12 years, that percentage increases to 90%. Considering that many of our feline patients are living well beyond 15 or even 20 years of age, it is important to be on the lookout for the impact of OA during examinations of cats.
Signs of OA in cats can be quite variable and often are unnoticed or attributed to concurrent conditions. Limping or lameness, as is most often appreciated in canine patients, is an uncommon finding in feline OA. Rather, behavioral changes are much more common symptoms of OA. These can include reluctance to jump or modifications of jumping habits, inactivity and increased sleeping, inappropriate litterbox habits, weight gain and other behavioral changes relating to aggression, interactivity and personality. The client interview becomes especially important in the care of middle-aged and older cats, as the signs of OA may not be apparent in hospital.
Appreciation of pain in cats has long been a challenge for both owners and clinicians. In cases of possible or probable OA, owners can be provided with a pain index (such as the Feline Musculoskeletal Pain Index) to aid in cataloguing behavioral changes that correlate to pain in cats.
Diagnosis of OA is often based on history and physical exam. Radiographs may contribute to the clinical picture in a given patient, but often don’t correlate closely with clinical signs. A cat with severe clinical signs of OA may have only mild to moderate changes on radiographs, while severe radiographic changes can be seen in cats with only mild clinical signs. The shoulders, elbows, coxofemoral joints and tarsi are described as the most common locations of feline OA, although any joint is susceptible.
The cause of OA is generally considered to be either 1) abnormal forces on a normal joint or 2) normal forces on an abnormal joint. Abnormal forces can occur secondary to things such as uneven load bearing, trauma and abnormalities in adjacent joints. A variety of conditions can lead to abnormal joints, including osteochondrosis dissecans, hip and elbow dysplasia, articular fractures and other causes of incongruity. Obesity is known to contribute to the progression of osteoarthritis, but its exact role in cats has not been well characterized.
Treatment of OA in cats should take a multi-modal approach. Considerations can include pharmaceuticals, nutraceuticals and adjunctive therapies, physical rehabilitation, surgery and weight loss.
Common pharmaceuticals of choice are gabapentin, buprenorphine and NSAIDs. Gabapentin is often a first-line treatment as there are few side effects, long-term administration is well-tolerated, and it can address aspects of both chronic and neuropathic pain associated with OA. Buprenorphine is effective and easy to administer, but can be expensive for long-term administration, and there is variable absorption with buccal administration. NSAIDs such as robenicoxib and meloxicam require consistent administration, but they are effective long-term – which has not been approved in the US. Long-term use is common in the UK, and studies have shown safety of long-term administration in both normal cats and cats with chronic kidney disease.
Nutraceuticals, most commonly including omega-3 fatty acids, glucosamine and chondroitin, are often employed as a means to slow the progression of OA. There has yet to be a study that shows a significant benefit to nutraceutical administration. Conversely, injectable polysulfated glycosaminoglycan has been shown to effectively reach the joints where it has anti-inflammatory and chondroprotective effects.
Physical rehabilitation (PR) has applications in many areas of veterinary medicine, although it is often only considered in the post-surgical setting and almost exclusively for canine patients. Osteoarthritis is an excellent target for rehabilitation. Cats can be willing participants and get benefit from the practice as well. Hydrotherapy is the most well-known aspect of PR and indeed is an excellent modality for the OA. There are additional modalities that can be employed both at home and with a rehabilitationist. These can include cat towers, obstacle courses, interactive play, and “hunting” for meals; and manual therapy, laser, and ultrasound, respectively. Benefits of PR include encouraging mobility – which has been shown in humans to decrease the discomfort associated with PT, maintaining strength and function, and weight loss.
Surgery may be indicated in some patients with predisposing conditions affecting the joints. These conditions may include previous trauma, acquired or congenital incongruity, OCD and CCL injury. Although treatment of the underlying condition will not reverse the OA already present, it can remove the inflammatory stimulus and thereby slow the progression of OA.
Weight loss should be an important part of the management protocol for any feline patient with OA. Reduction of weight decreases the stress placed on arthritic joints. Additionally, studies in humans have suggested that obesity is associated with increased inflammatory mediators which contribute to the development of OA. Weight loss plans are generally two-fold, with a focus on food (prescription weight-loss diets, measured meals, counting calories) and on calories burned (increasing activity at home, physical rehabilitation.)
Monitoring for response to therapy can be difficult in cats, as in-hospital examinations are often unrewarding. Practically speaking, client surveys (Feline Musculoskeletal Pain Index, client specific outcome measures, quality of life and temperament scores) are often the most informative tool. Follow-up physical exams, charting weight loss and repeat radiographs are additional monitoring tools.
Enlisting clients to participate in diagnosis and rehabilitation of OA can help forge a lasting veterinary-client-patient relationship. Although osteoarthritis in cats is often overlooked or attributed to “slowing down” with old age, marked improvements in quality of life and functionality can be obtained with deliberate, multimodal treatment. We often tell our clients that “age is not a disease” and a proactive approach to OA management is an excellent opportunity to prove that.
Obesity and Osteoarthritis in Canines
The incidence of obesity is continuing to trend upwards, with the most recent AAHA weight management guidelines for dogs reporting that as many as 59% of our canine patients are obese. Obesity is defined as excess body fat capable of causing or exacerbating disease. When a body condition scale of 1-9 is used, each uptick in score beyond ideal is equivalent to 10-15% excess body weight.
Osteoarthritis (OA) affects at least 20% of dogs over one year of age. It can be very difficult to discuss weight management with owners; however, it is one of the most effective (and safe) treatments for OA in dogs. The take-home message for the owners of any obese dog with OA is that dogs are expected to live longer and more comfortably if they are a healthy weight. Labrador retrievers kept at a lean body weight (BCS 4-5/9) lived, on average, two years longer than their overweight littermates (BCS 6-7/9). In addition, continual pharmacologic treatment for OA is necessary in obese animals three years earlier than in those kept at a healthy weight.
Weight loss may be a daunting process for many owners. Start with small, achievable goals. Positive reinforcement is key – encourage the owners to stop by for a weight check on the clinic scale every 2-4 weeks, and make adjustments as necessary. It has been experimentally demonstrated that as little as 6% weight loss in obese animals can increase weight bearing and quality of life in dogs with osteoarthritis. Encourage moderate, controlled exercise. Gradually increasing distance of leash-walks, especially during the cooler times of day (dawn and dusk) will help maintain joint comfort and muscle mass and facilitate shedding the pounds. As the weather gets warmer, swimming is also a fantastic means of exercise. Encourage owners to get into the water up to their knees to prevent their pets from running into and out of the water. Finally, professional physical therapy in conjunction with weight loss has shown more benefit than weight loss alone.
The first step to achieving weight loss is to determine exactly what is being fed. Encourage the owners to keep a journal of everything that is offered over a week’s time. Remember to keep it simple. Owners are less likely to be compliant if a “crash diet” is recommended. In addition, dogs that lose weight gradually are more likely to keep the weight off than those that quickly drop weight.
Calculate the patient’s energy requirement, and ensure that the owners are weighing the food at mealtime or using an eight-ounce measuring cup for precision and repeatability. Encourage low-calorie treats or breaking treats into multiple small pieces. Fruits and vegetables make excellent low calorie snacks (no grapes or raisins). It is important to remember that the nutrient composition of any food is calculated to provide balanced nutrition of all essential nutrients when fed based on caloric density. Therefore, if appropriate weight loss is not achievable on the diet the patient currently eats, it is recommended to switch to a weight control diet rather than substitute large volumes of food with green beans, pumpkin, etc., as deficiencies may result.
Finally, a multimodal approach to OA therapy including use of neutraceuticals, chondroprotectants, specific joint diets, NSAIDs and other analgesics is key in helping these animals be as comfortable as possible while achieving their weight loss. If an owner feels that their pet is exceedingly uncomfortable after exercise, they are unlikely to continue. When sedentary, these animals gain weight, become increasingly lame, and continue on a downward spiral.
Adam R. Lancaster, DVM, DACVECC
BluePearl in Michigan
Common causes of hypoglycemia in dogs and cats include puppy/kitten hypoglycemia, sepsis, xylitol toxicity, liver dysfunction, insulinoma and exogenous insulin overdose. The brain is reliant on a constant stream of blood glucose for its energy needs. When low blood sugar occurs, neuroglycopenia (hypoglycemia of the central nervous system develops). Clinical signs of neuroglycopenia include altered mentation or dullness, sleepiness, weakness, ataxia, blindness or altered vision and seizures. Prolonged neuroglycopenia can lead to permanent brain injury and neurologic signs that persist beyond the resolution of the hypoglycemia. Other clinical signs may include pacing, restlessness, shaking, trembling, vomiting, anorexia, panting, diarrhea or urination.
Regardless of the etiology of the hypoglycemia, emergency medical treatment is similar. Administration of 0.5-1 ml/kg of 50% dextrose (diluted 1:2 to 1:4 should be administered) should be administered to patients with hypoglycemia that present with the above signs. Additional dextrose containing fluids (2.5-5%) should be administered until the underlying cause can be determined and the patient is capable of maintaining euglycemia on their own.
Insulinomas are insulin-secreting tumors of the pancreas. Diagnosis is made by documenting a high insulin level during a period of hypoglycemia. Patients with insulin secreting tumors (such as an insulinoma) require special consideration. While a bolus of dextrose is still indicated for management of life-threatening side effects of hypoglycemia (such as seizures), a rebound hypoglycemia may occur after dextrose supplementation due to increased insulin release. Therefore, routine administration of dextrose boluses in the absence of clinical signs should not be performed. For these patients, administration of anti-insulin medications such as steroids and diazoxide will increase blood sugar without the risk of rebound hypoglycemia. Surgery may ultimately be required to remove the tumor.
Hypoadrenocorticism – Addison’s disease
Hypoadrenocorticism is an uncommon endocrinopathy that commonly affects middle-aged female dogs; although any age, sex or breed may be affected. Classical hypoadrenocorticism results from a mineralocorticoid deficiency leading to severe electrolyte derangements. While an atypical form may also occur from the result of glucocorticoid deficiency only, it is unlikely to present as an emergency.
Patients affected with hypoadrenocorticism often have vague clinical histories and clinical signs may include anorexia, vomiting, diarrhea, weight loss and lethargy. These signs may be intermittent or chronic and mild or severe. Other clinical signs include tremoring, shaking, weakness, PU/PD, bradycardia and hypotension. As mentioned, there is a sex predilection for females, and most dogs are middle-aged (mean age of 4-5 years) at the time of diagnosis. A variety of breed predilections have been reported including the Portugese water dog, great Dane, West Highland white terrier, standard poodle, Wheaton terrier and Rottweiler. However, mixed breed dogs are affected more than any other dog breed. Cats are rarely affected.
Common clinicopathologic abnormalities include lack of a stress leukogram, hypoglycemia, pre-renal azotemia, hyponatremia and hyperkalemia. A sodium/potassium ratio <27 is suggestive and a Na/K ratio less than 23 is highly suggestive of hypoadrenocorticism. An ACTH stimulation test is required for definitive diagnosis, however. Differential diagnoses for a low Na/K ratio include severe whipworm infestation, kidney failure, ascites and chylothorax.Treatment of a hypoadrenocortical crisis involves aggressive fluid resuscitation, correction of hypoglycemia and electrolyte abnormalities, and glucocorticoid and mineralocorticoid supplementation. Fluid resuscitation typically involves the administration of isotonic crystalloids (0.9% saline or balanced buffered solutions may be used). Large volumes of crystalloids may be required to restore perfusion and correct hypotension. Hypoglycemia may be corrected as previously discussed. Electrolyte abnormalities will resolve with administration of crystalloids and mineralocorticoid supplementation. Fluid resuscitation is the single most important treatment in the emergency management of these patients. Once fluid resuscitation has commenced, supplementation of glucocorticoids in the form of dexamethasone SP, hydrocortisone or prednisone may occur. It is important to note that only DexSP should be administered if an ACTH stimulation test is yet to be completed as other glucocorticoids will affect the results. While hydrocortisone is likely the best injectable glucocorticoid for use in this situation, it is not readily available and is expensive. Mineralocorticoid supplementation can occur in the form of DOCP (Percorten®) or fludrocortisone (Florinef®).
Diabetic Ketoacidosis (DKA) and Hyperosmolar Hyperglycemic Syndrome (HHS)
Diabetic ketoacidosis is a disorder characterized by a relative or absolute insulin deficiency. Insulin has many effects on body function with the main effect being to decrease blood glucose. The net effect of insulin is storage of carbohydrate, proteins and fat. It also had numerous effects on electrolytes, enzymes and growth. Various hormones also exist to counter the effects of insulin. These include glucagon, epinephrine, growth hormone and cortisol. These counterregulatory hormones antagonize the effects of insulin and increase blood glucose by increasing glycogenolysis, gluconeogenesis and lipolysis. These hormones are very important in the development of DKA.
The development of DKA occurs from an absolute or relative deficiency of insulin resulting in increased gluconeogenesis, accelerated gylcogenolysis, and impaired glucose use by tissues. Despite increased blood glucose the cells become starved for energy shifting to the use of free fatty acids as an energy source. The progression from an unregulated but compensated diabetic to DKA is due to an increase in counterregulatory hormones. These “stress” hormones are thought to be due to a secondary or coexisting disease process. An increase in these counterregulatory hormones causes a vicious cycle of elevated blood glucose with cellular “starvation,” and eventually DKA or hyperglycemic hyperosmolar syndrome (HHS) ensues. Common co-existing disease processes include pancreatitis, urinary tract infections, hyperadrenocorticism, neoplasia, pneumonia, pyelonephritis and chronic kidney disease. HHS is a form of diabetic crisis marked by severe hyperglycemia (>600 mg/dl), minimal or absent urine ketones, and serum osmolality >350 mOsm/Kg. The development of HHS occurs similarly to DKA but it is believed that small amounts of insulin and hepatic glucagon resistance inhibit lipolysis, thereby preventing ketogenesis.
Diabetes occurs most commonly in middle-aged to older animals, although younger animals may also be affected. There is no sex predilection and dogs and cats can both be affected. Common clinical signs include PU/PD, weight loss (despite a ravenous appetite), weakness and lethargy. When animals become sick with DKA they often will develop anorexia, vomiting or diarrhea. Confirmation of a diabetic crisis can be made with routine bloodwork. Persistent hyperglycemia with glucosuria is indicative of diabetes mellitus. A blood gas and serum or urine ketones should also be performed to confirm ketosis +/- acidosis. Additional diagnostics should be performed to assess for comorbidities and include a CBC, serum chemistry, urinalysis, urine culture, thoracic radiographs and abdominal ultrasound.
The goals of therapy for DKA are to restore intravascular volume, correct electrolyte disturbances, correct dehydration, correct acid-base imbalance, decrease blood glucose, rid the body of detectable ketones and treat any underlying or coexisting disease.
Fluid therapy is the cornerstone of DKA treatment. NaCl 0.9% has traditionally been advocated due to the presence of hyponatremia in many of these patients. This may worsen acidosis, however as 0.9% NaCl is an acidifying fluid. Balanced buffered solutions including LRS, Norm-R or plasmalyte may contribute to the management of acidosis and hypokalemia (also very common). Ultimately, the type of isotonic crystalloid is not as important as remembering to use one. Fluid therapy increases renal perfusion and urine excretion which will decrease blood glucose, ketones, and counter regulatory hormones. It also restores intravascular volume and dehydration deficits. It is important not to initiate insulin therapy until volume and dehydration deficits have been restored as this will worsen hypovolemia and may lead to cardiovascular collapse.
Electrolyte disturbances are very common in diabetic emergencies and most commonly include hyponatremia, hypokalemia, hypophosphatemia or hyperphosphatemia, and hypomagnesemia. Hypokalemia is a common and potentially life threatening electrolyte derangement. Patients with normal blood potassium levels may actually be whole body depleted in potassium, and insulin administration will worsen hypokalemia. As such, potassium supplementation should be administered to all patients with DKA with normal or low potassium levels.
Once hypovolemia, dehydration, and acid-base and electrolyte derangements have been corrected, insulin therapy should be started. Insulin therapy is more important in DKA than it is in HHS as insulin is required for reduction of ketones. Regular insulin should be administered to patients with DKA or HHS. This can be administered either via insulin CRI or intermittent intramuscular administration.
Lilies: Fatal Attraction
Lilies are a common fixture in households across the country this time of year. What many clients don’t know is the risk that these flowers hold for curious household cats. Many members of the lily family are toxic to cats, and ingestion of very small amounts of the plant can lead to toxicity. All parts of the plant, including leaves, stems and flowers are considered to be toxic. Related flowers such as the tiger lily, daylily, and stargazer lily have similar toxicity.
Lily toxicity affects the kidneys, and kidney failure can develop rapidly. The feline kidney appears to be extremely sensitive to this toxin while this effect is not observed in dogs. As the toxicity progresses, the kidneys become less capable of clearing waste products from the body. When these waste products accumulate in the blood, clinical signs of illness become evident.
Symptoms can develop within a few hours but may be delayed as long as a few days after ingesting or chewing on the plant. Clients may observe vomiting, loss of appetite, and depression in their cats. Astute owners may also notice changes in water consumption and litter box habits.
Early recognition and treatment are critical to a successful outcome.
We always recommend immediate emergency care, either with a family veterinarian or BluePearl emergency hospital, for a cat who was seen chewing on or ingesting a lily plant. Lab work may reveal significant elevations in kidney values and alterations to the body’s electrolytes. The cornerstone of treatment is to provide aggressive fluid support through an IV catheter. Other medications may be added to the treatment to prevent stomach upset and stimulate urine production. In severe cases, dialysis may be considered.
If your patient recovers from the acute toxicity, it is likely that there will be some long-term effects in the form of chronic kidney disease. Fortunately, cats are tolerant of low levels of kidney dysfunction and can still have extended, good quality lives. Our BluePearl clinicians are available to answer any questions you might have about lily toxicity.
VSEC BluePearl is strongly committed to the veterinary community. One of the ways we demonstrate this commitment is through our continuing education program, which is subsidized in part by our Partners in Education.
All BluePearl lectures are free and open to all area veterinary professionals. Registration is required, please. To register please visit our website.
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