High-risk neonatal puppies and kittens are those that become severely dehydrated or systemically ill, or are falling behind in weight gain. A variety of factors can contribute to these circumstances, of which husbandry is the most common. Failure of passive immunity and/or infectious disease can also contribute.

Caring for these high-risk neonates requires knowledge of normal newborn parameters. Healthy puppies and kittens should be gathered in a loose pile within their enclosure (

), should have good mucous membrane coloring and should be noted to be “twitching” while asleep; they should not be extremely vocal.

A healthy puppy or kitten will twitch noticeably, almost continuously, while sleeping (

). This can even startle them awake or cause them to readjust their sleeping position. In my experience, evaluating for this twitching has been the most important factor when monitoring neonates. A significant decrease or lack of twitching could signify that the animal is not doing well and requires professional evaluation.

Several other factors should be monitored as well when caring for high-risk neonates, including environment, hydration, nutrition, excrement, weight and immunity.

In the first week of life, puppies and kittens rely solely on their external environment for warmth; they are unable to maintain their own body temperature. Environmental temperatures ranging from 75°F to 80°F will support maintaining an optimal neonatal rectal temperature of 98°F to 99°F. Only when a puppy or kitten is maintained at an appropriate temperature is it able to digest milk and thus ready to be fed.

High-risk neonates are typically solitary individuals; an entire litter of high-risk neonates is rare. Those at high risk prefer to snuggle against something warm. IV fluid bags warmed in the microwave (make sure the bag is neither too hot nor too cold) and covered with a tube sock can provide a nice substitute for littermates. A sock will be more inviting to the neonate and, because they can be changed and laundered easily, socks also help keep the area clean.

A well-hydrated puppy or kitten will have adequate skin turgor and good pigment color. Light-colored animals should have bright pink mucous membranes (

). As for adults, it can be challenging to assess mucous membranes in darkly pigmented neonates. However, there should be areas where assessment is possible, such as the belly.

Any fluids administered to a neonate, regardless of route, should be warmed. For mildly dehydrated newborns, subcutaneous fluid administration is appropriate. Crystalloid fluids should be administered at a dose of 1 ml/30 g. In cases of severe dehydration, an intravenous or intraosseous catheter is greatly preferred. Jugular intravenous catheters may be the easiest to obtain, and the femur is an excellent bone for intraosseous placement using a hypodermic 22- or 20-gauge needle. Both routes can be used to administer fluids, blood products, diluted dextrose and antibiotics. Severely hypovolemic neonates can receive approximately 60 ml/kg of crystalloid fluid total during one resuscitation event. In cases of dehydration, the rehydration process should be more gradual.

Dehydration deficits in neonates are calculated in the same way as for adults: Percent dehydration multiplied by body weight in kg will provide the total fluid deficit in liters.

 The neonate’s maintenance fluid is about 60 to 100 ml/lb/day.

 Colloids can be used in urgent circumstances and are dosed the same as in adults.

Any species-specific milk replacer or goat’s milk can be used to feed neonatal puppies and kittens. Neonates need to be fed every two hours until they are gaining weight steadily and becoming more glossy in appearance. They can be bottle fed only if they are vigorous enough to perform the task adequately. Bottle feeding should not be attempted until the neonate’s Apgar score is between 7 and 10 (

 Neonates with Apgar scores between 4 and 7 should be tube fed via a red rubber catheter (size 8-10 Fr for canine neonates and 5 Fr for neonatal kittens.)

Correct tube length is imperative when tube feeding. The tube should be aligned from the mouth and extended down to the last rib. When placing the tube in the stomach, you will feel resistance as the tube passes the lower esophageal sphincter. Place the animal in sternal recumbency and insert the tube toward the back of the throat on the left side, advancing rather swiftly. A puppy or kitten that is alert enough to be fed will also fight you to some degree during tube placement. Holding the mouth closed and the neck extended while milk is instilled will help keep the tube in place.

It is very common for neonates to grunt and vocalize while being fed. Hearing this is a sign that the tube has been placed correctly. An animal that is too lethargic to swallow the tube and provide some resistance is not quite ready for enteral nutrition. While feeding the neonate, be sure to palpate the area below the lower rib on the left side of the body to ensure you are not overfeeding. A good guideline for feeding volume is approximately 4 to 5 ml/100 g. If the puppy or kitten is showing signs of discomfort during feeding, do not proceed with the entire volume but work up to it incrementally. To prevent residual milk from dripping into the pharynx, risking aspiration, kink the tube before removing it.

Because neonates cannot urinate or defecate without assistance, they should be stimulated both before and after feedings. To stimulate urination, rub the ventral caudal abdomen/inguinal area. Urine should be almost clear in a well-hydrated neonate (urine specific gravity < 1.017). A neonate with darker urine will need a more aggressive fluid therapy plan.

Some neonates may urinate and defecate simultaneously, while others need separate stimulation to produce feces. Do not rub directly on the anus repeatedly to stimulate defecation; this can result in ulceration of the anal tissue and make defecation uncomfortable. Instead, wipe a damp, warm cloth or gauze bilaterally on either the ischium or the pelvis (or both). If ulcerations do occur, use vitamin A & D ointment in between stimulation events.

Neonatal feces should resemble varieties of mustard. It can be bright yellow or darker yellow, with or without “seed” material in it. The seeds are fatty excrement. The feces can be very wet in appearance but should not be completely liquid. The meconium is much darker and gelatinous. At-risk neonates that have not had adequate nutrition may pass meconium much later after birth.

A healthy puppy or kitten will gain about 10% of its body weight daily. High-risk neonates should be weighed twice daily using a gram scale. This will allow minor weight losses and gains to be observed more closely to allow for a necessary intervention sooner rather than later.

Neonates that have failed to nurse on their dam or queen within 18 hours of birth will not have had the opportunity to ingest colostrum. In these cases, plasma or serum can be used as a substitute. If administered within the first 18 to 24 hours of life, the plasma or serum can be given orally to the neonatal puppy. Puppies should receive 0.1 ml/g of adult dog serum.

In kittens, care should be made to ensure the serum blood type matches that of the kitten. Dosing for kittens is 15 ml non-hemolyzed adult serum/100 g of body weight. This serum should be divided into three total injections given every eight hours for the first 24 hours of life.

Newborn puppies and kittens can become compromised quickly, particularly in the first week of life. Their owners may miss early warning signs of compromise, only noticing that something is amiss when the neonate has entered a high-risk state.

Dr. Simermeyer is an emergency practitioner at Mount Laurel Animal Hospital in Mount Laurel, NJ. Her professional interests include emergency and critical care, and canine reproduction. She has been breeding Cardigan Welsh Corgis for the past 23 years.

Thomovsky EJ. How to treat the sick neonate. Presented at the Atlantic Coast Veterinary Conference; 2015.

Veronesi MC, Panzani S, Faustini M, et al. An Apgar scoring system for routine assessment of newborn puppy viability and short-term survival prognosis. 

Articles

Newborn puppies and kittens can become compromised quickly. Here’s what you need to know when caring for these fragile animals.

Neonatal nursing care for high-risk puppies and kittens

The disruption of normal joint mechanics may lead to or result from injury to the various components of a joint. Frequently, this injury results in osteoarthritis (OA),

 which often leads to physical incapacity, pain and reduced quality of life for the affected pet. OA is the most common form of arthritis and is recognized in humans and in all veterinary species. It is often a slowly progressive condition characterized by two main pathologic processes: degeneration of articular cartilage with a loss of both proteoglycan and collagen, and proliferation of new bone. In addition, there is a variable, low-grade inflammatory response within the synovial membrane.

In North America, OA prevalence is reported to range from 20% in dogs older than 1 year up to 80% in dogs over age 8.

 The objectives of OA treatment are multifaceted: reduce pain and discomfort, decrease clinical signs, slow disease progression, promote repair of damaged tissue and improve quality of life.

It has been suggested that the best results in dogs with chronic pain due to OA result from a combination of anti-inflammatory and analgesic medications, disease-modifying OA agents, specific nutrients, nutraceuticals, weight reduction, exercise programs, physical therapy and therapeutic diets. Applying an individualized combination of these management options to each patient will enhance quality of life, which is the ultimate goal of therapy.

It is well recognized that obesity is epidemic in companion animals. In 2018, the Association for Pet Obesity Prevention estimated that 56% of dogs in the United States were overweight or obese.

 In addition, a long-term study has documented that the prevalence of OA is greater in overweight/obese dogs compared with ideal weight dogs (83% vs. 50%).

 Given these data, it is reasonable to assume that a significant portion of arthritic dogs will be overweight/obese and vice versa. Managing these comorbid conditions presents a variety of challenges.

As disease entities, OA and obesity present diagnostic challenges for very different reasons. Clinical signs of OA may not be obvious on examination, particularly early in the disease process. Although signs of pets being overweight or obese are readily apparent, these signs are often overlooked or dismissed as inconsequential. Diagnosis of OA generally requires a combination of history, physical examination findings and radiographic evidence of degenerative joint disease. Although this seems straightforward, historical clues, which are vital to creating an index of suspicion, may be elusive and clinical signs are often subtle and not evident on routine veterinary examination. Owners may attribute many signs of OA to normal aging and therefore fail to report them unless prompted (see 

Owners of dogs at risk for obesity and OA should be educated on the importance of lifelong weight management. The incidence and severity of OA secondary to canine hip dysplasia can be influenced significantly by environmental factors such as nutrition and lifestyle.

Clinical signs of OA include difficulty rising from rest, stiffness and lameness. A thorough disease-specific history may reveal evidence of subtle changes early in the course of OA, such as reluctance to walk, run, climb stairs, jump or play. Signs may be as inconspicuous as lagging behind on walks. Veterinary teams must listen to owners when they are describing that their dog is reluctant to walk on tile or hardwood floors, or that their pet no longer wants to go for car rides—something that was once a favorite activity.

Owners are often unaware of the correlation between behavior changes and OA. Yelping or whimpering, and even personality changes such as withdrawal or aggressive behavior may be indicative of the chronic pain of OA. Additionally, the veterinary team may uncover subtle signs caused by OA pain that the owner did not notice, such as longer nails (indicating that the dog is not walking and so nails are not being worn down by hard surfaces) or abnormal fur patterns over joints (indicating the dog has been licking the area). Consistent use of an owner questionnaire may facilitate early detection of OA.

Dietary factors can potentially modify some of the underlying processes involved in OA, including modulation of the inflammatory response, provision of nutrients for cartilage repair and protection against oxidative damage. Where effective, dietary management may help reduce or eliminate the need for conventional drugs, some of which are associated with adverse effects.

As the building blocks of proteins, amino acids play a role in the makeup of tissues and organs throughout the body. Methionine is a unique amino acid that produces several  molecules that are essential for proper cell function. Methionine, which contains sulfur, can produce other sulfur-containing molecules in the joint and is involved in protein production. Manganese is an essential nutrient involved in many chemical processes in the body, including bone formation. Manganese plays a role in the health and maintenance of bone and cartilage in joints. In addition, manganese supports collagen formation for joint strength. Methionine and manganese are building blocks for cartilage in joints.

Carnitine is an amino acid that enables the body to turn fat into energy. Carnitine aids in muscle maintenance and transports long-chain fatty acids and their derivatives into the mitochondria of cells. By strengthening skeletal muscle and turning fat into energy, the severity of OA may be lessened.

Hyaluronic acid is a principal component of synovial fluid and works in the joint to maintain joint viscosity, aid in joint lubrication and help with shock absorption. Additionally, vitamins C and E are antioxidants that neutralizefree radicals to maximize mobility. N-acetyl-D-glucosamine “shortcuts” the glycosaminoglycan pathway to maintain healthy joint structure and function.

Omega-3 fatty acids have been shown to aid in canine OA management. Studies show that foods with high levels of total omega-3 fatty acids and eicosapentaenoic acid (EPA) can improve the clinical signs of canine OA.

In normal canine cartilage, there is a balance between synthesis and degradation of cartilage matrix. In arthritic joints, damage to chondrocytes incites a viscous cycle that culminates in cartilage destruction, inflammation and pain. The mechanisms responsible for the demonstrated clinical benefits of omega-3 fatty acids include controlling inflammation and reducing the expression and activity of cartilage-degrading enzymes.

Cartilage degradation starts with loss of cartilage aggrecan followed by loss of cartilage collagens, resulting in the inability to resist compressive forces during joint movement. EPA significantly decreases the loss of aggrecan in canine cartilage by inhibiting the upregulation of aggrecanases by blocking the signal at the level of messenger RNA.

Omega-3 fatty acids result in a decrease in membrane arachidonic acid (AA) levels because omega-3 fatty acids replace AA in the substrate pool. This produces an accompanying decrease in the capacity to synthesize inflammatory eicosanoids from AA. Studies have documented that inflammatory eicosanoids produced from AA are depressed when dogs consume foods with high levels of omega-3 fatty acids. In addition to its role in modulating the production of inflammatory eicosanoids, omega-3 fatty acids have a direct role in the resolution of inflammation.

Shellfish supplements have been used to manage arthritis in humans and, in recent years, interest has focused on the potential benefits of a nutritional supplement prepared from the New Zealand green-lipped mussel (GLM), 

 GLM is known to contain anti-inflammatory components and other nutrients that benefit joint health. Heat processing of GLM has been shown to destroy its activity. Therefore, the processing of whole GLM and incorporation of the GLM product into food products requires special care and processing techniques to avoid destroying any efficacy of the final product.

GLM has been shown to contain a unique omega-3 fatty acid, eicosatetraenoic acid, which appears to act as a dual inhibitor of arachidonic acid oxygenation by both the cyclooxygenase and lipoxygenase pathways.

 GLM is a rich source of nutrients, including glycosaminoglycans (e.g. chondroitin sulfates), vitamins, minerals and omega-3 series polyunsaturated fatty acids.

Nutrition, and specific nutrients, provide an effective and safe way to manage OA in dogs. Foods with high levels of omage-3 fatty acids have the dual benefit of controlling inflammation and pain while slowing disease progression by decreasing cartilage degradation.

Successful treatment and prevention of obesity and OA require a comprehensive approach that includes preventive measures and a multimodal treatment program. Documenting the presence of comorbid conditions is critical.

Clinical signs of OA are often not obvious on examination, particularly early in the disease process. Early diagnosis of OA facilitates early intervention, which will likely improve long-term outcome. Nutritional management should be part of the multimodal approach in dogs with joint disease. Mobility is powerful and allows humans and dogs to live healthily and happily in body and mind. Joint health is fundamental to moving in comfort and should be addressed with every dog that comes into the hospital.

DeCamp CE, Johnston SA, Déjardin LM, et al. Arthrology. In: DeCamp CE, Johnston SA, Déjardin LM, et al, Eds. 

Brinker, Piermattei, and Flo's Handbook of Small Animal Orthopedics and Fracture Repair

Anandacoomarasamy A, Caterson I, Sambrook P, et al. The impact of obesity on the musculoskeletal system. 

Anderson KL, O’Neill DG, Brodbelt DC, et al. Prevalence, duration and risk factors for appendicular osteoarthritis in a UK dog population under primary veterinary care. 

Burns KM. Are your patients suffering in silence? Managing osteoarthritis in pets. 

2018 Pet obesity survey results: U.S. pet obesity rates plateau and nutritional confusion grows. Association for Pet Obesity Prevention website: 

Kealy RD, Lawler DF, Ballam JM, et al. Evaluation of the effect of limited food consumption on radiographic evidence of osteoarthritis in dogs. 

Roush JK, Dodd CA, Fritsch DA, et al. Multicenter practice assessment of the effects of omega-3 fatty acids on osteoarthritis in dogs. 

Fritsch D, Allen TA, Dodd CE, et al. Dose-titration effects of fish oil in osteoarthritic dogs. 

Roush JK, Cross AR, Renberg WC, et al. Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis, 3-month feeding study. 

Fritsch DA, Allen TA, Dodd CE, et al. A multi-center study of the effect of dietary supplementation with fish oil omega-3 fatty acids on carprofen dosage in dogs with osteoarthritis. 

Bui LM, Bierer TL. Influence of green lipped mussels (

) in alleviating signs of arthritis in dogs. 

Treschow AP, Hodges LD, Wright PF, et al. Novel anti-inflammatory omega-3 PUFAs from New-Zealand green-lipped mussels, Perna canaliculus. 

Kara Burns is a licensed veterinary technician with masters’ degrees in physiology and counseling psychology. She is founder and president of the Academy of Veterinary Nutrition Technicians and teaches nutrition courses around the world. Kara is a consultant for 

, the U.K.’s #1 hip and joint supplement for dogs. She’s a member of, and holds board positions with, numerous associations, including the American Academy of Veterinary Nutrition, Western Veterinary Conference, NAVTA, Pride VMC and the Pet Nutrition Alliance.


Osteoarthritis in dogs is often diagnosed late owing to several factors. Here’s why, plus tips for managing this debilitating disease through nutrition.


Mobility matters: nutritional management of canine joint disease 

Gastrointestinal (GI) motility disturbances are widely underrecognized in dogs and cats, primarily because we do not have good tools to diagnose them. Delayed transit disorders are suspected commonly by clinicians and may involve the esophagus (megaesophagus and dysmotility), stomach (delayed gastric emptying), small intestine (postoperative ileus and pseudo-obstruction), or colon (constipation and megacolon).

This two-part article discusses general causes of GI motility disorders affecting the esophagus to the colon, and offers insight for appropriate diagnostic evaluation and treatment options for these disturbances. This article covers the GI tract as a whole; a second article will focus on esophageal diseases that cause motility disturbances.

Vomiting is the predominant clinical sign in dogs and cats with gastric motility disorders. Gastric mucosal disorders may cause motility disturbances due to hypomotility or pyloric outflow obstruction. The most common causes of outflow obstruction are foreign bodies and/or intraluminal masses (e.g., mucosal and/or muscular proliferative diseases), whereas infiltrative diseases may cause generalized hypomotility. Gastric dilatation and volvulus may also cause outflow obstruction but is not further discussed here. Gastric hypomotility and defective propulsion may also be associated with diverse inflammatory conditions and metabolic/systemic diseases, such as chronic gastritis, inflammatory bowel disease (IBD), 

 spp infection, ulceration/erosions, pancreatitis, hypokalemia, hypocalcemia and hypoadrenocorticism.

Gastric retention (i.e., retained gastric contents eight to 10 hours after meal ingestion) has two causes: gastric hypomotility and pyloric outflow obstruction. With pyloric outflow obstruction due to foreign bodies (an especially common cause in young animals;

), an acute onset of vomiting typically occurs. These patients may be painful in the cranial abdomen on physical examination. Therefore, clinicians should take the time to rule in or out a foreign body with a diagnostic workup that includes abdominal imaging (survey radiographs for radiodense objects), with barium contrast if necessary to demonstrate a filling defect if the object cannot be visualized on survey radiographs (

Contrast radiography can be beneficial if ultrasound is unavailable or unrewarding. Gastroscopy serves to confirm the cause of obstruction, and can help with removing the obstructing object and/or sampling mass lesions via exfoliative cytology or forceps biopsy (

). With infiltrative disease (e.g., nonspecific chronic gastritis, IBD), intermittent episodes of vomiting food and bile, hematemesis, melena, abdominal discomfort and weight loss may occur. In patients with chronic gastritis, retained gastric fluids and ingesta noted on gastroscopy may be a clue that a concurrent motility disturbance is present (

Keep in mind that gastric motility disturbances other than mechanical obstruction (e.g., delayed gastric emptying) have diverse causes, including mucosal inflammation (e.g., chronic gastritis, IBD), infection (gastric 

 spp), and dysmotility of unknown cause. Delayed gastric emptying has also been associated with with numerous secondary conditions, including hypokalemia, metabolic disorders (e.g., Addison’s disease, uremia, diabetes mellitus), use of concurrent drugs (e.g., anticholinergics), and acute abdominal inflammation.

Treatment of gastric motility disorders is as follows:

 gastric polyp (polypectomy), tumor (biopsy/gastrectomy +/- chemotherapy), foreign body (endoscopic/surgical removal)

 inflammation/IBD (hydrolyzed diet +/- prednisone), infection (antibiotics), idiopathic (hydrolyzed/ultra-low-fat diet + prokinetic drugs [e.g., cisapride, ranitidine, erythromycin])

Small and large intestinal motility disturbances

As noted earlier, intestinal motility disturbances can be difficult to document due to inadequate diagnostic tools that yield variable results. For example, methods to measure intestinal transit may include barium contrast studies (with or without food), ultrasonography (very operator dependent), and wireless motility capsule. If a structural disorder (e.g., mechanical obstruction) is suspected, it is advisable to start with survey abdominal radiography followed by contrast radiography to rule out specific intestinal diseases.

Ultimately, identifying and treating the underlying disease process is key to clinical remission. Enteroscopy may be useful for removal of proximal duodenal foreign bodies (

). Clinical signs suggestive of small intestinal diarrhea include large stool volume, watery diarrhea, fetid smell, presence of melena and systemic signs (hyporerexia, ravenous appetitie and/or weight loss); whereas normal stool volume, hematochezia, mucoid stools and/or frequent attempts to defecate are most characteristic of large intestinal diarrhea.

Obstruction of the small intestine is a common reason for dysmotility, especially with luminal foreign bodies. While these objects can lodge anywhere along the small or large intestine, many are diagnosed as lodged jejunal foreign bodies. Linear foreign bodies cause obstruction because of their ability to gather/pleat the intestine to cause partial or complete obstruction, and potential perforation, if not resolved. Intussusception in younger dogs and cats (< 1 year of age) can also cause bowel obstruction (

Patients with complete intestinal obstruction often present with acute signs of vomiting, whereas chronic clinical signs (vomiting, diarrhea hyporexia, and/or weight loss) are most consistent with chronic obstructive disorders. Other causes of intestinal dysmotility include dysautonomia, postoperative ileus, viral enteritis, opioid-induced dysmotility, and the rarely occurring idiopathic pseudo-obstruction (i.e., intestinal dilation with no evidence of mechanical obstruction).

Canine parvovirus can cause hypomotility (functional ileus) of the small intestine as a consequence of severe intestinal inflammation/necrosis secondary to viral infection. Because parvovirus is viral in origin, the mainstay of therapy is supportive care. By supplementing nutrition, correcting hydration and providing other supportive measures (e.g., anti-emetic therapy), motility disturbances and clinical remission can be addressed adequately. With infiltrative disease, such as IBD, alimentary lymphoma, and GI histoplasmosis, obtaining mucosal biopsies will generally yield a definitive diagnosis and the need for specific therapy.

Colonic motility disturbances are characterized predominantly by constipation and megacolon. Constipation denotes infrequent or difficult defication with the passage of dry feces. The causes of constipation are numerous and include intra- or extraluminal mechanical obstruction (bones, hair, neoplasia, pelvic fracture), neuromuscular dysfunction (dysautonomia, lumbosacral disease), metabolic/endocrine disease (hypokalemia, hypothyroidism), and medications (opioids, anticholinergics). Megacolon is characterized by excessive colonic dilation thought to be associated with functional disurbances in colonic smooth muscle. 

Treatment strategies for colonic dysmotility are aimed at removal of the underlying cause; adding dietary fiber; using enemas, stools softeners, or manual extraction of hard feces; and administering promotility drugs (ciasapride, erythromycin, misoprostil). When mass lesions present in the colon are causing partial obstruction, the main differentials are adenocarcinoma and inflammatory polyp, both of which usually can be removed (surgically or via endoscopy) without further complications.

Medical therapy for GI motility disturbances

The primary drug choices for GI motility disorders include agents that stimulate intestinal smooth muscle. These include metoclopramide, cisapride, erythromycin, ranitidine, and misoprostol, each of which has a different mechanism of action. For gastroesophageal reflux and gastric hypomotility, metoclopramide (a dopamine antagonist) and cisapride (a serotonin 5-HT [hydroxytryptamine] agonist) are the primary therapeutic choices because they promote gastric emptying and increase lower esophageal sphinter tone to prevent reflux. Metoclopramide will have limited effect distal to the pylorus but will likely facilitate gastric contractions and movement of fluid/ingesta through the pylorus. Because cisapride affects the smooth muscle of the entire GI tract, it may be beneficial in treating different causes of GI hypomotility involving the stomach and intestines.

For small intestinal dysmotility, cisapride, ranitidine and erythromycin are good treatment options. Ranitidine is a histamine 2 antagonist but has prokinetic activity, especially when treating small intestinal hypomotility. Erythromycin works via motilin-like activity and has prokinetic activity at sub-antimicrobial doses; it is also useful for stimulating smooth muscle of the small intestine. Occasionally, dogs with small intestinal IBD that are experiencing continued diarrhea despite diet and immunosuppressive therapy will respond to a promotility drug, suggesting that infiltrative diseases are associated with dysmotility. A suggested trial period of four to six weeks is recommended in these cases.

For colonic dysmotility/constipation, cisapride is recommended as a first choice agent. Unfortunately, there are few effective promotility medication options for stimulating colonic motility. Pilot study data suggest that misoprostil following meal ingestion may stimulate colonic motility in dogs.

Dr. Jergens is an internist and holds the Donn E. and Beth M. Bacon Professorship in Small Animal Medicine and Surgery, and serves as associate chair for research and graduate studies in the Department of Veterinary Clinical Sciences at Iowa State University College of Veterinary Medicine.

1. Fioramonti J, Frexinos J, Bueno L. Oral prostaglandin E analogues induce intestinal migrating motor complexes after a meal in dogs: Evidence for a central mechanism. 

Gastrointestinal motility disorders are a diagnostic and therapeutic challenge for many practitioners. Here’s how to narrow down the affected area so you can identify the cause and provide appropriate treatment.

Diagnosis and management of GI motility disorders

As a result of the COVID-19 pandemic, veterinary practices have been forced to change how we serve our clients. While at first these changes may have seemed like a great hindrance to practicing veterinary medicine, the reality is that many of the innovative protocols we devised will continue to benefit our practices, clients and patients long after the pandemic is over.

Many clients have really appreciated the convenience of curbside service. In my practice, we had discussed offering curbside service for a couple years, but just never ripped off the Band-Aid because we were comfortable with the status quo. With no other choice during COVID-19, we realized how successful curbside care could be and will continue to offer this option to our clients for several services:

Medical appointment admits and discharges

Technician appointments (nail trims, anal gland expression, vaccine booster, etc.)

We knew during our first week of curbside service that we had to come up with ways to improve efficiency. The demand for appointments far outweighed (and still does) anything we had ever experienced. But our appointments were consistently exceeding their allotted time slots, causing us to fall behind most days. When we analyzed our system, we saw that what was taking up so much time was history taking, especially when the person bringing the pet to the appointment was not the owner.

We quickly realized that obtaining the patient history before the appointment would speed things up immensely. Many types of patient history forms can be sent to clients to fill out electronically well before the appointment, or even while the client is waiting to be seen:

Health questionnaires (senior pets, annual exams, etc.)

Once clients start coming back to your practice, obtaining as much information as possible prior the appointment will continue to be beneficial. Collecting patient histories in advance can shorten 30-minute appointments to as little as 15 to 20 minutes, and the doctors can review the information before the appointment. With their thoughts already on the case, they pair that with the physical exam and are able to convey treatment options more efficiently.

The “witching hour”—typically the stretch from 4 to 6 p.m. when everyone comes to pick up their pets, prescriptions or food after work—can cause stress even for the most well-run practices. Combine that mayhem with your scheduled appointments, and your client service representatives quickly need a floatie to get through those rough seas.

When we implemented curbside service, we had no choice but to switch gears when it came to processing payments. About a week in, we had two clients dispute a credit card phone authorization and had to jump through hoops to prove we performed the services in question. After a quick chat with our merchant service provider, we started emailing invoices with a link for payment. Sending invoices to clients ahead of time allows them to pay via the link in their email, so when they come to the practice all we have to do is deliver the pet, prescription or food right to the car. Clients love not having to wait, and I cannot express how much it speeds up the checkout process and makes the “witching hour” less chaotic. We should have started this years ago and will continue to do so after the pandemic is over.

Over the past few years, telemedicine has incited panic in some practices and excitement in others. No matter what your opinions of telemedicine were prior to COVID-19, there is no doubt that this service has been beneficial for clients and practices alike during the pandemic. With some clients unable or unwilling to visit the practice and some practices short-staffed due to quarantined team members, telemedicine became a game changer. What’s more, telemedicine consults can be completed in almost half the time of a regular appointment. After the pandemic, we will continue to use telemedicine in our practice for several types of appointments:

Manning the eight phones lines in our practice has been a monumental challenge during the pandemic. Fortuitously for us, we onboarded with practice management software provider 

 just before the pandemic hit. We encouraged our clients to download the app and use it to reach us with almost instantaneous results:

Because our phone traffic has lessened dramatically, we can now serve our clients more proficiently.

As I reflect on our practice experiences over the past couple months, I am amazed by our ability to adapt to change. Practices that make pandemic changes part of their 

 protocols will be the ones that will thrive once it is over.

Emily Shiver is practice manager at Cleveland Heights Animal Hospital in Lakeland, Florida.

A practice manager reflects on the many protocol changes implemented during COVID-19 that will benefit veterinary hospitals, clients and patients well into the future. 

Pivot during the pandemic for success on the other side

Immune-mediated hemolytic anemia (IMHA) is far from a simple disease with a straightforward treatment plan. Difficult to treat and confusing to manage over time, this disease has many clinicians referring patients to internists for both short- and long-term management. The difficulties may be due largely to the fact that each patient is so different in how they present, how the disease progresses, how they respond to treatment and how they fare over the long term:

 A patient with IMHA may present clinically normal with abnormal routine lab work, or may come in nearly dead.

A dog with questionable bloodwork can crash in a hemolytic crisis within 24 hours after a normal physical exam.

The protocol that keeps one dog alive can appear to be useless for another patient, or a protocol that worked initially can appear ineffective after a relapse.

 One dog never relapses, the next never seems to stop relapsing or ever get out of its initial crisis.

At a recent Fetch dvm360 conference, Elisa Mazzaferro, MS, DVM, PhD, DACVECC, a criticalist at Cornell University Veterinary Specialists and adjunct associate clinical professor at Cornell University College of Veterinary Medicine, shared her approach to IMHA cases. A previous article discussed Dr. Mazzaferro’s insight on the causes and diagnosis of IMHA.

 Here she sheds light on short- and long-term treatment, as well as patient monitoring.

Initial treatment for IMHA depends on the severity of the clinical presentation, the clinician’s preference and the owner’s cost limitations. Any moderately affected patient is better off being hospitalized than being monitored at home, but this is not always something you can convince owners to do.

First, Dr. Mazzaferro said, identify and remove any inciting cause, if possible. These may include ticks, pennies or other metals (e.g., zinc intoxication); note that zinc-containing ointments such as sunblock and Desitin can also be culprits.

Glucocorticoids and other immunosuppressive agents

“Steroids, steroids, and more steroids”—this is the one and only proven treatment, and sometimes it is the only immunosuppressive treatment chosen, Dr. Mazzaferro said, adding that “you cannot skip steroids, but you will need to wean them sooner or later and you may need to add a second drug.” The current recommended dose for prednisone (or prednisolone) is 1 to 2 mg/kg/day, divided (it is no longer 2-4 mg/kg/day). With vomiting animals, you can start with injections of dexamethasone sodium phosphate at about 0.1 to 0.2 mg/kg IV every 12 hours, which is roughly equivalent to the prednisone dose.

If there is proof of autoagglutination, or in severe cases that require multiple transfusions, Dr. Mazzaferro will start a second immunosuppressive drug and thromboprophylactic therapy right away, but when to do this is not clear from the literature (see Is combination therapy effective?). None of the drugs below have proven efficacy by themselves in patients with IMHA

Cyclosporine suppresses T cells and inflammatory cytokines and has a rapid onset; the dose is 5 to 10 mg/kg PO every 12 hours. Side effects include infections, gingival hyperplasia and, occasionally, renal or liver toxicity.

Azathioprine suppresses T-cell function, and takes one to two weeks to start working; the dose is 2 mg/kg/day PO for five to seven days and then every other day. It can cause vomiting, diarrhea, pancreatitis and myelosuppression.

Mycophenolate inhibits T and B cells, and inhibits B-cell antibodies; the dose is 10 mg/kg/day PO or IV. This drug has variable bioavailability, and can cause lethargy, vomiting, diarrhea, lymphopenia and pyoderma. 

Leflunomide, a newer agent, blocks both T and B cells; the dose is 2 to 4 mg/kg/day PO. Side effects include vomiting, diarrhea and bone marrow suppression. (Leflunomide is not used commonly — consult with your local internist.)

If your patient is symptomatic for anemia (weak, pale, elevated respiratory rate or heart rate), or the packed cell volume (PCV) is 13% or lower, immediate transfusion is required. This will likely need to be done at a 24-hour care facility using the freshest packed red blood cells (RBCs) available.

Note that cross-matching can be difficult for dogs that are already macroagglutinating, but the RapidVet-H cross-match kit (DMS Laboratories) is not supposed to be affected by this. If the dog has never had a transfusion, it can be done without cross-matching. If the patient is four days or more out from a recent transfusion, you must cross-match as they may have started making antibodies against foreign RBCs already.

Several other medications can also be used to treat IMHA. Crystalloids (ideally, intravenous fluids) can help flush out bilirubin, which can be nephrotoxic.

An estimated 50% to 80% of dogs with IMHA develop life-threatening thromboem-bolic complications. Steroids are pro-coagulable, and the systemic inflammation from hemolysis can trigger clots, consumption of clotting factors and other clotting dyscra-sias. To prevent these compli-cations, patients should be started on one of the following anticoagulant drugs:

Aspirin: 0.5-1 mg/kg/day PO (can be compounded for small dogs) Dr. Mazzaferro noted that this dose is largely ineffective as an antiplatelet drug in dogs, but this is the "recommended" dose.

Clopidogrel: 10 mg/kg/day PO loading dose on day 1, then 2 mg/kg/day PO

Unfractionated heparin: may be useful only if dose adjustments are based on an individual patient's daily anti–factor Xa activity measurements, so it is not widely used or recommended at this time 

Fractionated heparin (enoxaparin): 0.8 mg/kg SC every six to eight hours, with dose adjustments based on anti–factor Xa activity

Gastrointestinal protectants, such as proton pump inhibitors, histamine blockers, anti-emetics and/or sucralfate, may also be considered for these patients.

Dr Mazzaferro prefers to start doxycycline empirically at 5 to 10 mg/kg every 12 to 24 hours in all patients with IMHA. She will stop if there are signs of gastrointestinal upset and restart it later if indicated by the infectious disease panel. Doxycycline can be discontinued if an infectious cause is no longer suspected.

These are tailored to the indi-vidual patient and also guided by clinician preference. Monitoring and long-term treatment can get complicated, but here are some basic guidelines.

Once the patient is out of the hospital, recheck the PCV/total protein every seven to 14 days initially, then every two to four weeks, and do blood smears and a full complete blood cell count (CBC) as often as owners will allow. Each CBC should have an add-on review by a pathologist.

Taper the prednisone when (1) PCV has risen to a normal level, (2) there are no longer any reticulocytes or evidence of regeneration, and (3) all of the spherocytes and abnormal RBCs (including nucleated RBCs) are gone from the comprehensive CBC with a pathol-ogist’s review. (You can roughly monitor in-house with cytology if you are skilled, Dr. Mazzafero said, but send blood to the lab for confirmation that everything has normalized.)

Do not taper too hastily. Decrease prednisone by 25% and then recheck every three to four weeks. If the pathologist’s review reveals ongoing evidence of IMHA (spherocytes, reticulocytes, anemia, abnormal blood cells or recurrence of anemia), increase the prednisone dose. If CBCs remain normal with no evidence of reticulocytosis or spherocytosis, lower the dose by another 25% of the original dose every four to six weeks.

Wean steroids in total over three to six months, and be aware that relapse can occur at any time. In the face of an altered immune system, regularly check for urinary tract and skin infections, and treat these based on culture and sensitivity results.

Stop the anticoagulant therapy when prednisone is stopped.

If using adjunctive cyclosporine, start to decrease it in the same way as the prednisone, at about 20 weeks out, and check lab work monthly.

Due to patient variability, there will be many exceptions to these guidelines. More often than not, Dr. Mazzaferro says, you will seek a consultation with or refer to an internal medicine specialist— and you should. With a complicated disease, however, having some simplification allows us to manage a good portion of the care, helps us catch relapses and diagnose the disease on initial presentation, and allows us do our part in co-managing these cases. Maybe we can save more of them.

Dr. Johnson practices emergency medicine at Berkeley Dog and Cat Hospital in Berkeley, California, and general practice at Cameron Veterinary Hospital in Sunnyvale, California. Her nonveterinary loves are writing, dressage with her Iberian warmblood mare Synergy; watercolor painting on yupo; vinyasa yoga; and running with her dog Tyson. Try as she might, her curly-coated Scottish Fold, Hootie, refuses to go jogging with her.

Johnson C. Possible IMHA dog—now what? Vetted. 2020;117(7):10-12.

Swann JW, Garden OA, Fellman CL, et al. ACVIM consensus statement on the treatment of immune-mediated hemolytic anemia in dogs. J Vet Intern Med. 2019;33(3):1141-1172. doi:10.1111/jvim.15463

Best practices for short- and long-term therapy, as well as monitoring, in patients with IMHA.

Managing immune-mediated hemolytic anemia

I’ve been researching stress and anxiety in our profession and talking to veterinarians about their daily struggles. It’s becoming clear to me that much of our stress comes from expectations about—and interactions with—our clients. We stress about diagnoses, treatment success and our surgery skills, but the things that seem to hit us the hardest are the things our clients think about us, what say to us and how they treat us on social media.

I think there are three main assumptions we make about clients and their complaints, and if we could think differently, we might do a better job at managing the stress.

Mistake No. 1: We think clients know more than they do

Sure, veterinary clients often check with “Dr. Google” about their pet’s symptoms, and sometimes they’re in the ballpark, but they really don’t have the medical knowledge to discern whether their research makes practical sense or to understand the tests needed to confirm that Dr. Google diagnosis.

When I ask clients questions about diet, clinical signs, length of illness or past medical history, I often get answers that don’t add up. For example, when I see a mammary mass on a dog that’s encompassing one-quarter of the abdomen and the client tells me it just popped up in the past few weeks. I know this cannot be true. I know that this really means the client was busy with everyday life, so they didn’t see anything wrong until it was seriously wrong. If I choose to be upset by this fact, I will cause myself undue stress. If I accept that this is where we are and then do my very best to make proper treatment recommendations from this point in time, I can proceed without taking on stress about it.

Mistake No. 2: We think we always know what our clients should do

We think we know what's best for a patient, but it's our clients who get to decide what’s best for their pet and their situation. “Best” is a matter of opinion. We may not always agree with the choices our clients make when it comes to their pets, but our job is to give them the options we’ve been trained to give. It’s not up to us to judge their decisions. We’re there to support them in whatever decision they make without taking on the emotions or personal responsibility for these decisions. We should assume they’ll do what they believe is best for their pet and love them through any “best” decision.

Mistake No. 3: We think our clients know how hard our job is

We know we’re not God and cannot save every life. We understand our limitations. We assume that clients realize this as well. We think they know we’re doing our best to help them in every situation. We know how much it costs to run a veterinary hospital, but clients may think us uncaring when we give them a treatment plan they can’t afford. We know we stress over every one of their pets’ problems, but they don’t see our pain. Continuing to communicate with the public about how difficult some of our days can be is the first step in bridging this gap.

So, whether you’re a veterinary client or a working veterinarian, realize that we all care about the same thing: loving and healing pets. Clients, you need veterinarians to be healthy and whole to help you. Veterinarians, you need your clients to pay for the valuable work you’re passionate about. We’re on the same team, and we should treat each other with respect, compassion and understanding.

Julie Cappel, DVM, works as a small animal and exotic pet veterinarian, and leadership and life coach. She has been a practice owner for more than 20 years, running a four-doctor veterinary hospital in Warren, Michigan.

Making assumptions about what our clients do and don’t understand can cost much more than lost revenue.

3 erroneous assumptions veterinarians make

Creating building blocks for a practice can lead to major payoffs for the veterinary team in the long run. (whyframeshot/stock.adobe.com)You got the job … now what? As a new associate veterinarian at a practice, you have two choices. First, if you were hired to replace someone, you can simply fill that spot and maintain the status quo as a 

	How do you make the leap from filler to builder? By finding your niche, engaging the community and developing an online presence, you could be the injection of energy, inspiration and medicine you, your hospital and your team need.    

	Entering a new veterinary practice means you're the fresh pair of eyes. Perform a needs assessment during your first few months as an associate and look for the niche you can carve out for yourself. Try out one or more of these ideas:

 For example, I did additional training to start offering in-house ultrasound; I perform the ultrasounds and a board-certified radiologist reads them.

 Laser therapy and holistic therapies such as acupuncture and chiropractic are common ones to consider.

Study more to be the practice expert on a matter involving a specific patient group

-for example, orthopedic processes for sporting or active breeds, hospice or in-home care for elderly pets, behavior training or breed-specific diseases and/or surgeries (think 

 I created and organized an open house around the holidays. We ran a tour of the hospital, drug company reps offered giveaways, and we let people take pet pictures with Santa. Many clients commented they'd never seen the entire hospital and were so excited about the Santa pictures.

Become the “new client” veterinarian.

 Develop a spiel about how you and your hospital are uniquely caring. Call back all new clients the next day for a quick check in. You'd be amazed how many clients appreciate hearing from the actual veterinarian themselves. 

	Now, look outward to opportunities available in the community. Play to your strengths as you look for ways to become better known in the area. While I enjoy educating the public and feel comfortable speaking to large groups, you may not. There are still many ways to build community as a veterinarian:

Attend local horse shows, dog park openings and pet-focused community events.

Find opportunities to interact with the owners of feed stores and pet stores.

 Ask to leave your cards on their bulletin boards.

Join the city council animal advisory board or offer your services to consult on animal issues.

Support the local school system and engage with any pre-vet or agriculture programs.

Offer reduced surgery prices for a local animal shelter.

 This is especially welcome if their building doesn't have its own surgery suite. 

Speak at community events and/or join your city's Chamber of Commerce.

Participate in career days at local schools.

 Every kid wants to hear from an animal doctor.

Welcome high school students interested in shadowing or getting volunteer hours at your hospital. 

		Hungry for some words on clinical topics to go with your cool photos on Instagram, Facebook and more? 

	Practice-builders take to their keyboards and smartphones to increase their reach as veterinarians. These days the search for knowledge is continuous-taking place at all hours in online forums and on social media platforms. Building an online presence is an important tool to reach new clients and promote yourself (and your hospital). Here are ways you can engage on the internet: 

Congratulations, associate veterinarian! Youve been hired to fill a position. Now, ask yourself: Who do you want to be? Filling a slot or filling your practice with new ideas and enthusiasm?

Vetted July 2020

Neonatal nursing care for high-risk puppies and kittens

Mobility matters: nutritional management of canine joint disease

Diagnosis and management of GI motility disorders

Pivot during the pandemic for success on the other side

Managing immune-mediated hemolytic anemia

3 erroneous assumptions veterinarians make

Be a veterinary practice builder, not a practice filler

The drug-resistant client: Why pet owners refuse anti-anxiety medicationsand what to do about it

Considerations for adding a dedicated veterinary dental space

Medium-chain triglycerides and seizure control in dogs