• Breed-associated inherited macrothrombocytopenia 
  • Cavalier King Charles spaniels
  • Norfolk and cairn terriers
  • Identified sporadically in:
    • Bichons frises 
    • Boxers 
    • Chihuahuas 
    • Cocker spaniels 
    • English toy spaniels 
    • Havanese 
    • Jack Russell terriers 
    • Labradoodles 
    • Labrador retrievers
    • Maltese
    • Poodles 
    • Shih tzus
  • Inherited macrothrombocytopenia resulting from May-Hegglin anomaly (rare; reported in a pug crossbreed)
• Breed-associated thrombocytopenia
  • Akitas
  • Greyhounds
  • Other sight hounds (eg, whippets, deerhounds)
• Decreased platelet production
  • Acquired immune-mediated amegakaryocytic thrombocytopenia 
  • Aplastic anemia/bone marrow panhypoplasia 
    • Drug-associated effect (eg, chemotherapeutic, estrogen, griseofulvin [cats], chloramphenicol, sulfadiazine)
    • Infectious cause (eg, canine parvovirus, feline panleukopenia virus, FeLV, chronic Ehrlichia canis infection)
    • Other less common cause (eg, exposure to radiation, chemicals, mycotoxins, plant toxins)
  • Cyclic hematopoiesis in gray collies (ie, gray collie syndrome)
  • Myelophthisis (eg, myelofibrosis; lymphoid, myeloid, or metastatic neoplasia)
• Dilutional thrombocytopenia (eg, after massive transfusion, particularly of platelet-poor products)
• Gestational thrombocytopenia 
  • Occurs in humans, cows, and mice
  • May occur in dogs and cats 
• Increased platelet consumption
  • Disseminated intravascular coagulation
  • Envenomation (eg, snake bite)
  • Thrombotic microangiopathy (eg, thrombocytopenic thrombotic purpura, hemolytic uremic syndrome)
  • Vasculitis
• Increased platelet loss
  • Hemorrhage (eg, secondary to anticoagulant rodenticide toxicity or trauma)
• Increased platelet sequestration
  • Splenomegaly (eg, due to hypersplenism secondary to portal hypertension)
  • Splenomegaly ± hepatomegaly (eg, hypothermia, endotoxemia)
  • Other blood pooling
• Platelet destruction
  • Immune-mediated thrombocytopenia
    • Primary (ie, no underlying disease identified)
    • Secondary (eg, infection, neoplasia, drug-associated effect)
  • Non-immune–mediated platelet destruction, often due to infection (eg, rickettsial disease [eg, anaplasmosis, ehrlichiosis]), protozoal infection (eg, babesiosis), drugs, or neoplasia 
    • Hemophagocytic syndrome or lymphohistiocytosis
• Pseudothrombocytopenia, possibly due to:  
  • EDTA 
    • Platelet satellitism and/or phagocytosis
  • Overlap in size between RBCs and platelets (depending on methodology of platelet enumeration)
  • Platelet clumping (especially in cats)

Beyond the basics of pet food regulation, owners should be educated on obtaining information from manufacturers to determine the ideal food for their pet, such as quality control, level of testing, and expertise behind food formulations. Gathering as much information as possible about the food and manufacturer can help guide conversations.

The WSAVA Global Nutrition Committee’s nutrition toolkit provides a stepwise approach to selecting high-quality food through a series of questions for owners to ask manufacturers.¹ Examples of the criteria and questions used to determine high-quality pet food are explained below.

Many manufacturers offer a wide spectrum of nutritional expertise; some companies market based on the perception that cost equals quality. However, the manufacturers that follow the WSAVA Global Nutrition Guidelines are not necessarily those with the most expensive food.

A few example questions from the WSAVA guidelines that pet owners should ask include¹:  

• Does the manufacturer employ at least one full-time, qualified nutritionist (ie, has a PhD in animal nutrition and/or is a veterinarian and certified by the American College of Veterinary Nutrition)? Asking about full-time employment is important, as companies need the continued expertise of a nutritionist to ensure ongoing quality throughout production.
• What are the qualifications of the person who formulates the food (if not the nutritionist)? Although the qualifications noted above are ideal, there is a wide range of experience and expertise between someone with a PhD and someone with no prior formal training, and asking this question can help clarify the level of expertise of the person formulating the pet food.

Clinicians should remind owners that their pet needs nutrients—not ingredients—and the effects of processing (or not processing) the food, interactions between ingredients, and the extent of testing for bioavailability and digestibility should be considered. Not every manufacturer can perform extensive testing, but those that do can provide more information on nutritional adequacy. Larger manufacturers may have more resources to provide stringent quality-control protocols and employ expert nutritionists and food scientists. For example, a study evaluating thiamine deficiency in commercially available foods showed that foods from smaller companies are more likely to have lower thiamine levels as compared with foods from larger companies.² However, this information should not be assumed, and there is no official definition of a large company, so owners should contact manufacturers to ask about their quality-control methods and testing. Suggested questions include¹: 

• What quality control measures are in place? Strict quality-control measures are critical to ensuring safe, consistent, and nutritious food. These measures can vary widely among manufacturers but should include certification of their procedures by the Global Food Safety Initiative, Hazard Analysis and Critical Control Points, and/or American Feed Industry Association; testing of ingredients and end products for nutrient content, pathogens, and toxins; and supplier audits.
• What kind of product research has been conducted, and have the results been published in peer-reviewed journals? Feeding trials or further evaluation of a food after being fed to the intended species provide the most information about the food’s bioavailability and digestibility. Foods may be on the market without having undergone more than a computer formulation or analysis, neither of which assesses bioavailability.

Every food, excluding treats, should have an accompanying AAFCO statement that describes whether the food is complete and balanced and the life stage for which it is appropriate. Only foods that are labeled as complete and balanced by AAFCO feeding trials have been evaluated in live animals (vs laboratory analysis). Three important things can be determined by these statements³:

If not, the food label will state (often in small print) that the product is only intended for intermittent or supplemental feeding. This means the food does not have all essential nutrients; owners should not feed this to their pet unless otherwise instructed by a clinician (eg, therapeutic diets). 

Companies can either perform noninvasive feeding trials (AAFCO feeding trials last 6 months) or an analysis of their product to determine the food is complete and balanced. Foods that have undergone feeding trials will carry a statement confirming that feeding tests or trials using AAFCO procedures substantiate the food provides complete and balanced nutrition; foods that have undergone nutritional analysis only will carry a statement that the food is formulated to meet AAFCO nutrient profiles. Ideally, companies should test food using both methods to ensure it is safe and perform longer trials to ensure long-term safety and adequacy. 

AAFCO provides nutrient profiles and feeding trial requirements for growth (differentiated by breeds expected to weigh more or less than 70 lb [32 kg] at adult weight), reproduction, and adult maintenance. There are no guidelines for senior animals. Foods labeled for all life stages must meet minimum levels for both growth and adult maintenance.

Owners should be instructed to look for companies that produce high-quality products and use evidence from peer-reviewed studies as opposed to companies that focus on negative traits of other pet food companies. Owners should also watch for a lack of nutritional knowledge, including promulgating assumptions that human nutrition applies to cats and dogs. An example might be adding ingredients that are potentially toxic to animals (eg, onion, garlic). Another caution to advise pet owners against might be a nutritionally incomplete food (ie, with an AAFCO statement denoting supplemental or intermittent feeding only) marketed in way that implies it provides a pet the nutrition it needs.

There is more to understand about optimal nutrition for companion animals, and owners may easily become frustrated and confused by contradictory information. Using a follow-the-evidence communication style allows recommendations to change as more information becomes available and promotes a team-based approach between clinicians and owners to determine what is best for a pet. The author suggests conveying the following communication points:

• There are no good or bad foods—just foods with more available information.
• Food without testing is not “bad,” but its adequacy is unknown.
• An informed consumer is one who is familiar with all the testing a company conducts on a food. 

For owners who may feel overwhelmed, the Pet Nutrition Alliance’s Dare to Ask project provides many manufacturers’ answers to the WSAVA Global Nutrition Committee’s guideline questions⁴; this resource can provide a quick comparison of information among pet food brands. This may be helpful for owners who are confused or trying to decide between multiple foods.

Providing expert assistance can be helpful to owners who may be overwhelmed by the available pet food information. This can also help focus information gathering on adequacy and evidence (eg, feeding trials or peer-reviewed clinical trials on various pet foods) as opposed to unfounded information in the form of marketing (eg, health claims on food that have not been tested on animals). Providing vetted resources and specific guidelines to help owners make improved food choices can strengthen the clinician–owner relationship and avoid well-intentioned but ill-informed—and possibly inadequate—food choices for pets.

Dogs and cats with oral tumors may exhibit halitosis, ptyalism, bleeding from the oral cavity, facial asymmetry, and/or dysphagia. Patients may be presented for dental prophylaxis due to perceived or actual dental disease. A thorough, systematic oral examination should be performed during physical examination, dental prophylaxis, and procedures with general anesthesia, because this is when oral tumors are often discovered. Clinicians should be prepared to conduct a diagnostic investigation, such as incisional biopsy, during these procedures.

Patients with oral tumors should undergo a thorough physical examination, including a digital rectal examination, to rule out other malignancies (eg, anal sac adenocarcinoma or transitional cell carcinoma that can metastasize to other bone sites such as the mandible).

Staging tests may include dental radiography, 3-view thoracic radiography, and aspiration of the mandibular lymph nodes. A CT scan of the head and thorax is typically recommended for local and distant staging and surgical planning, especially for gingival tumors (Figure 1). For acanthomatous epulides, a CT scan of the thorax may not be necessary, as these tumors are locally aggressive but do not metastasize. Additional testing prior to surgery should include CBC, serum chemistry profile, urinalysis, and, in case blood transfusion becomes necessary, blood typing.

Definitive diagnosis is required once an oral tumor is identified. Common differential diagnoses for oral tumors in dogs include malignant melanoma, squamous cell carcinoma, fibrosarcoma, osteosarcoma, and acanthomatous epulis.¹ In cats, squamous cell carcinoma, osteosarcoma, and fibrosarcoma should be considered. Although it is beneficial to ensure that the oral cavity is as clean as possible prior to surgical resection and/or radiation, some pet owners may prefer to know diagnostic and treatment options before proceeding; therefore, the pros and cons should be discussed with the owner before biopsy or dental prophylaxis is performed.

Definitive diagnosis is best achieved via histopathology (vs cytology), and incisional biopsy of the oral cavity is recommended. The biopsy tract should be removed with definitive resection, as it will likely be contaminated with tumor cells; this is especially important for tumors of the maxilla, as biopsy through overlying skin can complicate reconstruction techniques after maxillectomy. The oral mucosa can heal quickly and—in patients in which an oral mass has been marginally excised—the removal site may no longer be evident by the time histopathology results are received; this can lead to a suboptimal outcome when wide tumor resection or radiation treatment is planned. Thus, excisional biopsy is not recommended for oral masses. Shaving off the mass should be avoided. It is also recommended that digital photographs of the mass be taken while the patient is under anesthesia or sedated, especially if the patient is to be referred to a specialist.

In dogs, high-low fibrosarcomas are an extremely locally aggressive fibrosarcoma subtype that is biologically high-grade but appears to be low-grade on histopathology (Figure 2).² A high-low fibrosarcoma has the potential to be misdiagnosed on incisional biopsy because the tissue can appear microscopically as a histologically bland or benign inflammatory lesion. A description of the mass and the presence of bone lysis on radiographs or CT images are critical to histopathologic interpretation. A pathologist should be consulted if the histopathologic diagnosis does not fit clinical characteristics.

In cats, squamous cell carcinoma is the most common oral tumor, followed by osteosarcoma.¹ Although the underlying cause of most oral tumors is poorly understood, eating canned tuna, wearing flea collars, and living with humans who smoke have been associated with potential oral tumor risk in cats.^3,4 Oral papillomavirus may be associated with some cases of squamous cell carcinoma in dogs.^5,6

In dogs and cats, malignant tumors of the oral cavity should generally be treated with wide excision (ie, cheilectomy, glossectomy, mandibulectomy, or maxillectomy, depending on the tumor location) of the mass. Most malignant tumors of the gingiva invade the underlying bone to some degree, and the affected portion of the mandible or maxilla should be removed with a minimum margin of 1 cm; this is similar for lip and tongue tumors. In dogs, ≤70% to 80% of the tongue can be removed and still have the potential to return to function.^7,8 Wide excision is not possible for tonsillar tumors, for which marginal excision is generally recommended. Elective lymph node dissection⁹ and/or sentinel lymph node mapping¹⁰ is recommended for surgical staging of disease.

Mandibulectomy and maxillectomy (Figure 3) are the most common surgical procedures for gingival tumors in dogs and cats. For specimens, margins should be inked for histopathology and evaluation. Potential complications include hemorrhage, infection, dehiscence, incomplete excisional margins, mandibular drift, malocclusion, anorexia, dysphagia, and mass recurrence. Seroma formation is common at the lymph node dissection site.

Although novel techniques to restore the mandible are becoming available and involve either a 3D-printed implant¹¹ or plate reconstruction and bone morphogenic protein, they are not commonly used.¹² Clinicians should be prepared for blood transfusion. After maxillectomy or mandibulectomy, most dogs will eat within 24 to 48 hours postoperation and do not require placement of a feeding tube; however, feeding tubes should be considered for radical resections, especially radical maxillectomy. Although it is generally believed that cats do not do well after maxillectomy or mandibulectomy because they will not eat postoperatively, this has not been the author’s experience. There is potential for success with these procedures in cats. Feeding tubes are critical for cats, because they may not readily eat after surgery, and hepatic lipidosis is possible after even short periods of anorexia. A recent study of 8 cats that underwent radical mandibulectomy found that 6 cats ate on their own 3 days to 1 month postoperatively and had an estimated mean survival time of 712 days.¹³ A feeding tube is recommended in both cats and dogs after glossectomy.

In dogs and cats, multimodal pain control (primarily with a combination of opioids, NSAIDs, and local anesthesia) is recommended. Patients should be maintained on IV fluids and monitored for pain, hydration status, and evidence of ongoing hemorrhage. A patient’s ability to eat postoperatively may depend on the amount of tissue resected, amount of postoperative swelling, degree of pain control, and patient’s willingness to eat; canned food of different consistencies should be offered. Patients should wear an Elizabethan collar postoperatively.

Recommendations for adjunctive therapy in dogs depend on tumor type and stage, as well as margin evaluation. Follow-up radiation therapy should be considered if clean histologic margins are not achieved. Oral melanoma is responsive to hypofractionated radiation, which involves weekly radiation therapy for 4 weeks. This protocol has minimal adverse effects and should be considered in patients deemed nonsurgical or in cases in which the owner chooses not to pursue surgery. Melanoma can also generally be treated with the melanoma vaccine rather than with chemotherapy.^14,15 Systemic chemotherapy can be considered in dogs with osteosarcoma or patients with squamous cell carcinoma or fibrosarcoma in which there is evidence of lymph node involvement, a high-grade tumor, or high mitotic count.

Prognosis with surgical treatment varies based on tumor type. Long-term survival is possible for patients with squamous cell carcinoma and with some sarcomas that have no evidence of metastatic disease, low metastatic potential based on histopathologic features, and complete surgical margins. The median survival time for patients with oral melanoma treated with surgery is 1 year.¹⁶

Although it is generally not possible to prevent oral tumors, it is recommended that pets not be exposed to household smoke. Regular physical examinations including the oral cavity and dental prophylaxis may help with early diagnosis, generally resulting in a better outcome and decreased need for surgery.

Follow-up depends on the patient and disease, but oral examination, lymph node palpation, and 3-view thoracic radiography are recommended every 3 months for 1 year postoperatively. The owner should perform regular oral examinations at home and schedule a re-evaluation if there are any signs of recurrence or physical changes (eg, redness, swelling, mass development) in the area.

Following are 5 common indications for appetite stimulation according to the author. 

Several acute illnesses can impact appetite, and evidence suggests that many hospitalized dogs and cats fail to voluntarily meet nutritional requirements.^1,2 Previously well-nourished patients may tolerate short (ie, <48 hours) periods of anorexia, but persistently poor intake can impact numerous physiologic processes (eg, enterocyte turnover, GI permeability, systemic immune response) in various species.³  

Human studies have shown that inadequate nutritional intake typically results in longer hospital stays and increased mortality^4,5; this is typically less recognized in companion animals, although data indicate an association between inadequate food intake and poor patient outcomes.^1,2 Unless oral intake is directly contraindicated, patients should typically be encouraged to eat as soon as problems such as frequent regurgitation, gastric stasis, or intestinal ileus are effectively managed.⁶ Infrequent vomiting, diarrhea, and conditions such as pancreatitis should not be regarded as reasons to withhold food, as oral intake of even small amounts of food can protect GI tract health and function.⁷ Suboptimal intake should not be considered acceptable, as patients recovering from acute illness are often in a hypermetabolic state and need substantially more calories and protein than usual.⁴ An appetite stimulant should be introduced promptly in patients recovering from acute illness to support adequate intake of an appropriate diet.

Many chronic disorders (eg, renal disease, cardiovascular disease, cancer) are associated with progressive weight loss.^8-11 Affected patients may become cachexic, a state in which voluntary intake is poor and the body’s muscle proteins—rather than fat stores—are used to supply energy. The underlying disease process can increase metabolic rate, and weight loss can occur more rapidly than with simple starvation. 

The impacts of unaddressed protein–energy malnutrition have been well established in human medicine, and intervention in affected humans may improve quality of life and longevity.^12,13 Studies in companion animals with chronic kidney disease or heart failure have shown associations between BCS and longevity, and nutritional intervention may improve the well-being and outcome of these patients.^8,9,11 If weight loss regardless of appetite is noted when a patient is diagnosed with a chronic disorder, an appetite stimulant should be included as part of the initial treatment plan. The stimulant can be adjusted or discontinued as appropriate and may prevent further decline in physical status. 

In addition to the expected physiologic benefits of an improved energy balance, enhanced intake will likely reassure owners of their pet’s overall comfort and quality of life. Similarly, a consistent appetite supports compliance with complex medication plans; owners may become disheartened and frustrated by the effort needed to administer oral medications to a hyporexic pet. A full dietary history, including weight, BCS, and muscle condition score, should be obtained routinely in dogs and cats with chronic illness¹⁴ and an appetite stimulant prescribed as soon as concerns regarding intake are identified.

Specific nutrition is routinely recommended for the management of various conditions (eg, urinary tract disease, chronic enteropathy, atopic dermatitis, liver disease, chronic kidney disease, diabetes mellitus, pancreatitis).¹⁵ Diets often play a key role in successful patient management, but patients may be reluctant to eat an unfamiliar food. 

Owner compliance with a new diet can be problematic if the pet seems reluctant to eat; owners may be tempted to add treats or continue to mix in the old food under these circumstances. Administration of an appetite stimulant prior to introduction of a new food may support adequate intake during the transition and encourage owner compliance with feeding a therapeutic diet. The appetite stimulant can be gradually withdrawn after a few weeks while the patient’s intake is carefully monitored.   

Elective soft tissue or orthopedic procedures can result in short periods of postoperative hyporexia. Although the prevalence of postoperative anorexia in companion animals undergoing routine surgery has not been well studied, one study reported that only 7 out of 15 juvenile beagles given buprenorphine prior to routine ovariohysterectomy consumed food within 26 hours of extubation.¹⁶ There can be numerous reasons for poor postoperative intake, including discomfort, alterations in GI motility associated with anesthesia, anxiety related to hospitalization, and medications prescribed to manage pain or prevent perioperative infection. 

Because poor food intake is often a major concern for owners, preemptive strategies to promote adequate intake in postoperative patients can be helpful. An appetite stimulant should be incorporated into the in-clinic postoperative care plan for patients undergoing elective surgical procedures and continued briefly following discharge.

Changes in environment can cause a range of clinical and behavioral signs, including decreased food intake in both dogs and cats.^17,18 This is a particular concern in obese cats, as serum chemistry and histopathologic changes associated with hepatic lipidosis may be noted after only 2 weeks of fasting.¹⁹ Although dogs adapt better than cats to starvation, immune responses and GI function are impacted in both species by relatively short periods of anorexia.²⁰ 

Consistent intake encouraged by giving an appetite stimulant may also reduce the likelihood of diarrhea and other clinical concerns in boarding animals. In addition, owners of boarded animals are often worried when food intake is down and may be reluctant to board their pet in the future. Prescribing an appetite stimulant at the start of the boarding period may prevent stress-related hyporexia and weight loss and provide reassurance to anxious owners. 

Although this issue has not been specifically investigated, animals with chronic illnesses may be particularly vulnerable to poor intake when housed in a new environment, and preemptive use of an appetite stimulant may be especially beneficial.

Numerous conditions and situations can cause poor food intake, and clinicians should be attentive to changes in patient body weight and other evidence of decreased appetite. Food intake, including type and amount, should be discussed at every visit and assessed daily in hospitalized patients. Early intervention is ideal, and clinicians should consider an appetite stimulant in hyporexic patients and those vulnerable to inadequate intake.

Immune-mediated hemolytic anemia (IMHA) is an important differential for anemia in dogs and cats. Diagnosis relies on identifying signs of an immune-mediated RBC attack and hemolysis in anemic patients.

In this study, a survey was distributed to clinicians and veterinary technologists to discover which tests were being used to diagnose IMHA in veterinary patients. The study authors then performed a literature review to describe the utility of different tests that can support an IMHA diagnosis.

Most survey respondents were found to perform saline agglutination or Coombs tests to detect antierythrocyte antibodies. Autoagglutination of erythrocytes can occur when immunoglobulin is present on erythrocyte surfaces. The saline agglutination test is a useful method to identify RBC agglutination, which should not be present in a normal patient. This test can be performed by mixing 1 part RBCs with 4 parts saline to help disperse strong rouleaux that can cause false-positive results. True autoagglutination is most reliably identified after washing the cells 3 times in saline. In patients that do not demonstrate autoagglutination, a direct antiglobulin test should be used to identify presence of antiglobulin on erythrocyte surfaces.¹ This is most commonly achieved with a Coombs test performed at both 39.2°F (4°C) and 98.6°F (37°C).

In addition to these tests, a routine minimum database contains much information that can raise suspicion for IMHA. CBC will not only identify anemia but also signs of regeneration in many IMHA patients. Microscopic review of a fresh blood smear can identify evidence of ghost cells, which are consistent with hemolysis, and/or spherocytes, which are consistent with immune-mediated RBC lysis in dogs. Visual inspection of the plasma from a packed cell volume analysis, serum chemistry profile, and urinalysis can offer additional information regarding hemolysis (eg, the presence of hyperbilirubinemia, bilirubinuria, hemoglobinemia, and/or hemoglobinuria).

Hyper- or hypocoagulability can be found in patients with IMHA. Thrombocytopenia is a common finding in dogs with IMHA and could be a result of consumptive processes (eg, disseminated intravascular coagulation) or concurrent immune-mediated thrombocytopenia. If thrombocytopenia or signs of coagulopathy are identified, further coagulation testing is recommended.

Key pearls to put into practice:

Pet owners should be informed that a diagnosis of IMHA relies on findings from several tests to identify the anemia, hemolysis, and immune-mediated RBC destruction present in this disorder.

CBC results, including evaluation of a fresh blood smear, can identify many of the features consistent with IMHA, including anemia, changes in plasma color in the packed cell volume tube, and/or presence of spherocytes (dogs only) or ghost cells.

If autoagglutination is not present on the saline agglutination test, a Coombs test can provide further evidence for diagnosis of IMHA.

This retrospective study reviewed the clinical course and outcome of dogs after grape or raisin ingestion; a low prevalence of acute kidney injury (AKI) was observed after ingestion.

The study included 139 dogs with known grape or raisin exposure. Raisins were ingested in 87/139 (62.6%) dogs, and grapes were ingested in 51/139 (36.7%) dogs; 1 dog ingested both grapes and raisins. Cases were divided into early and late groups based on time from ingestion to evaluation (early group, ≤4 hours [n = 82]; late group, >4 hours [n = 57]). In the early group, 38 dogs were treated in-clinic and 44 treated as outpatients. In the late group, 35 dogs were treated in-clinic and 22 as outpatients. The median length of hospitalization was 24 hours in the early group and 36 hours in the late group; duration of hospitalization was significantly longer in the late group.

Vomiting was the most common clinical sign. Other clinical signs, in decreasing order of frequency, included lethargy, polydipsia, diarrhea, polyuria, abdominal pain, and inappetence. Decontamination was performed in 87% of dogs; both emesis and activated charcoal were used in 56% of dogs, activated charcoal alone was used in 19%, and emesis alone was used in 11%.

In dogs for which serum chemistry data were available, incidence of AKI was 8/120 (6.7%); no difference in AKI prevalence was observed between the groups. Two dogs received continuous renal replacement therapy, due to which one dog died from complications.

Key pearls to put into practice:

In this study, evidence of grapes or raisins was observed in the vomitus of 15 dogs in which emesis was performed. The longest time from exposure to emesis in which grapes were observed in the vomitus was 8 hours; 4 dogs had raisins in the vomitus 12 hours after ingestion. Although the exact toxicant that leads to AKI is unknown, if removal from the GI tract could help prevent AKI, induction of emesis should be considered in patients presented <6 to 8 hours postingestion, assuming emesis is not contraindicated.

The International Renal Interest Society (IRIS) AKI staging system was used in this study. For IRIS stage 1 patients (creatinine, <1.6 mg/dL), any progressive (hourly or daily) increase in blood creatinine >0.3 mg/dL in the nonazotemic range within a 48-hour interval may suggest AKI.¹ Of the 8 azotemic dogs in this study, 4 met these criteria. Thus, if a patient’s creatinine level remains within range but shows a 0.3 mg/dL increase, active AKI is evident and intervention and monitoring should be continued.

The level of intervention varies by patient, and not all pet owners can afford hospitalization and 48 hours of fluid diuresis. Between both the early and late groups, 66/139 (47.5%) dogs in this study were treated as outpatients. Outpatient care and continued monitoring for patient response to these interventions may result in good outcomes.

Essential fatty acids (EFAs) are unsaturated fatty acids that cannot be produced and therefore must be ingested. EFAs in dogs include linoleic acid and α-linolenic acid; in cats, EFAs include linoleic acid, α-linolenic acid, and arachidonic acid. Fatty acids are commonly used in oral form to decrease skin inflammation, reduce pruritus caused by atopic dermatitis, and improve skin barrier function, which may be measured as a decrease in transepidermal water loss. Oral supplements (eg, capsules, chews) or diets that contain high levels of eicosapentaenoic acid and docosahexaenoic acid may be selected. Diets labeled for skin or joint conditions are more likely to contain therapeutic levels of fatty acids.

This study aimed to assess, via an online survey, the frequency of and rationale for EFA use in a population of clinicians, including general practitioners and specialists. The type of EFA selected, factors influencing product choices, reason for choosing EFAs, and awareness of EFA oxidation over time were evaluated in the 309 respondents. Common reasons for using EFAs for skin disease included barrier dysfunction, atopic dermatitis (environmental or food induced), immune-mediated diseases, and food allergies. Veterinary-branded products were recommended most often, and scientific studies influenced product decisions. More than 50% of respondents were not aware that fatty acids could oxidize over time.

Key pearls to put into practice:

EFA products must be within date and kept in a cool, dry location away from direct sunlight to slow the rate of oxidation. Oral EFA supplements may take 8 to 12 weeks to take effect, and long-term use is required for continued efficacy. Topical fatty acid and ceramide products may improve skin barrier function, but continued use is needed for sustained benefit.

A dose of 60-70 mg/kg per day of combined eicosapentaenoic acid and docosahexaenoic acid is recommended. A veterinary formula is preferred and is typically easier to dose in larger dogs. Higher doses may lead to flatulence and diarrhea; pancreatitis is a rare but serious complication.

EFAs at recommended doses can lower steroid and cyclosporine requirements in the treatment of atopic dermatitis.

Brucella canis, a challenging bacterial pathogen, can cause significant reproductive disease and sporadic disease (eg, diskospondylitis) of other body sites  and can be carried long-term and subclinically.^1-3 It is also an uncommon but potentially important zoonotic pathogen.^4-7

Accurate diagnostic testing is critical for diagnosis of acute disease, for broader disease control purposes, and because diagnosis can have potentially severe outcomes for dogs (eg, euthanasia) and staff (eg, quarantine). However, diagnosis of canine brucellosis can be challenging due to the nature of the pathogen and limitations of available tests.

This study aimed to compare different serologic methods and PCR testing to identify B canis. Samples from 254 dogs (4 of which had active clinical brucellosis) from 5 breeding kennels in Brazil were evaluated. Serum and whole blood samples were collected and tested via agar gel immunodiffusion, rose Bengal plate testing, complement fixation testing, microagglutination testing (MAT), 2-mercaptoethanol MAT (2ME-MAT), dot-ELISA testing, and PCR testing. Rapid slide agglutination testing, 2ME-rapid slide agglutination testing, and immunofluorescence assay testing—tests commonly used in North America—were not included.

Overall, there was poor agreement between different serologic tests, with positive results ranging from 6.3% to 16.5%. PCR and 2ME-MAT were the only tests with even reasonable statistical agreement. Using latent class analysis, positive MAT results were most strongly associated with positive PCR results, even though discordant PCR and MAT results were common.

The authors concluded that diagnosing brucellosis remains challenging. Available tests have different inherent limitations in sensitivity and specificity, and sensitivity can be impacted greatly by the type of infection (clinical vs subclinical) and time of sampling with respect to onset of infection. The difficulty in diagnosing canine brucellosis in a population in which the disease is strongly suspected highlights the challenges in screening clinically normal dogs and/or dogs with less overt disease.

Key pearls to put into practice:

Brucella canis infection can be difficult to confirm or rule out definitively. Combinations of tests are often required. Sensitivity and specificity of selected tests must be considered when interpreting results.

Approaches to testing of dogs with reproductive disease, disseminated infection (eg, diskospondylitis), and subclinical infection vary, as tests may perform differently in these patient populations.

Because of the potentially severe consequences of a positive test result, it is critical clinicians understand the strengths and limitations of individual tests.

Bacterial culture can provide a definitive diagnosis but is of limited availability due to the enhanced required biosafety practices and often low sensitivity in chronic subclinical infections.

Congestive heart failure (CHF) can trigger detrimental systemic effects due to upregulation of neurohormonal and inflammatory systems¹; cardiac cachexia is one such example of a systemic effect. Several definitions of cardiac cachexia have been proposed in human medicine, with most including weight loss as a primary criteria; however, muscle loss may be a more sensitive marker of cachexia,² particularly in CHF patients with fluid accumulation that can significantly influence body weight. Approximately 50% of dogs and cats with CHF demonstrate some degree of muscle loss and cachexia.^3,4 Although cardiac cachexia is a well-documented negative prognostic indicator in humans,¹ it has not been well studied in cats with CHF.

The primary goal of this study was to determine the prevalence of cachexia in cats with CHF based on definitions in human and veterinary literature. Differences in clinical findings, laboratory values, and outcomes in cats with and without cardiac cachexia were evaluated.

Clinical records of 125 cats with CHF secondary to acquired heart disease were retrospectively reviewed. The authors identified 7 definitions of cardiac cachexia that appeared applicable to small animals; only 1 definition exclusively used muscle condition score (MCS) to identify patients with cardiac cachexia. MCS was assessed as normal, mild, moderate, or severe muscle loss as defined by WSAVA guidelines.⁵

Prevalence of cardiac cachexia in this group ranged from 0% to 66.7%, depending on the definition applied. Muscle loss was noted in cats of all BCSs, including 11 of 61 cats that were considered overweight (ie, BCS >5/9). When the definition of cardiac cachexia that exclusively used MCS was applied to the entire study group, 41.6% of cats met the criteria for muscle loss and thus were considered to have cachexia. Cats with muscle loss were more likely to have pleural effusion and had significantly higher BUN and BUN:creatinine ratios, lower body weights and BCSs, higher neutrophil concentrations, and lower hematocrit and hemoglobin concentrations. Cats with muscle loss also had significantly shorter survival times (ie, ≈95 days) as compared with cats without muscle loss (ie, ≈281 days). Thin body condition (ie, BCS <4/9) was also associated with decreased survival as compared with overweight cats (ie, ≈35 days vs ≈216 days).

Overall, cardiac cachexia prevalence in cats with CHF varies widely, depending on its definition. MCS appears to be a good clinical marker to identify cats with cachexia. Of note, cachexia can be present prior to overt weight loss; many cats considered to have a normal or overweight BCS had muscle loss based on MCS. Based on the finding of decreased survival with muscle loss, detection of cachexia based on MCS appears to be a useful prognostic indicator for cats with CHF.

Key pearls to put into practice:

Cachexia can be present in cats with a normal or overweight BCS.

Assessment of MCS in cats with advanced heart disease should be performed at each visit to detect early signs of cachexia.

Muscle loss and low body weight can occur secondary to advanced heart disease and have been shown to decrease survival times in cats with CHF.

Ischemic dermatopathy can refer to multiple syndromes that share common features but have different etiologies. Few recent studies have focused on nonfamilial variants of ischemic dermatopathy or cases in which a vaccine trigger has not been identified. Few case reports have shown improvement after administration of vitamin E combined with pentoxifylline ± prednisone or with oclacitinib.^1,2

This retrospective study reviewed 177 cases of canine ischemic dermatopathy, excluding familial dermatomyositis; 93 cases had complete medical records. Results showed that small breeds (weighing <22 lb [10 kg]) represented most cases; Chihuahuas, toy/miniature poodles, Maltese, and Yorkshire and Jack Russell terriers were significantly overrepresented.

Of the 93 dogs with complete records, alopecia was the most common lesion, followed by crusting, scale, erythema, erosions/ulcers, and hyperpigmentation; pruritus was noted in one-third of the dogs. The median number of lesion sites was 4; however, some dogs had a single lesion. Most dogs with a single lesion had been vaccinated at that site; those with lesions not at a vaccine site were older and had greater body weights. Lesions were found most commonly on the pinnae, vaccination sites, and the periocular region/face. The most frequently reported systemic signs were lethargy, fever, inappetence, and lameness. In dogs receiving concurrent medication, there was no clinical suspicion that medication triggered the disease. Dogs having only pinnal lesions or increased systemic signs required more medications/potent immunosuppressive agents for treatment.

Pentoxifylline was the most commonly used medication, followed by steroids, vitamin E, and cyclosporine. The use of steroids was associated with a worse outcome and prognosis. Overall remission was generally achieved without significant changes in medication or combination therapy. Half of the cases had a good outcome and could be maintained on medication long-term. Factors associated with a worse prognosis included a weight <22 lb (10 kg), increased age, increased number of lesion sites, presence of systemic signs, and lesions at specific sites, including the pinnae and paw pads.

More than half of the cases in this study were likely not induced by vaccination, highlighting the need to investigate other underlying causes of ischemic dermatopathy. Previous reports show that vaccine-induced disease is seen primarily in small-breed dogs, but results in this study contraindicate those prior results. Although vaccines appear to play a role in some cases, generalized idiopathic ischemic dermatopathy more likely encompasses a diverse group of diseases, with variations in severity and unidentified but wide-ranging triggers.

Key pearls to put into practice:

Small-breed dogs weighing <22 lb (10 kg) are typically overrepresented in cases of ischemic dermatopathy; thus, this disease should be on the differential list for patients displaying appropriate clinical signs.

More than half of the cases of ischemic dermatopathy in this study were likely not induced by vaccination; thus, a specific trigger for this disease may not be apparent from a patient's history.

Overall remission was achieved without the use of significant numbers of medications. Approximately half of the cases had good outcomes and could be maintained on medication long-term.

Glycemic monitoring is a cornerstone of managing diabetic ketoacidosis (DKA) and is generally performed using portable blood glucose meters. Minimally invasive flash glucose monitoring systems (FGMSs) continuously measure interstitial blood glucose (IG) concentrations. IG can be evaluated as often as every minute through FGMSs, but the sensor needs to be scanned with a reader to obtain a measurement rather than having the glucose continuously displayed (as with continuous glucose monitoring). IG has been shown to closely reflect circulating blood glucose concentrations in steady state conditions, but when blood glucose rapidly increases or decreases, IG lags and will be lower or higher, respectively.^1,2 The FGMS has recently been evaluated in uncomplicated diabetic dogs but not in dogs with DKA.³

In this study, the performance of an FGMS was assessed in 14 dogs with DKA, during the DKA crisis and after its resolution. IG measurements obtained with the FGMS were compared with blood glucose concentrations obtained via a validated portable blood glucose meter. BCS, lactate concentration, severity of ketosis, acidosis, and time wearing the device were evaluated for their effects on sensor accuracy.

The FGMS provided clinically accurate estimates of blood glucose concentration as compared with the portable blood glucose meter and can be a useful device for monitoring blood glucose concentration in critically ill dogs with DKA. Changes in metabolic variables (eg, acid–base status, ketosis, lactate concentrations), BCS, and time wearing the device did not seem to influence sensor accuracy. Application of the FGMS appeared to be painless and easy to perform and was well tolerated by all dogs. No relevant adverse events were recorded. One dog had mild erythema at the application site that resolved spontaneously within 24 hours of removal. 

Further studies are required to evaluate precision, effects of hydration status, skin and SC adipose tissue thickness at the site of application, and location of the sensor on the accuracy of the device.

Key pearls to put into practice:

FGMSs are less invasive than portable blood glucose meters and have acceptable clinical accuracy. They can minimize pain and prevent complications secondary to frequent phlebotomies (eg, iatrogenic anemia), particularly in small-breed dogs and cats. They are cost effective and productive for ≤2 weeks.

FGMSs provide IG results every minute across a wide range of glucose concentrations between 40 mg/dL and 500 mg/dL. Glucose readings are stored every 15 minutes for ≤8 hours on the sensor and uploaded to the reader when scanned, allowing pattern and trend generation that can be used to guide treatment decisions. The authors of this review article discharge their DKA patients wearing the FGMS to optimize insulin dosing in the subsequent 1 to 2 weeks.

Evaluating blood glucose concentration with a validated portable blood glucose meter is strongly recommended when unexpected or low FGMS results (<70 mg/dL) are obtained.

Approximately 40% of US homes include cats,^1,2 and homes with cats are more likely to have multiple animals, averaging 1.8 cats each.² Close contact among cats, however, can be associated with an increase in behavior problems; urine spraying and urinating outside the litter box are significantly more common in multicat homes.³ Conflict behaviors—from tail twitching to aggressive interactions—can also occur and cause stress within the household.

This study represents the first large statistical evaluation of intercat relationships in households and the factors that may influence them. Multicat homes included in this study (n = 2492) had between 2 and 4 cats.

Affiliative behaviors among individual cats were found to be more common than conflict signs. These behaviors included sleeping in the same room as another cat, grooming another cat by licking around the head or ears, sleep-touching with another cat, and nose-touching with another cat. Almost 90% of cats slept in the same room as other cats at least once a day, and cat–cat touching was observed during ≈50% of this time. Mutual grooming of the head and ears was also common.

Conflict signs were slightly less common, although the frequency of signs increased as cat numbers increased. The number of conflict signs that owners could report was limited to 7 and included staring, chasing, stalking, fleeing, tail twitching, hissing, and wailing/screaming. Almost 75% of owners noticed conflict when a new cat was introduced into the home, and in ≈50% of cases, conflict among the cats continued over time. Staring and chasing conflict signs occurred at least daily in 44% of cats, with stalking occurring in 35% of cats. Almost 17% of households reported intercat aggression, indicating potential for clinics to provide behavioral treatment.

These results were obtained through an internet survey; thus, responders were self-selective and may or may not be representative of all cat owners. Nevertheless, the sample size of 2492 multicat households containing 6431 cats yields good insight into intercat relationships.

Key pearls to put into practice:

Recommending ways to promote friendly introductions of new cats into the home can result in fewer negative interactions among household cats.

Results from this survey appear to indicate that owners observe their cat’s behavior; thus, asking questions regarding behavioral concerns during routine visits may provide opportunities for earlier intervention.

Developing protocols for intercat aggression can be helpful for owners with cats prone to conflict.

Newer technology that includes the use of biomarkers and algorithms has been developed to aid in prediction and early disease detection, resulting in earlier treatment and, ultimately, a more favorable patient outcome. Mitzi was one such patient that received testing with this technology and experienced early CKD prediction and a positive outcome as a result.

Mitzi, a 12-year-old, spayed domestic shorthair cat, was presented for a wellness examination. Physical examination revealed diffuse muscle wasting but was otherwise unremarkable. CBC, serum chemistry, thyroid testing, and urinalysis were performed; BUN was normal, but creatinine was in the upper end of the reference range and isosthenuria and proteinuria were evident. A urine protein:creatinine ratio of 0.4 confirmed borderline proteinuria. Noninvasive blood pressure measurement also revealed hypertension (systolic, 160 mm Hg). Urine culture and susceptibility testing was performed and was negative for bacterial growth.

A RenalTech status was reported as a part of Mitzi’s wellness screening to further assess her unique risk for CKD. RenalTech utilizes artificial intelligence and machine learning to measure and compare 6 key values (ie, urine specific gravity, urine protein, urine pH, creatinine, BUN, WBC count), as well as patient age, at 2 different time points (ideally, 6 months apart). The analysis is able to detect subtle changes over time and predicts the development of CKD in a patient within the next 2 years with >95% accuracy.^5,6

Possible statuses generated from the RenalTech algorithm include positive, negative, and inconclusive:

• A positive result indicates that the patient already has CKD or is likely to develop CKD within the next 2 years. If the result is positive, the patient should be closely monitored and, when CKD is diagnosed based on IRIS guidelines, treatment recommendations should be provided based on IRIS staging.
• A negative result indicates the patient is not likely to have a diagnosis of CKD within the next 2 years; the patient should be re-evaluated at their next annual wellness examination, with no further action necessary until re-evaluation.
• Investigating for concurrent comorbidities that might predispose to, increase the risk for, or impact management of CKD should also be performed. This includes but is not limited to systemic hypertension, diabetes mellitus, hyperthyroidism, electrolyte abnormalities, and urolithiasis.
• If the result is inconclusive, it is recommended to re-evaluate and re-test the patient in 3 to 6 months.

Investigating for concurrent comorbidities that might predispose to, increase the risk for, or impact management of CKD should also be performed. This includes but is not limited to systemic hypertension, diabetes mellitus, hyperthyroidism, electrolyte abnormalities, and urolithiasis.

SDMA is a renal biomarker used to detect CKD earlier than can creatinine, when approximately only 40% of renal function has been lost.⁷ SDMA is used in the IRIS staging guidelines to help improve early diagnosis of CKD and individual patient management and recommendations. SDMA, which provides a snapshot of renal function at a single point in time, can be used alongside the RenalTech predictive algorithm to support an earlier CKD diagnosis and staging, as well as for monitoring of treatment and disease progression.

Mitzi returned to the clinic 3 weeks later for reassessment of her SDMA and creatinine levels. Although Mitzi’s creatinine was at the upper end of the normal laboratory reference range, she was diagnosed with IRIS stage 2 CKD based on interpretation of both her creatinine and SDMA levels. Studies have documented that, unlike serum creatinine levels which decline with muscle wasting, SDMA levels remain unaffected by this age-related change and are more highly correlated with glomerular filtration rate than serum creatinine.⁸

Mitzi’s isosthenuria, proteinuria, and hypertension were also supportive of kidney dysfunction and helped substage her CKD (ie, borderline proteinuric, hypertensive) and individualize her treatment plan moving forward. Before attributing her proteinuria and hypertension to kidney disease, it was crucial to rule out the presence of other comorbidities such as endocrine disease (eg, hyperthyroidism, diabetes mellitus) and lower urinary tract disease (eg, UTI, urolithiasis) that could also cause these abnormalities.

By utilizing both RenalTech and SDMA technologies, Mitzi was appropriately diagnosed with IRIS stage 2 CKD earlier than if her diagnosis had relied on creatinine alone. Mitzi was started on a renal therapeutic diet and an antihypertensive medication. It was recommended that Mitzi return in 2 weeks for repeat diagnostics to monitor her response to treatment and allow for additional medication adjustments.

Incorporating both RenalTech and SDMA technologies allows veterinarians to provide early care and recommendations for patients with CKD. RenalTech can help shape the approach to CKD in cats from a reactive perspective to a proactive one; by using and interpreting more than traditional serum BUN and creatinine levels, patients are able to be diagnosed with CKD sooner and receive individualized treatment plans that are tailored to their unique health status.² RenalTech can help improve owner confidence and compliance, ultimately leading to improved patient care and outcome. As early care strategies continue to emerge, the outlook for CKD continues to improve.

Meniscal injury in dogs and cats primarily occurs secondary to stifle instability resulting from cranial cruciate ligament (CCL) rupture.^7-18 Isolated meniscal tears are rare and may be more likely to occur secondary to trauma or in canine athletes; a limited number of these cases have been reported.^8,10-12 CCL rupture is the most common cause of pelvic limb lameness in dogs, and ≥85% of dogs—and 67% of cats—with CCL rupture have been reported to have meniscal tears diagnosed at the time of surgery.^12,13 Postoperatively, meniscal tears can also occur secondary to persistent stifle instability and have been reported in 0.7% to 27.8% of dogs, with the lowest rates generally following tibial plateau leveling osteotomy (TPLO) surgery and the highest rates generally following tibial tuberosity advancement surgery.^15-18

Spayed/neutered, older, and obese dogs, as well as certain breeds (eg, rottweilers, Newfoundlands, Staffordshire terriers), have been shown to have a higher risk for CCL rupture.^19,20 Specific risk factors for the development of meniscal tears after CCL rupture include increased stifle instability, increased duration of lameness, increased weight, and older age.^21-23

Although there are 2 menisci in the stifle joint, >96% of meniscal tears occur in the medial meniscus alone.^{1,2,4,13,15,16,24} This is secondary to anatomic differences between the medial and lateral menisci. Both menisci are attached cranially to the tibia, but the medial meniscus is more closely associated with the tibial plateau because of its firm attachment at the medial collateral ligament, peripheral attachment to the joint capsule, and primary caudal attachment to the tibia at the meniscotibial ligament. The lateral meniscus lacks an attachment at the collateral ligament, has looser capsular attachments, and has its primary caudal attachment on the femur versus the tibia. When the CCL is ruptured (Figure 1), the femoral condyles translate caudally during weight-bearing, leading the lateral meniscus to translate caudally with the lateral femoral condyle. The medial meniscus, which is more firmly attached to the tibia, is then crushed by the medial femoral condyle when it translates caudally. Excessive rotational forces in the stifle, either from CCL rupture or supraphysiologic loads, can also lead to meniscal injury.^8,25,26 Tears may be partial or full thickness through the meniscus.

The caudal pole region between the medial collateral and meniscotibial ligaments is the most commonly injured portion of the medial meniscus. Common configurations include vertical longitudinal (ie, bucket handle) tears, maceration of the caudal pole, peripheral capsular detachment, and radial tears. The most clinically relevant tears are medial meniscal; however, 77% of arthroscopically evaluated dogs with CCL rupture had some degree of damage to the lateral meniscus.^24,25,27 Lateral meniscal tears tend to be radial or longitudinal and, although the clinical significance is unclear, a recent report found significant cartilage lesions associated with isolated lateral meniscal tears in dogs, suggesting that there is a negative impact on joint health.^12,24

Dogs and cats with meniscal tears are typically presented with chronic or acute pelvic limb lameness that is often only partially alleviated with conservative management (including NSAIDs and rest); CCL rupture may or may not have been previously diagnosed, and stifle surgery for CCL rupture may have been previously performed.^{10,11,24,28-30} Development of a meniscal tear is typically associated with sudden worsening of lameness in patients that were previously diagnosed with CCL rupture or a new onset of lameness in dogs that have previously undergone surgery for CCL rupture.^17,18,24 The presenting lameness is often more severe in dogs that have CCL rupture and meniscal tears as compared with dogs that have only CCL rupture; it is not uncommon for this to be nonweight-bearing lameness.^22,23 Some owners report hearing a popping or clicking sound when their pet is ambulating. Meniscal injury should be a differential diagnosis for dogs that have had stifle surgery for CCL rupture and are presented with subtle or acute profound lameness or have poor clinical recovery after surgery.^{15,16,22,24,30}

Because meniscal disease primarily occurs in conjunction with CCL rupture, clinical findings support both conditions. Orthopedic examination often reveals partial to nonweight-bearing pelvic limb lameness and variable amounts of musculature atrophy on the affected pelvic limb.^8-11,22,23 Palpation of the stifle joint can reveal periarticular thickening and palpable joint effusion.^9,11,18 Stifle range of motion may be decreased secondary to pain or periarticular fibrosis in the case of chronic disease. Pain with flexion of the stifle joint is an indicator of meniscal injury in some cases.^11,23 Approximately 28% to 38% of dogs with meniscal injury have an audible popping sound (ie, meniscal click) during flexion and extension of the stifle that occurs when the medial femoral condyle slides up and over the caudal pole of the medial meniscus.^8,23,24,31 Dogs with meniscal tears are often positive for cranial drawer motion and tibial thrust secondary to CCL rupture.

Clinical history and orthopedic examination are key to diagnosing meniscal injury, but diagnosis cannot be confirmed using only these methods. Orthogonal radiography of the affected stifle joint can be used to evaluate the presence and severity of osteoarthritis and can help rule out other pathologies (eg, osteochondritis dissecans, fracture, neoplasia) of the stifle. In dogs with CCL rupture and possible meniscal injury, osteophytosis, increased soft tissue opacity in the joint space (ie, joint effusion), and increased soft tissue opacity on the medial aspect of the joint (ie, medial buttress) are commonly seen on radiographs (Figure 2); however, it is possible to see little to no osteoarthritis in acute injuries. The meniscus cannot be directly visualized on radiographs and identification of meniscal tears is limited, even with computed tomography arthrography.^32,33 A skilled ultrasonographer may be able to identify some tears in the meniscus^34-37; however, MRI is a more readily available and reliable, noninvasive method to evaluate the presence of meniscal tears.^37-40

Surgical exploration of the stifle joint is typically used to identify tears in the meniscus. The most accurate method for diagnosing a meniscal tear is joint evaluation by arthroscopy or arthrotomy, combining visual evaluation and careful palpation of the meniscus with a meniscal probe.⁴¹ A stifle distractor or Hohmann retractor may be necessary to facilitate adequate access to inspect the caudal portions of the joint (Figure 3). Both menisci should be carefully evaluated to identify all damaged regions.⁴¹ Failure to identify and treat meniscal tears is a common cause of poor function following surgery for CCL rupture.^24,30,41,42

Because there is poor blood supply to the menisci, meniscal tears are unlikely to heal on their own, and surgery should be the primary treatment. Surgical treatment usually involves removing the torn portion of the meniscus; however, it may be possible to repair specific meniscal tears located in the outer 25% of the meniscus where the blood supply is better.¹⁴ Better success with meniscal repair or regeneration in dogs and cats is possible in the future.^42,43

Treatment for meniscal tears depends on the tear location and severity.^14,24,28-30 If the entire caudal pole is damaged, it should be removed via caudal pole hemi-meniscectomy.⁴⁴ If only the inner rim of the caudal pole is damaged, a partial meniscectomy (ie, removal of the damaged inner rim), leaving the periphery intact and possibly preserving some of the function of the meniscus (Figure 4), can be performed. The normal meniscus is generally left in situ.

If there is instability of the stifle secondary to CCL rupture, surgery to stabilize the stifle is indicated following treatment of the meniscal tear. Common methods of stabilizing a CCL-deficient stifle include TPLO, lateral fabellotibial suture, and tibial tuberosity advancement. The potential risks and benefits of performing a meniscal release—in which the medial meniscus is transected to allow more movement of the meniscus—are debated. This procedure can reduce, but not eliminate, the chance of meniscal tears postoperatively; however, it changes the contact mechanics in the stifle joint, subsequently reducing stability and causing osteoarthritis.^41,45,46 Physical rehabilitation can improve the speed and extent of recovery postoperatively and may have long-term benefits.^47,48

Because dogs and cats can develop progressive osteoarthritis and decreased stifle range of motion secondary to meniscal injury, ongoing medical therapy with weight management, joint supplements, physical rehabilitation therapy, and pain medication may be needed.^12,49,50 After TPLO surgery, dogs fed a protein-rich omega-3 fatty acid diet were shown to have increased limb use as compared with dogs fed a standard adult diet.⁵¹

Surgical removal of the torn meniscus often results in rapid resolution of pain and lameness.^{11,15,24,28,29} The long-term functional outcome can be variable depending on the preoperative disease state of the joint and the surgical procedure performed to address the concurrent CCL disease, if applicable. TPLO currently has the best evidence supporting the ability of dogs to consistently return to normal clinical function and the lowest reported rate of postoperative meniscal tears.^17,52 Although removing the torn meniscus can change biomechanics in the stifle joint and cause osteoarthritis, a difference has not been seen in the functional outcome between dogs with TPLO treated with and without meniscectomy for CCL rupture.^28,29

Meniscal tears are common in dogs and cats with CCL rupture and can occur rarely as isolated events. Incidence increases with increased stifle laxity and chronicity of CCL rupture. Radiography and orthopedic examinations alone are not sensitive enough to diagnose meniscal injury. MRI or surgical joint exploration using arthroscopy or arthrotomy with meniscal probing can confirm diagnosis. Meniscal tears are commonly treated with surgical debridement; concurrent surgical stabilization of the CCL-deficient stifle is advised. Although the postoperative outcome for meniscal injury is typically good, stifle osteoarthritis may require ongoing management.

Tucker, a 6-year-old, 56.9-lb (25.8-kg) neutered male German shepherd crossbreed, was presented for vomiting and lethargy of 24 hours’ duration. A distal jejunal foreign body was suspected on abdominal radiographs and confirmed with exploratory laparotomy. Enterotomy was performed without complication. Cefoxitin (22 mg/kg IV) was administered 30 minutes before surgery and again every 90 minutes until surgery was complete.^1-4 Postsurgical antimicrobial administration was deemed unnecessary because the bowel was healthy and intact at the foreign body site, and there was no abdominal contamination by GI material.^5,6 Tucker recovered uneventfully and was discharged after 48 hours. Five days later, the owners noticed purulent discharge at the surgical incision site. He was also reported to be progressively lethargic and anorexic, although vomiting had not been observed.

Tucker was returned 7 days postoperatively for assessment of the abdominal incision.

On presentation, Tucker was quiet but alert and responsive. Vital signs were normal except for an elevated rectal temperature (103.3°F [39.6°C]). CBC and serum chemistry profile were unremarkable other than mild leukocytosis (15.3 × 10⁹/L, reference range 5.0-14.1) characterized by mature neutrophilia (13.0 × 10⁹/L, reference range 2.9-12.0).

Examination of the surgical incision showed generalized erythema, pain and heat on palpation, and purulent discharge and dehiscence of the wound at the cranial aspect (Figure 1). A point-of-care sonogram revealed scant abdominal fluid consistent with a postoperative procedure. Surgical exploration of the wound was recommended.

Tucker was placed under general anesthesia, and sterile wound preparation, debridement, and exploration were performed. Tissue devitalization and necrosis were noted to extend subcutaneously with involvement of the superficial abdominal musculature, leading to a diagnosis of deep surgical site infection (SSI).^3,7

Sharp debridement of necrotic tissue, thorough lavage with sterile saline, and a deep tissue swab were performed for cytology, which revealed gram-positive cocci and gram-negative rods. A small portion of the deep tissue was also excised for culture and susceptibility testing.

Open wound management was performed with twice-daily, medical-grade honey dressings. Enrofloxacin (10 mg/kg IV) and ampicillin (20 mg/kg IV) were administered based on cytology results and the anticipated spectrum of activity against gram-positive cocci and gram-negative bacilli. Drug therapy was transitioned to amoxicillin/clavulanic acid (20 mg/kg PO every 12 hours) and enrofloxacin (10 mg/kg PO every 24 hours) after surgical recovery. Following initiation of local wound management and antimicrobial therapy, Tucker showed evidence of clinical improvement with a reduction in periwound erythema and exudative discharge. Broad-spectrum antimicrobial therapy is recommended while waiting for culture and susceptibility testing results; antimicrobial de-escalation is encouraged (see Discussion) after results are received.⁸

Culture results (Table 1) obtained 2 days after Tucker was readmitted revealed an SSI with evidence of methicillin-resistant Staphylococcus pseudintermedius, extended spectrum β-lactamase–producing Enterobacter cloacae, and Enterococcus faecalis. S pseudintermedius is the leading cause of SSI in dogs with methicillin resistance; this is an increasing concern in veterinary medicine and highlights the need for prudent antimicrobial use.⁹ Decisions to change antimicrobials should be made based on culture and susceptibility results in conjunction with the patient’s clinical signs.¹⁰ Antimicrobial de-escalation (ie, enrofloxacin continued; amoxicillin/clavulanic acid discontinued) was warranted based on reported susceptibility of the isolated methicillin-resistant S pseudintermedius and E cloacae. Despite the intermediate susceptibility of S pseudintermedius to enrofloxacin, this was considered an appropriate antimicrobial choice given Tucker’s clinical improvement. Enterococcus spp were not targeted because they are not commonly true pathogens, although they are commonly isolated.¹¹ 

Antimicrobial therapy was continued for 5 days until the wound was clean and dry, the periwound erythema was resolved, and a healthy bed of granulation tissue was observed. Delayed secondary closure of the wound was performed without any complications.

The incision was completely healed when Tucker was presented 2 weeks after discharge for suture removal. This case demonstrates that, with appropriate and timely intervention, the prognosis for complicated SSI can be good to excellent.

There are many risk factors for development of SSI; however, key factors include time of clipping prior to surgery, duration of anesthesia and surgery, comorbidities, surgical wound classification, and appropriate perioperative antimicrobial administration.^1,3 To minimize the risk for SSI, perioperative administration of antimicrobials should be timed so that bactericidal concentrations reach the appropriate tissue at the time of incision and throughout the duration of the procedure.¹² 

Standard SSI definitions are critical for accurate diagnosis and play an important role in surgical site surveillance programs.⁷ Active surveillance programs allow monitoring for SSI and trending of procedures with which SSI is commonly associated. Clear guidelines have been established in human medicine and subsequently adopted in veterinary medicine (Table 2).^3,7

Accurate diagnosis of SSI relies on an appropriate sampling technique.¹ It is preferable to perform deep tissue sampling away from active draining tracts that are likely to be contaminated with skin commensals. This can be achieved using standard wound swabs, by aspirating deep tissue, or surgically (Table 3), depending on the patient. Flocked swabs (vs traditional cotton-tipped swabs) can be used to maximize sample collection and results, particularly if the yield is expected to be low.¹³ Sampling should ideally occur prior to antimicrobial administration; however, if this is not practical, antimicrobials can be withheld for 24 hours prior to sampling, or the sample can be obtained just prior to when the drug is given next.¹⁴

Local wound management is significant in managing SSI and is important for effective treatment.¹⁰ Surgical intervention may not be necessary in patients with a first-time, superficial SSI that does not have extensive tissue involvement. Normal wound management practices should be applied and aimed at improving the local environment to favor healing. No strict criteria exist for surgical debridement use in the management of SSI, and clinician discretion is required. However, further exploration should be considered in severe, recurrent, or chronic infectious processes.¹ Repeated debridement may be necessary, as bacterial biofilms can rapidly recover (in ≈24 hours) and prove highly resistant to systemic antimicrobial therapy.¹

Cytology should be performed in all SSI patients and should be compared with culture results to help determine relevance. Consideration of culture results should be based on whether isolates are common causes of infection, resident organisms at the site, or common contaminants. Consideration should also be given to the clinical response to initial antimicrobial treatment.

Antimicrobial de-escalation generally refers to a reduction in the spectrum of administered antimicrobials. Although no specific recommendations exist, studies have shown that antimicrobial de-escalation is not associated with poorer outcomes.⁸ Because it is expected to improve antibiotic resistance profiles and reduce antibiotic-related adverse events, antimicrobial de-escalation should be recommended in all cases when possible.⁸ Culture results are essential in effective de-escalation strategies and for improving patient outcomes through reducing inappropriate antimicrobial selection.^11,15 Tissue culture should be performed in all patients with suspected SSI, except those that have sporadic superficial SSI that can be managed with local therapy alone.¹⁰