Determining whether to collect a specimen and which diagnostic tests are necessary should be the first step. Although culture is useful in most situations, sampling for culture is less important (or should be avoided) in cases for which systemic antimicrobial therapy is not likely needed, a proper representative sample cannot be collected, contamination is likely, or sampling may compromise unaffected sites.

Bacterial culture is useful when the disease process is unclear and/or when systemic antimicrobials are to be used. Culture is particularly important when there is a greater likelihood that resistant pathogens are involved, such as infections that have failed empiric treatment or infections in patients with a history of antimicrobial treatment and/or hospitalization.

Although culture is often the focus of wound sampling, cytology should be considered whenever a specimen is being collected for culture. A specimen should always be submitted for cytology, which can be useful to confirm the presence of bacterial infection, rule out other causes, corroborate culture results, or identify fastidious organisms. Beyond routine aerobic culture and cytology, additional testing may be indicated in some situations, particularly chronic infections, infections that have not responded to appropriate treatment, and infections that are clinically atypical. This could include addition of special stains (eg, acid-fast, periodic acid–Schiff) or fungal culture. Anaerobic culture may be indicated in infections potentially associated with a penetrating wound or those that have a clinical appearance suggestive of anaerobic infection (eg, emphysematous tissue).

When possible, tissue samples should be collected for culture. Although more invasive than fine-needle aspirates or swabs, tissue samples can have a higher sensitivity and specificity, particularly with deeper infections in humans.^1,2

Fine-needle aspiration can be performed on deeper sites and are preferred over superficial swabs of draining tracts. The small volume collected and small area of the site sampled can limit sensitivity. Ideally, ≥2 samples should be collected, as positive results from >1 sample provide more convincing information of the clinical relevance of an isolated bacterial species.

Swabs are typically easier to collect and can be useful in many clinical situations. When performed properly, swabs are more prone to isolation of contaminants but yield fairly similar results as compared with other methods.³ Although tissue biopsy should be performed when possible, the following discussion focuses on collection of swabs, as this is the most common approach. Important concepts for wound sampling are presented in Important Considerations when Collecting a Specimen from a Wound.

Flocked swabs should be used when available, as they recover bacteria from infected sites as well as cotton- or rayon-tipped swabs but are more effective at releasing recovered bacteria into the culture medium.⁴

A properly collected swab often appears relatively clean, with only some blood-tinged fluid present (Figure).

Of note, fungal culture can be considered in any case, but fungal infections are uncommon. Fungal culture is more important in infections that do not respond as expected to antimicrobials, in infections with unusual clinical presentation or progression, or when cytology suggests fungal involvement.

Loss of viability (ie, false negatives) and contamination (ie, false positives) are of concern. Swabs for culture should be placed in an appropriate transport medium. Most commercial culture swab sets are effective at preserving viability of aerobic bacteria for the time typically required for a sample to reach the diagnostic laboratory. Anaerobes are more prone to death during transit, and either anaerobic transport media or combined aerobic/anaerobic transport media should be used if anaerobic culture is to be performed.

Swabs should be stored at room temperature if they will be processed by the laboratory within 2 hours. However, this will be difficult in most clinical situations; when delays will be encountered, swabs should be stored at refrigeration temperature (39°F [4°C]) until shipping and kept cool during shipping. Slides for cytology should be prepared immediately after collection. Ideally, the same swab should not be used for both cytology and culture, as contamination could occur while the swab is being rolled on a slide and preparing the cytology slide will remove some of the bacterial biomass.

Despite the use of optimal techniques, sampling will never be 100% sensitive and specific, and laboratory error (both technical error and abnormal behavior of bacteria in vitro) can occur. Any culture result must be carefully interpreted, with consideration of the body site, common pathogens, sample type, and the organisms that were isolated. Mixed infections can occur but are probably uncommon. Isolation of multiple organisms should be approached with caution, as one (or all) could be a contaminant. Although many commensals are opportunistic pathogens, isolation of bacteria that are common members of the commensal microbiota and typically of limited virulence (eg, coagulase-negative staphylococci, enterococci) is typically not clinically relevant.

When determining whether an isolated bacterium is likely clinically important, antimicrobial resistance is irrelevant. Resistance and virulence are different, and a multidrug-resistant bacterium is not more likely to be clinically relevant than a susceptible counterpart. Therefore, the bacterial species, infection site, and degree of bacterial growth—not the susceptibility pattern—should be considered.

Assemble all required supplies. Determine the degree of physical or chemical restraint that is necessary for proper sample collection.

Irrigate the wound with sterile saline (A). Debride any existing necrotic tissue. Then, using gauze, remove excess saline from the site (B), leaving a clean wound bed devoid of pus, debris, or necrotic tissue for sampling (C). If possible, let the site dry for ≈1 minute.

Replace gloves if they are contaminated and/or wet. Remove a sterile swab from its packaging, taking care not to contaminate it via contact with other surfaces. Rub the swab back and forth over ≈1 cm³ of viable tissue in the affected area for ≈5 seconds, taking care to avoid contact of the swab with sites that have a commensal microbiota (eg, skin and mucous membranes). Apply pressure to the swab to help express fluid from the wound bed.

For culture specimens, place the swab into a transport medium and label the tube. Keep the swab at room temperature if it will be processed within 2 hours; otherwise, refrigerate the swab. Complete the laboratory submission form; include the specific sample location.

For cytology, roll a second swab onto a glass slide. Label the slide and allow it to air dry.

Indicate the swab site, disease process, species (along with any other relevant information), and patient history of antimicrobial therapy on the laboratory submission form.

• Acute pancreatitis
• Acute tumor lysis syndrome
• Artifactual hypocalcemia
  • EDTA or citrate contamination of serum sample
• Critical illness (likely multifactorial), including sepsis
• Drug-induced effect
  • Bicarbonate infusion
  • Bisphosphonates
  • Enrofloxacin
  • Furosemide
  • Phosphate enema
  • Tetracyclines
• Eclampsia
• Ethylene glycol toxicity
• Hyperthyroidism
• Hypoalbuminemia (most common cause)
• Hypomagnesemia
• Massive blood transfusion (excessive citrate)
• Medullary thyroid carcinoma (increased calcitonin)
• Metabolic (eg, secondary to protracted vomiting) or respiratory (eg, hyperventilation) alkalosis
• Postsurgical correction of primary hyperparathyroidism or hyperthyroidism
• Primary hypoparathyroidism
• Protein-losing enteropathy
• Renal secondary hyperparathyroidism
  • Chronic or, less commonly, acute renal failure
• Secondary hyperparathyroidism due to nutritional (eg, vitamin D) deficiencies
• Severe rhabdomyolysis or soft tissue trauma
• Snake envenomation
• Urethral obstruction
• Vitamin D-resistant rickets (types I and II)

On examination, Marcus was tachypneic with a respiratory rate of 60 bpm and a mild increase in expiratory effort. His heart rate was 144 bpm, mucous membranes were pink, and pulses were strong and synchronous. His temperature was mildly elevated at 103.2°F (39.6°C). On auscultation, heart and lung sounds were normal on the right side but decreased on the left. The remainder of the examination was unremarkable.

Right lateral thoracic radiographs revealed a large amount of fluid/soft tissue opacity obscuring the cardiac silhouette. Ventrodorsal radiographs showed increased soft tissue opacity in the left hemithorax, primarily in the cranial and middle lung fields. A mild interstitial pattern, a pleural fissure line, and border effacement of the heart were noted in the left hemithorax (Figure 1).

Radiography findings suggested a combination of pulmonary and pleural space disease. Differential diagnoses included pleural effusion (eg, hemothorax, pyothorax, chylothorax, hydrothorax, neoplasia) and pleural space mass or mass effect (eg, neoplasia, lung lobe consolidation or torsion, abscess/granuloma).

CBC, serum chemistry profile, venous blood gas, urinalysis, and coagulation panel (prothrombin time, activated partial thromboplastin time) results were within normal limits.

Pleural effusion was confirmed via thoracic ultrasonography, and therapeutic thoracocentesis was performed; 650 mL of serosanguinous fluid was removed from the left side (Figure 2) and 150 mL from the right side. Packed cell volume and total solids of the fluid were 4% and 3.5 g/dL, respectively, and cytology demonstrated a chronic hemorrhagic, neutrophilic, and histiocytic inflammatory exudate with mesothelial cell hyperplasia, suggesting inflammation without overt evidence of infection or neoplasia.

Radiographs obtained after thoracocentesis demonstrated improved pleural effusion and consolidation of the left middle lung lobe (Figure 3). Based on the soft tissue bulge near the hilum and the air bronchocram extending cranially, the primary differential was lung lobe torsion (LLT). Other considerations included pulmonary mass, abscess, or granuloma.

CT demonstrated bilateral moderate pleural effusion with an abnormal appearance of the left cranial lung lobe, stippled gas collections, and truncation of the bronchus that suggested LLT (Figure 4).

Left lateral thoracotomy revealed LLT in the caudal portion of the left cranial lung lobe, and a lung lobectomy was performed. A 20 Fr thoracostomy tube and pleural catheter were placed for postoperative recovery, monitoring, and pain control (Figure 5). Two days postoperation, the amount of pleural effusion aspirated from the thoracostomy tube was still significant in quantity (72 mL/kg/day) and off-white in color (Figure 6). The fluid was confirmed to be chylous effusion based on cytologic examination results (ie, lipid droplets, moderate numbers of mature lymphocytes, and a few macrophages) and paired serum (95 mg/dL) and effusion (819 mg/dL) triglyceride levels.

Fluid continued to be produced in large quantities over the next week, with a plateau at >30 mL/kg/day. Treatment options discussed with the owner included medical management, placement of a long-term SC pleural port, and surgery. Surgery was elected, and pericardiectomy, thoracic duct ligation, and ablation of the cisterna chyli were performed.

Marcus did well during the second surgical procedure; chylothorax resolved quickly, and he was discharged after 3 days. His condition was reported as normal 3 years after the procedure.

LLT can be idiopathic or secondary to pleural effusion, other pulmonary or pleural space disease, trauma, or thoracic surgery.^1,2 Deep-chested, large-breed dogs (especially Afghan hounds) and certain small-breed dogs (eg, pugs) have been reported to have a higher occurrence of LLT.^1-6 Lobectomy of the affected lung lobe is the treatment of choice for LLT. Previously, survival rates were 50% to 78%^1,2,6; however, more recent studies report a survival-to-discharge rate of 92%.⁴ 

Chylothorax can occur secondary to intrathoracic pathology that causes obstruction of the thoracic duct and normal lymph flow. Common causes include granuloma, trauma, congenital abnormalities of the thoracic duct, diaphragmatic hernia, cardiac disease, thoracic surgery, and intrathoracic neoplasia.^7,8 Although the underlying cause of chylothorax should be treated, a primary cause (ie, idiopathic chylothorax) is not identified in many cases.⁷

Chylothorax is a common pre- and postoperative finding with LLT.^1,2-5,9 Pleural effusion is thought to increase the risk for LLT, and chylothorax that develops after lung lobectomy may be caused by trauma to the thoracic duct during surgery or pleuritis from LLT, which alters lymphatic flow.^1,2,9 When LLT is diagnosed and pleural effusion is present, presurgical serum and fluid triglycerides should be tested to diagnose chylous effusion, as chyle may not always have a milky appearance, and the presence of chylothorax may warrant additional surgical procedures at the time of lung lobectomy.⁵

Several therapeutic options are available for idiopathic chylothorax.^10-16 Medical options include feeding a low-fat, medium-chain triglyceride diet and administering rutin (a benzypyrone) with or without octreotide (a somatostatin analog). Medical therapy alone has a low success rate (eg, 40%).^10-12 Surgical options include ligation of the thoracic duct, subtotal pericardiectomy, and cisterna chyli ablation. Success rates of 53% to 88% have been reported when these surgical procedures are used in combination.^10,13-16 Other surgical procedures with variable success rates have also been reported, including thoracic omentalization, pleurodesis, placement of pleuroperitoneal or pleurovenous shunts, and placement of permanent pleural space catheters for intermittent evacuation of fluid.^10,13-16

Clinical history and physical examination findings are helpful in establishing differential diagnoses. For example, a young cat with weight loss and hyperproteinemia is more likely to have an inflammatory effusion from FIP than from a neoplastic process. Likewise, an older large-breed dog with acute collapse and a large splenic mass is more likely to have hemorrhagic effusion from a ruptured hemangiosarcoma than from a transudate associated with hyperadrenocorticism.

Typically, only several milliliters of fluid are present in the thorax, abdomen, and pericardial sac in dogs and cats. The fluid is clear, colorless, and minimally cellular (<3 × 10⁹ cells/L) with a relatively low total protein concentration (<2.5 g/dL).¹ There is some variability in classifying effusions, and several schemes and algorithms are presented in the literature.^1,2 Recent classification schemes have simplified effusion categories into low-protein transudates (<2.5 g protein/dL and <3 × 10⁹ nucleated cells/L), high-protein transudates (≥2.5 g protein/dL and <3 × 10⁹ nucleated cells/L), and exudates (≥2.5 g protein/dL and ≥3 × 10⁹ nucleated cells/L).¹ A hemorrhagic effusion is suggested if the fluid packed cell volume is ≥25% that of the peripheral blood or if >0.5 × 10¹² RBCs/L are present.^1,3 Neoplastic processes can be associated with any fluid type, emphasizing the importance of microscopic evaluation.

Examples of the types of cells that occur in effusions are included in this image gallery.

Ischemic dermatopathy is composed of a heterogenous group of vasculopathic syndromes with indistinguishable clinical and histopathologic appearances. The underlying pathology for any of the syndromes in this heterogenous group is a process by which immunologic damage is directed against vessel walls. Ischemic dermatopathy appears clinically as alopecia with crusting and postinflammatory hyperpigmentation or depigmentation. In more advanced cases, erosions and ulcers are present, particularly over bony prominences. Treatment is variably successful and has traditionally included pentoxifylline and vitamin E ± immunosuppressive therapy (eg, corticosteroids, modified cyclosporine).

This article describes 4 cases of canine ischemic dermatopathy; all dogs were <1 year of age, and diagnosis was made based on signalment, clinical presentation, and/or histopathologic changes. Three of the 4 dogs were littermates, and skin biopsies were performed on only 1 of these 3 dogs.

One dog required daily prednisolone (initial dose, 2.4 mg/kg every 24 hours) despite concurrent treatment with modified cyclosporine (5 mg/kg every 24 hours). In this patient, the cyclosporine dose was progressively increased (≤13 mg/kg every 24 hours) for over a year, with only poor clinical improvement observed; cyclosporine was then replaced with mycophenolate mofetil (16 mg/kg every 12 hours). Although clinical improvement was observed with mycophenolate mofetil, severe diarrhea developed. Mycophenolate mofetil was discontinued for 14 days then reinstituted at a lower dose; however, diarrhea reoccurred. Treatment was modified to include prednisolone (0.4 mg/kg every 24 hours) and oclacitinib (0.6 mg/kg every 12 hours), and disease was eventually well controlled with oclacitinib (0.5 mg/kg every 24 hours).

Cases 2, 3, and 4 were littermates that experienced disease control only when receiving modified cyclosporine (≤8.5 mg/kg every 24 hours) and prednisolone (≤0.8 mg/kg every 24 hours). Complete remission was achieved with administration of oclacitinib (0.5-0.7 mg/kg every 12 hours) and prednisolone (0.5-1 mg/kg every 24 hours) for 30 days. The prednisolone dose was tapered and eventually discontinued; lesions remained in complete or near full remission with monotherapy of oclacitinib (0.2 mg/kg every 24 hours in 1 dog, 0.4-0.6 mg/kg every 12 hours in 2 dogs).

Key pearls to put into practice:

Canine ischemic dermatopathy—except for vaccine-associated ischemic dermatopathy—is either genetic (eg, dermatomyositis) or idiopathic in origin.

Initial therapy with immunosuppressive doses of prednisolone with or without concurrent immunosuppressive agents (eg, modified cyclosporine, mycophenolate mofetil) is typically required for treating generalized ischemic dermatopathy.

Monotherapy with oclacitinib may be another treatment option for dogs affected by ischemic dermatopathy.

This prospective cohort study sought to evaluate whether the use of focused cardiac ultrasonography (FCU) performed by nonspecialist clinicians would improve the detection of occult heart disease in cats. Nonspecialist clinicians received FCU training via class, video, and hands-on practice. Cats (n = 289) were evaluated by a nonspecialist clinician via physical examination, which was sequentially followed by ECG, FCU, and point-of-care N-terminal proB-type natriuretic peptide assay. A board-certified cardiologist then conducted an evaluation of each cat, and levels of agreement between the nonspecialist clinician and specialist diagnoses were evaluated. Agreement between nonspecialist clinicians and cardiologists was increased significantly after FCU, particularly in cases of moderate and marked heart disease. It was determined that FCU is a feasible, helpful tool for nonspecialist clinicians, and further investigation of this technique is warranted.

Intestinal flora contributes to several protective and homeostatic mechanisms in the body; alterations to these microbial communities can contribute to systemic inflammation and disease.¹ Diabetes mellitus is a common endocrinopathy in middle-aged to older cats, with a complex pathophysiology that often involves insulin resistance and β-cell dysfunction and injury, culminating in progressive loss of insulin-secreting ability.

In this study, the enteric microbial compositions of 82 cats (23 diabetic; 24 lean and 15 overweight, nondiabetic) were described and compared. The authors also assessed the impact of a 4-week, high-protein, diabetic-formulated diet change on microbial composition in a subset of these cats (11 diabetic; 12 lean and 13 overweight, nondiabetic).

Breed, age, and sex were not found to influence enteric microbial composition. Similarly, no differences in microbial composition were found between lean and obese cats. However, as compared with lean cats, diabetic cats were found to have reduced microbial richness (ie, number of gut microbial genes), gut microbial diversity, and bacteria able to produce the short-chain fatty acid butyrate, a known energy source for colonic epithelial cells and a factor in intestinal glucose and insulin regulation. Most differences found between these groups were caused by a relative reduction in enteric microbial communities, specifically in diabetic cats as compared with lean cats. In addition, following the 4-week diet trial, diabetic cats maintained a reduced microbial richness and diversity as compared with both lean and obese nondiabetic cats. Lower concentrations of various butyrate-producing bacteria were observed in diabetic cats both before and after the diet trial, with additional predictive models suggesting that the gut microbiota in diabetic cats may have an impaired ability to produce vitamin K. Although vitamin K is a known factor involved in hemostasis, the authors describe its potential additional role in regulating systemic insulin sensitivity.

Of several reported associations between serum chemistry or clinical parameters and enteric microbial composition, the most clinically relevant finding was that serum fructosamine concentrations were negatively correlated with high numbers of gut microbiota of the family Prevotellaceae, which have been associated with improved glucose tolerance, and positively correlated with high numbers of Enterobacteriaceae, a bacterial family associated with low-grade systemic inflammation.

Key pearls to put into practice:

Diabetic cats appear to have relative enteric dysbiosis as compared with healthy lean and obese cats, which could impact diabetes mellitus pathogenesis or, possibly, patient response to management.

Results of blood glucose testing, including serum fructosamine concentrations, may be influenced by a patient’s enteric microbial composition.

High-protein, diabetic-formulated diets appear to increase enteric microbial diversity in nondiabetic cats but do not exert a similar influence in diabetic cats. Further study is needed to determine if other interventions (eg, probiotics) can assist in overcoming this dysbiosis.

Gastric dilatation-volvulus (GDV) is a rapidly progressing, life-threatening condition that affects large-breed, deep-chested dogs. Even with surgical treatment and aggressive care, mortality in GDV cases ranges from 16% to 24%.¹ Elective prophylactic gastropexy can be performed in susceptible dogs to prevent volvulus of the stomach. Gastropexy can be performed laparoscopically, via laparoscopically assisted methods, or via traditional laparotomy. The risk for GDV after prophylactic gastropexy performed using appropriate surgical technique is low, and there are no long-term risks.² Among the many different methods for gastropexy, incisional gastropexy is commonly used and involves making an incision in the pyloric antrum and a right-sided incision in the transverse abdominis muscle caudal to the last rib. The typical length of the incision is 3 to 5 cm, but the optimum length and number of suture strands has not been determined.

In this study, the stomach and abdominal wall of 36 crossbreed hound dogs euthanized for reasons unrelated to the study were harvested, and gastropexy was performed by a single surgeon. The samples were divided into 4 groups: 2-cm incision using 2 sutures, 2-cm incision using 1 suture, 4-cm incision using 2 sutures, and 4-cm incision using 1 suture. All incisions were closed using 2-0 polyglyconate suture on a tapered-point needle. Mechanical testing was performed to assess the load to failure of each gastropexy construct.

Results showed that the load to failure was affected by the length of the incision but not the number of sutures used. Although the 4-cm incision was stronger than the 2-cm incision, the difference was negligible. Clinically, the strength required for safe gastropexy is unknown, so all constructs may be strong enough in a live animal.

Key pearls to put into practice:

Owners should be educated about the need for prophylactic gastropexy in large-breed, deep-chested dogs, as the risk for GDV after gastropexy is low. Prophylactic gastropexy should particularly be considered when spaying dogs or performing abdominal surgery in any at-risk dog.

Using either a 1- or 2-suture line when closing the incision in the pyloric antrum and a right-sided incision in the transverse abdominis muscle should be sufficient for prophylactic gastropexy.

Mechanically, 1- and 2-suture lines were found to be of similar strength; however, if only 1 suture is used and it fails, the entire gastropexy could unravel. Thus, a second suture line can act as potential reinforcement.

Diagnosis of pyelonephritis in cats is usually based on clinical signs, laboratory testing, and ultrasonographic findings, although definitive diagnosis requires positive urine culture obtained via pyelocentesis. MicroRNAs have been studied as biomarkers of renal injury in humans. This prospective case-control study sought to evaluate the presence and stability of microRNAs in cat urine and the discriminatory potential of selected urinary microRNAs for pyelonephritis. Several microRNAs were detected in urine, although storage temperature affected yield. There was upregulation of miR-16 in cats with pyelonephritis, but further research is needed to determine whether this is pyelonephritis-specific, pathogen-specific (ie, Escherichia coli), or both.

Collectively, mast cell tumors (MCTs) are the most common malignant neoplasms diagnosed in dogs, accounting for <≈20% of all skin cancers.¹ Significant clinical and research efforts have been made to better understand the biologic behavior of MCTs, which, in turn, informs clinical prognosis and helps guide treatment options for affected patients.

Although several variables have been evaluated in the prediction of canine MCT behavior,^2,3 histopathologic evaluation remains a cornerstone for assessing whether MCT biology is benign or aggressive and includes histopathologic grade and proliferative indices.^4-6 Although valuable, histopathology alone is an imperfect predictor of MCT biologic behavior, and the synergistic integration of clinical factors, along with pathology, can provide improved MCT biology prediction. As such, correlative investigations can provide actionable findings and should be conducted to identify new—and strengthen previously observed—associations between histopathologic grade and unfavorable clinical variables of the host (eg, breed) and tumor (eg, location). Findings derived from such studies offer opportunities to combine traditional pathology with clinical acumen for the best clinical management practices for canine MCTs.

Over a 15-year period, this retrospective study examined tumor and host variables of dogs that had MCTs. Of 400 MCTs identified, 90 were categorized as having a high histopathologic grade (via the Patnaik, Kiupel, and/or mitotic index classification) and were associated with a variety of tumor and host factors identified through physical examination and owner–clinician communication. Tumor-specific variables included lesion size and anatomic location, and host factors focused on patient signalment (eg, breed, age, sex, neuter status).

Although tumor size was not identified to be associated with a high histopathologic grade, MCTs arising from the inguinal or head regions had an increased risk for having a high histopathologic grade. In addition, MCTs arising from collective “unfavorable” sites, termed PIMP (ie, perineal, inguinal, mucocutaneous junctions, and perianal) locations, were also more likely to have a high histopathologic grade. Of the host factors examined, the shar-pei breed had an increased risk for being diagnosed with histopathologically high-grade tumors. In aggregate, MCT location and patient breed were also correlated with high histopathologic grade pathology findings.

Key pearls to put into practice:

MCTs are common skin cancers that can be benign or malignant.

Histopathology remains the gold standard for disease prognostication but is imperfect and should not be used as a sole predictor of biologic behavior.

This article reviews common causes of nonregenerative anemia in cats and provides a stepwise approach to diagnostic investigation and management. The authors divide differentials into 2 categories for pathologic mechanism. The first category is ineffective erythropoiesis involving conditions impacting bone marrow production of RBCs; this category includes nutrient deficiencies (eg, iron, vitamin B₁₂), infectious diseases (eg, FeLV, FIV), and primary bone marrow disorders (eg, precursor-directed immune-mediated anemia). Conditions outside the bone marrow that can cause nonregenerative anemia (eg, chronic inflammatory states, lack of erythropoietin associated with later stages of chronic renal disease) are also included in this category. The second category is reduced RBC lifespan and includes conditions leading to the premature removal of RBCs from circulation (eg, following oxidative stress or injury).

Nonregenerative anemia involves insufficient numbers of identifiable aggregate reticulocytes in circulation. This is typically defined as an absolute aggregate reticulocyte count of <60,000/μL; however, gradations in regenerative response (ie, strongly, moderately, and weakly regenerative) have been reported based on the absolute reticulocyte number and reticulocyte percentage. The authors stress the importance of assessing reticulocyte counts immediately, as the cells will continue to mature following collection, thereby preventing accurate reticulocyte quantification. Because the differentials list for feline nonregenerative anemia is long, use of an algorithm can help guide diagnostic decisions to minimize unnecessary testing and maximize the chance of obtaining a diagnosis. Minimum database testing as indicated is often followed by more specific investigations (eg, infectious disease screening, assessment for systemic disease [eg, chest and/or abdominal imaging], specific nutrient analysis [eg, iron panel, cobalamin concentration]). If a causative disease is not identified noninvasively, bone marrow aspiration ± core biopsy will likely be necessary.

Treatment is specifically targeted toward the underlying condition diagnosed. This may include supportive therapies for chronic blood loss or supplementation of nutrient or erythropoietin deficiencies. Autoimmune conditions are treated similarly to peripheral hemolytic anemia, with immunosuppressive protocols usually including a glucocorticoid and occasionally requiring a secondary agent. Cats that are hemodynamically unstable should receive blood type evaluation and a packed RBC transfusion.

Key pearls to put into practice:

Due to the diversity of differentials for feline nonregenerative anemia, consideration should be given to primary bone marrow disorders as well as systemic infectious, inflammatory, and neoplastic conditions known to impact RBC production and survival.

A reticulocyte count should be obtained soon after blood sampling to maximize accuracy of the quantification.

Because treatments are often targeted toward a specific causative condition, the diagnostic investigation should be comprehensive and may require assessment of a bone marrow aspiration ± core biopsy.

This study describes a technique for performing regional anesthesia in canine ears, which is particularly important during otoscopy and deep ear flushing. Otoscopic procedures can be painful and require profound sedation or anesthesia. Regional nerve blocks with lidocaine and bupivacaine block sensation to the affected area and allow for decreased anesthetic doses. These blocks may also be useful in dogs undergoing total ear canal ablation and bulla osteotomy. The 2 nerves that provide sensory innervation of the ear canal and pinna are the great auricular nerve and auriculotemporal nerve.

To block the great auricular nerve, the transverse process of the atlas (C1) should be palpated. A 22 g × 3.5” spinal needle is inserted at the skin caudal to C1 and aimed toward the deep fascia at the level of the transverse process of C1. Needle insertion is superficial, with the tip of the needle pointing rostrally. Negative aspiration of blood should be ensured. The total dose is injected in 3 equal amounts along the transverse process as the needle is retracted.

To block the auriculotemporal nerve, the temporomandibular joint (TMJ) is first localized by opening and closing the mouth while palpating the area over the TMJ. After locating the TMJ, a 22 g × 1.5” spinal needle should be inserted perpendicular to the skin toward the TMJ. The needle should be held in contact with the zygomatic arch at the level of the masseteric margin. After negative aspiration of blood is ensured, the drug can be injected.

Lidocaine or bupivacaine can be used. The upper dose limit is 5 mg/kg for lidocaine and 2 mg/kg for bupivacaine. The desired total volume for injection for the great auricular nerve is 0.2 mL/kg; the volume for the auriculotemporal nerve is 0.04 mL/kg. The dose can be diluted with saline to achieve total volume in cases in which the upper limit of the dose prohibits using the desired volume of the drug by itself (eg, in smaller dogs).

Key pearls to put into practice:

Deep ear flushing in dogs with severe otitis can be painful and thus requires significant sedation or anesthesia. The ear blocks described can allow for lower doses to be administered; as a result, recovery can be improved and anesthetic depth can be lighter.

Ear flushing is an underused tool to treat chronic otitis and should be considered in any patient that has chronic otitis or suspicion of otitis media.

Cannabis sativa is a plant that has been used for both medicinal and recreational purposes for centuries. Industrial hemp is the legal term for any strain of Cannabis sativa with <0.3% of Δ-9-tetrahydrocannabinol (THC), and marijuana  is a strain of Cannabis sativa with greater THC content.¹

Cannabis sativa has chemical compounds known as phytocannabinoids and other phytochemicals (eg, terpenes, flavonoids). There are >100 different phytocannabinoids that have been identified and may be present in the different strains of Cannabis sativa.² The amount and type of phytocannabinoids present can be influenced by many factors, such as strain and growing location.³ Two well-known and researched phytocannabinoids are CBD and THC. These phytocannabinoids work in the endocannabinoid system (ECS) of the body, a newly discovered body system.⁴

The ECS is a broad-spectrum system that acts as a modulator or regulator for many different body systems. It is also involved, to some degree, in most basic bodily functions. The overall guiding purpose of the ECS is to maintain a stable state (ie, homeostasis) in each system it is involved in.⁵

Endogenous compounds bind to ECS receptors throughout the body. Several ECS receptors have been identified, but CB1 and CB2 are the most well-known. CB1 and CB2 are G protein-coupled receptors found in the cytoplasm of cells. CB1 receptors are most commonly found  in the CNS, whereas CB2 receptors are primarily associated with immune cells, but both can be found throughout the body. The body synthesizes endocannabinoids, with the 2 best characterized endocannabinoids being anandamide (AEA) and 2-arachidonoylglycerol (2-AG). AEA and 2-AG, both endogenous endocannabinoids, are capable of acting as agonists or antagonists on their corresponding receptors. Phytocannabinoids that are not endogenous but plant-based (eg, CBD, THC) appear to alter the ECS system similarly to AEA and 2-AG either by directly binding to the cannabinoid receptors or through a host of other receptors that regulate body responses (eg, appetite, behavior, inflammation).^6,7 

There are 3 main classifications of hemp oil in the market: isolate, broad-spectrum hemp, and full-spectrum hemp. An isolate is usually described as a product that isolates and contains a single phytocannabinoid, typically CBD. Broad-spectrum hemp oils are a group of extracted isolates like phytocannabinoids, terpenes, and/or flavonoids that are blended together with a carrier oil. Full-spectrum hemp oils contain all of the phytocannabinoid, terpenes, and/or flavonoids that are present in the plant. The “entourage effect” occurs when all of these components are able to work with each other to potentially provide additional or greater benefits than the phytocannabinoids and terpenes could provide individually.²

There are few published studies that have researched the safety, efficacy, and pharmacokinetics of hemp oil in dogs. Ongoing efficacy studies are evaluating hemp oil for possible use for other indications. Because not all hemp oil products are equal, selecting a product from a company with a known history of excellent quality control and assurance is crucial. In a recent study of commercial veterinary hemp products, only 23% (3/13) of hemp oil extracts met the levels stated on the label; the remaining 77% (10/13) either made no label claim or contained less than what was stated on the label.⁸

Additional studies of the pharmacokinetics in both dogs and cats are also being performed at major veterinary universities. Auburn University has been conducting some initial pharmacokinetic research on Chroniquin, a fullspectrum hemp oil product.⁹ This initial pharmacokinetic research on Chroniquin was compared with the published pharmacokinetic data on other veterinary hemp oil products; Chroniquin was shown to provide a longer CBD half-life and higher serum concentrations of CBD 24 hours postadministration as compared with published data on other products, despite some of those products having administration rates up to 5 times higher than that of Chroniquin (2 mg/kg).^10,11 

As the use of hemp oil products increases and more CBD-rich research is published, veterinary healthcare providers should become aware and knowledgeable of CBD products, as well as the laws and regulations regarding the legality of recommending CBD products in their area of practice. Clinicians should also be able to relay to pet owners the importance of selecting a safe, quality product from a trusted company for their pets.

Acute pancreatitis is a common disease in dogs. Severity can range from mild pancreatitis with GI signs to necrotizing pancreatitis that leads to multiorgan failure and death. Early detection of pancreatitis has improved with recently developed diagnostic tests,¹ but these tests are imperfect. In humans, early recognition of the more severe forms of pancreatitis are critical to improving patient outcome, and multiple scoring systems are used.²

This multicenter, retrospective cohort study sought to develop a scoring system based on independent predictors of short-term death (ie, within 30 days) in dogs that had acute pancreatitis (n = 138) and to validate the scoring system in an external population of dogs that had acute pancreatitis (n = 31). In the cohort of 138 dogs, the case fatality rate 30 days after admission was 33%.

Independent risk factors for short-term death identified in this study included presence of systemic inflammatory response syndrome, coagulation disorders, increased creatinine, and ionized hypocalcemia. Using these risk factors, the authors proposed 2 scoring systems: the Canine Acute Pancreatitis Severity scoring system and a simplified version of this system that could be used for a faster calculation.

Key pearls to put into practice:

Secondary causes of acute pancreatitis (eg, foreign body obstruction, neoplasia) should be ruled out via imaging prior to considering primary pancreatitis, as early intervention can impact outcome.

Acute kidney injury evidenced by a rising creatinine value—even if still in the normal range—has been identified as a negative prognostic indicator for many severe illnesses; creatinine should be closely monitored in acute pancreatitis patients.

Frequent re-evaluation of dogs with acute pancreatitis is critical for early recognition of risk factors so that treatment may be altered to improve outcome and provide realistic prognoses.

HSA can develop in any vascular organ or tissue but is most commonly found in the spleen (≈50%), right atrium and/or auricle (≈25%), and skin or SC tissue (≈15%; Figure 1).⁴ Most dogs diagnosed with HSA are geriatric, with a predisposition observed in German shepherd dogs, golden retrievers, and Labrador retrievers.^5-7 Splenic HSA is a common splenic malignancy and is accompanied by life-threatening complications (ie, hemoabdomen and distant metastases).^8-11 The mode of metastatic spread varies for patients with HSA that involves the abdominal visceral organs (eg, spleen, liver, kidneys). Regional dissemination of disease in the abdominal cavity or retroperitoneal space is enabled by the local deposition of tumor cells following primary tumor rupture, but distant metastasis requires hematogenous circulation, vascular entrapment, and successful colonization of detached tumor cells. Common metastatic sites include the liver, omentum, mesentery, and lungs.^7,12 HSA also tends to metastasize to the CNS.^13,14

Although HSA involving visceral organs is typically uniformly malignant, the biologic behavior of cutaneous HSA varies in aggressiveness and depends on the extent of localized (dermal, hypodermal/SC, or muscular) invasion. In dog breeds with short hair and minimal pigmentation, sun exposure (ie, actinic induction) is a risk factor for superficial cutaneous HSA.^15,16 This dermally confined variant of HSA tends to be less aggressive due to lack of subdermal penetration and reduced capacity for establishing distant metastases as compared with HSA that involves deeper adnexal structures (including tissues of the subcutis and muscle).^15,17-21

Many dogs with HSA remain clinically normal for relatively long periods of time (ie, months) during malignant progression. An HSA diagnosis involving visceral organs is often precipitated by sudden life-threatening signs related to hemodynamic collapse following acute, nontraumatic organ rupture and consequent hemoabdomen. In affected dogs that do not experience life-threatening hemorrhage, clinical signs of nonspecific lethargy may fluctuate and an episodic pattern related to intermittent hypovolemia associated with acute third-space blood loss may be exhibited.

Clinical signs are nonspecific and depend on the anatomic location of the primary tumor as well as the magnitude and severity of resultant hemorrhage and hypovolemic shock. Common clinical signs include acute-onset lethargy, weakness, collapse, pale mucous membranes, delayed capillary refill time, tachycardia, cardiac arrhythmias, and poor pulse quality. If blood loss is self-limiting, these hemodynamic perturbations are not imminently life-threatening; clinical signs may be episodic in nature and a full clinical recovery may follow within days. However, when hemorrhage is severe, hemodynamic collapse and sudden death are possible.

A large space-occupying mass may be palpable with visceral organ (splenic or hepatic) HSA. In addition, tumor rupture can result in abdominal distention and ballottement of a fluid wave secondary to hemorrhagic effusion. With cardiac HSA, malignant arrhythmias (eg, ventricular premature contractions), muffled heart sounds, venous congestion (eg, jugular pulses, facial edema, hepatic venous congestion with effusion) associated with right-sided heart failure, and signs compatible with cardiac tamponade may be observed. Primary HSA lesions involving the superficial dermis may appear as well-defined blood blisters. HSA from the SC and IM tissues may appear as large and firm or fluctuant masses (Figure 2); overlying skin may have extensive ecchymosis, swelling, discoloration, and ulceration.

Although HSA can be presumptively diagnosed based on multiple clinical and physical findings and patient signalment, baseline diagnostic tests (see Baseline Diagnostic Tests) should be considered in patients that have probable HSA. Detailed images of HSA lesions arising from visceral organs, SC tissue, and deeper muscle structures can be acquired with advanced imaging modalities (eg, CT; Figure 3).

Definitive diagnosis of HSA requires microscopic identification of tumor cells through cytology or histopathology. Due to the poorly exfoliative nature of mesenchymal tumors coupled with the hemorrhagic nature of HSA, fine-needle aspiration cytology often produces samples of low cellularity with rare identification of malignant cells (Figure 4). Cytologic examination of hemorrhage effusions is not typically helpful or diagnostic for HSA because of the low numbers of neoplastic cells admixed with a large volume of blood. Biopsy is suggested for definitive diagnosis because benign lesions (ie, splenic hematoma) can have clinical presentations (ie, splenic mass with associated hemoabdomen) similar to malignant HSA. Excisional biopsy is preferred because it is diagnostic and therapeutic. All resected tissue samples should be evaluated for histologic features of malignancy and immunohistochemically stained for endothelial markers (eg, CD31).

Effective management of HSA is difficult, as therapeutic options (eg, surgery for cardiac HSA) can be associated with high morbidity, and palliative treatments (eg, radiation therapy) result in only marginal improvements in overall survival times. However, based on the biologic behavior of most HSA cases, comprehensive treatment plans should include a combination of localized and systemic therapeutic strategies except in cases of superficial dermal HSA, which can be treated with surgical resection alone. In patients with cardiac HSA, local treatment performed by a skilled surgeon can be attempted with the aim of resecting or cytoreducing primary tumors that involve the atrium or auricle; however, morbidity (and mortality) can be associated with these interventions. Pericardiectomy may be performed to mitigate the development of cardiac tamponade and associated hemodynamic compromise.^22,23 Ionizing radiation therapy can also be used for localized treatment of SC- or muscle-invasive HSA, in which effective surgical intervention is anatomically infeasible.²⁴ Although localized interventions (ie, surgery, radiation) are frequently palliative in nature and have the potential to control clinical signs associated with hemorrhage and pain, definitive efficacy of these treatment options remains speculative and prospective clinical trials are needed. Splenectomy followed by adjuvant systemic chemotherapy remains the standard of care for splenic HSA. In most anatomic forms of HSA, except superficial dermal involvement, regional and distant metastases can develop rapidly, and most dogs succumb to disseminated disease progression. The highly metastatic nature of HSA has been thoroughly documented in dogs with splenic HSA, in which a median survival time of 1.6 months is expected in dogs treated with splenectomy alone.¹¹

Chemotherapeutic approaches can support a marginally to modestly improved survival time (4-8 months) of dogs with HSA (mostly splenic) treated with systemic, maximum-tolerated-dose chemotherapy, primarily with a doxorubicin backbone protocol. Attempts to identify adjuvant and/or alternative systemic therapies (eg, metronomic chemotherapy, receptor tyrosine kinase inhibitors) to extend survival times have been largely unsuccessful.^12,25-27 Novel strategies that include administration of bispecific drug conjugates, inhibition of β-adrenergic signaling, and chemoimmunotherapy with dendritic cell vaccination and low-dose doxorubicin therapy are promising and under investigation^28-30; however, these strategies are not in mainstream use for dogs with HSA.

Dogs with HSA may also clinically benefit from alternative complementary therapies such as Yunnan Baiyao and a commercially available proprietary polysaccharopeptide (PSP) extract. Yunnan Baiyao has been recently investigated for its potential procoagulant properties.^31,32 In healthy beagles, Yunnan Baiyao has been shown in some studies, but not in others, to increase the strength of blood clot formation as measured by thromboelastography.^31,32 In dogs presented with presumed HSA, Yunnan Baiyao may improve postoperative surgical outcomes but requires future prospective studies to define its role in HSA management. Similar to Yunnan Baiyao, the PSP extract is a mushroom extract believed to act as an immunostimulant and has shown some potential in delaying the onset of abdominal metastases following splenectomy in a small pilot study.³³ Although initial results for the PSP extract are promising, additional and larger prospective studies evaluating its clinical benefit have not been published. The PSP extract’s role in HSA management therefore remains incompletely defined.

Early disease screening and tumor burden monitoring through routine radiography and sonography or molecular diagnostics can provide information on HSA disease status for pet owners and can improve clinical management of initial or recurrent HSA lesions. This is supported by superior survival outcomes in dogs diagnosed with early- versus late-stage disease.^11,34,35 Because HSA rapidly progresses, follow-up examination including blood work and monitoring (via thoracic radiography and abdominal ultrasonography) should be routinely performed, with follow-up scheduled depending on stage of disease, speed of disease progression, clinical signs, and owner compliance. Dogs treated with splenectomy and systemic chemotherapy that remain clinically stable should be re-examined every 8 weeks; this allows for local and/or systemic intervention when recurrent and/or metastatic disease is incipient.

A 12-year-old, 7.9-lb (3.6-kg) neutered male miniature pinscher was emergently presented to a veterinary dental specialist following a dental cleaning at his primary veterinarian. During the dental cleaning, significant periodontal disease bilaterally involving the mandibular first molars had been noted on periodontal probing. Although dental radiography and equipment to section teeth were not available at the primary veterinarian’s clinic, an attempt was made to extract the mobile teeth fully intact. However, both mandibles fractured at the level of the first molars, partially due to bone loss associated with severe periodontitis, and the patient was subsequently referred to the dental specialist.

On presentation to the specialist, the patient had a ventrally deviated mandible due to bilateral fractures. Physical examination findings were otherwise unremarkable; all vital parameters, aside from a BCS of 4/5, were within normal range. The tongue was slightly hanging out of the mouth on the left, and slight drooling was noted from the commissures of the mouth. Oral examination was not possible in the conscious patient due to behavior.

Preoperative blood work was in reference range. An IV catheter was placed, the patient was premedicated with hydromorphone, and maropitant was administered. Anesthesia was induced with diazepam and propofol. The patient was intubated and maintained with sevoflurane (2%) and oxygen. Monitoring included body temperature, ECG, pulse oximetry, noninvasive blood pressure, and capnography. A balanced IV crystalloid solution was also administered.

A complete oral examination confirmed stage 4 periodontal disease of numerous teeth (ie, first through fourth maxillary premolars, all maxillary molars, both maxillary canines, all remaining incisors). Dental radiographs confirmed bilateral mandibular fractures at the mesial root of the right mandibular first molar and distal root of the left mandibular first molar (Figures 1 and 2).

A regional anesthetic agent (0.5% bupivacaine [0.2 mL]) was injected where the mandibular nerve enters the mandibular canal (inferior alveolar nerve block). The affected teeth were surgically extracted to minimize distraction of the bones, the area was gently debrided, and each mandible was stabilized with a single intraosseous wire; the oral soft tissues were sutured in a simple interrupted pattern with 5–0 poliglecaprone-25 to completely cover the bone (Figure 3). This provided sufficient reduction of the fractures and adequate stability.

The patient recovered uneventfully and was discharged the same day with medication for pain management (ie, meloxicam, buprenorphine) and instructions for the owner to administer only soft foods.

The patient was presented 7 weeks later for a recheck oral examination under general anesthesia (performed in the same manner as previously). Dental radiographs demonstrated healing of the fractures (Figure 4). The interfragmentary wires were removed via an intraoral approach, and postoperative intraoral radiographs were obtained to confirm adequate healing (Figure 5). The patient recovered uneventfully.

Pathologic jaw fracture is a significant local consequence of chronic periodontal disease.^1,2 These fractures typically occur in the mandible due to chronic periodontal tissue loss, which weakens the bone in affected areas.³ Although these fractures can occur in any area of the mandible, they are especially common near the canine and first molar teeth.⁴ Pathologic jaw fractures are more common in small-breed dogs as compared with large-breed dogs due to their mandibular first molars being larger in proportion to the mandible itself.⁵ Small-breed dogs also have a minimal amount of bone apical to the tooth root, putting this area at high risk for fracture when apical bone loss occurs.⁶

Pathologic jaw fractures have a guarded prognosis due to the lack of remaining bone and poor bone quality, presence of infection, low oxygen tension in the area of the fracture, and difficulty in rigid fixation of the caudal mandible.^4,6 Regardless of the method of fixation used, diseased root(s) must be extracted to facilitate healing.^3,7

Pathologic jaw fractures typically occur as a result of mild trauma but can also occur during dental extraction procedures (ie, iatrogenic fracture).⁴ Clinical awareness can help reduce risk for iatrogenic fractures during at-risk dental procedures (eg, extraction of the mandibular canines in dogs and cats, the mandibular first molars in small-breed dogs, the mandibular fourth premolars in small-breed brachycephalic animals, and teeth in any area weakened by infection or neoplasia).⁶

Dental radiography is critical to the proper care of dental patients, as radiography can help identify risk factors for jaw fracture (eg, alveolar bone loss).⁷ In cases in which severe alveolar bone loss is noted, particularly if the mandibular canine or first molar is affected, owners should be informed of the possibility of iatrogenic jaw fracture prior to extraction of the offending tooth.^3,4

Regardless of the degree of bone loss, diseased teeth with minimal remaining bone can be successfully extracted using proper technique.

Multirooted teeth should always be sectioned prior to extraction. This is important because roots of most multirooted teeth are divergent, and thus root tips will break if extractions are attempted in one piece.^3,7-11 Root fracture can occur even if a tooth is relatively mobile. In addition, buccal bone removal may be performed if indicated, particularly if one of the roots or part of the root has significant periodontal attachment.⁸

This patient was successfully managed with a single interfragmentary wire on each side. This technique was elected because it was possible to achieve very good anatomic reduction of the fractures and provide clinically acceptable stability. However, when intraosseous wires are employed to fix fractures of the body of the mandible, it is important to ensure neutralization of bending forces with tension-band wire along the alveolar margin of the mandible and avoid tooth roots. A second area of fixation can also be considered at the ventral mandibular margin with a stabilization wire, which neutralizes rotational and shear forces. This will allow proper biomechanics for healing and prevent movement during the healing period.¹¹

Pet owners should be counseled about the importance of proper dental care to avoid the significant effects of periodontal disease. Further, dental radiography should always be performed prior to any extraction; it is particularly important to radiograph the mandible in small-breed dogs. Proper extraction techniques, including sectioning of multirooted teeth, should always be performed. Educating pet owners of the possibility of fracture is important from a legal aspect. In addition, patients with minimal apical bone should be referred to a veterinary dental specialist when possible.