Mable has congenital deafness but is otherwise healthy. Her BCS is 4/9. She was spayed at 6 months of age without complication. She receives routine flea, tick, and heartworm preventives. One other dog also lives in the household; both dogs are fed a commercially prepared raw diet. Mable’s owner reports she is a high-energy dog that performs in agility competitions and has traveled throughout the southeastern coastal part of the United States.

On physical examination, Mable is tachycardic (180 bpm) and panting. Her temperature is 103.1°F (39.5°C). When she occasionally places the affected limb on the ground, she has a plantigrade stance. Mable is sedated due to her high stress level. 

Pain is isolated to the hock region, and hyperflexion of the tarsus independent of the stifle is easily appreciated (Figure 1). During manual flexion of the tarsus, a crab claw appearance of the paw is noted. Diameter of the right Achilles tendon (ie, calcaneal tendon) is reduced by 25% relative to the left side. A firm knot is palpated deep in the gastrocnemius muscle bellies, a faint bruise is noted over the swelling on the caudal aspect of the thigh, and a 2-cm laceration is seen over the lateral aspect of the distal tibia (Figures 2 and 3). Radiographs of the right pelvic limb do not indicate fractures or luxations (Figure 4).

Surgery was performed to repair the full Achilles tendon rupture. The primary repair involved suturing the tendon ends to the calcaneus bone using bone tunnels and a 3-loop pulley with 0 polypropylene. Polypropylene mesh was used as additional reinforcement to reconstruct the Achilles tendon and its components (Figures 5 and 6). 

External coaptation was provided via a cast that was transitioned to a caudal splint after 4 weeks. At 8 weeks, the splint was transitioned to a soft bandage. All bandages (ie, cast, splint, soft) were changed weekly. At 10 weeks, all external support was removed, and Mable’s activity was restricted for an additional 4 weeks. At her 16-week follow-up, Mable had a normal gait and stance.

Canine inflammatory bowel disease (IBD) is characterized by idiopathic intestinal inflammation and lack of response to diet and antibiotic treatments.¹ Histopathology of the intestinal tract and response to immunosuppressive therapy are required for definitive diagnosis. Factors associated with negative outcomes for dogs with IBD include the chronic canine enteropathy clinical activity index (CCECAI), a high endoscopic score in the duodenum, hypocobalaminemia (<200 ng/L), and hypoalbuminemia (<20 g/L).²

Predictive markers are still needed to classify IBD-affected dogs into risk groups. One such prospective marker is the neutrophil:lymphocyte ratio (NLR). During inflammatory states, the neutrophil count may increase whereas the lymphocyte count may decrease.³ NLR is an accessible parameter that can easily be calculated as a ratio between absolute neutrophils and lymphocytes using a WBC count differential.³ In studies of human patients with IBD, NLR appeared to be higher in patients with active disease.⁴

This retrospective study evaluated the clinical and prognostic significance of NLR in dogs with IBD. NLR of healthy control dogs (n = 150) was compared with dogs with IBD (n = 41). The correlation between NLR and several variables, including CCECAI and endoscopic histology scores, was investigated. After one month of treatment with immunosuppressive therapy, differences in NLR between responders and nonresponders were assessed.

Results revealed that dogs with IBD had higher median NLRs than the control dogs (4.78 vs 3), although most dogs with IBD had neutrophil and lymphocyte counts within reference intervals. There was a moderate positive correlation between NLR and CCECAI at the time of admission, which supports the potential use of NLR as a marker of clinical disease severity in canine IBD. NLR seemed to be negatively correlated with total protein, albumin, and cholesterol levels. NLR was higher in dogs diagnosed with protein-losing enteropathy, potentially due to loss of lymphocytes through ruptured lacteals.⁴ The only significant histologic parameter associated with NLR was the presence of lacteal dilation. In the study population, NLR did not differ significantly between endoscopic or histologic score groups. After one month of immunosuppressive therapy, the median NLR was significantly higher in nonresponders than responders (12.23 vs 4.58).

Key pearls to put into practice:

Because of its poor sensitivity and specificity, increased NLR should not be used as the sole diagnostic criteria for canine IBD or lymphangiectasia. Although it can be used to further support suspicion of these disorders, histologic diagnosis is still required.

NLR has potential use as a marker of disease severity in canine IBD as well as for clinical monitoring of therapeutic response in cases of chronic enteropathies. NLR can be easily calculated by dividing the absolute neutrophil count by the absolute lymphocyte count using the results of routine blood work.

NLR can be impacted by stress and chronic disease states. The extent of impact has not been examined, and further studies are needed. 

Chronic enteropathy (CE) in dogs is categorized into subtypes according to responsiveness to food trials, antibiotics, or steroids/immunosuppressants. CE unresponsive to any of these treatments is classified as nonresponsive enteropathy. Differentiating subtypes can be difficult due to clinical and histologic similarities. The major histocompatibility complex (MHC) class II genotype in humans and the canine MHC (ie, dog leukocyte antigen [DLA]) genotype have been associated with several immune-mediated conditions. 

This study examined the potential for determining susceptibility to refractory CE through identification of risk and protective genotypes in French bulldogs and miniature dachshunds. No statistical difference was noted between dachshunds and controls. In French bulldogs, several significant associations were found between DLA class II genotypes and refractory CE. These findings support an immunogenetic component of CE in French bulldogs. Further studies involving larger sample sizes and different breeds may aid in early diagnosis, treatment, and prevention of CE through epigenetic approaches and breeding.

Congenital ocular malformations are rare in dogs and cats and include abnormalities present at birth, after the eye opens, or at ≈6 to 8 weeks of age. These malformations result from abnormal embryonic development, which may occur spontaneously or due to gestational teratogens, including both genetic and nongenetic factors. Some congenital ocular disorders have been identified as heritable within a breed (eg, collie eye anomaly) and form the basis for breeding recommendations by veterinary ophthalmologists. In humans, congenital ocular malformations are a leading cause of childhood blindness, and veterinary models are often used to investigate disease mechanisms and treatment options. 

This study sought to identify the prevalence and epidemiology of congenital ocular malformations in dogs and cats presented to a veterinary teaching hospital in Portugal. A prospective and retrospective evaluation of medical records included data on age, breed, sex, medical history, reason for presentation, clinical findings, vision impairment, and treatment options.

Of the 32,974 dogs and 13,977 cats evaluated, 103 (0.3%) dogs and 20 (0.1%) cats were diagnosed with a congenital malformation in one or both eyes. The most commonly identified ocular malformations in both dogs and cats were congenital cataracts, microphthalmia, and persistent pupillary membranes. Among dogs with ocular dermoids, French bulldogs were significantly overrepresented (75% of cases). No sex predisposition was identified for any congenital ocular malformation. 

Surgery was performed on 25 dogs to address congenital ocular malformations. The most common procedures were ocular dermoid removal (12 dogs) and cataract phacoemulsification with intraocular lens implantation (9 dogs). Four cats underwent surgery (3 for microphthalmos and/or entropion and 1 for enucleation due to congenital glaucoma).  

This study highlighted the rarity of congenital ocular malformations in dogs and cats and provided insight into these conditions. It is important to be aware of the most common congenital eye conditions, as treatment options may be available. Additional exploration of the possible hereditary nature of ocular dermoids in French bulldogs is warranted.

Key pearls to put into practice:

Congenital ocular malformations are rare in dogs and cats. The most frequently diagnosed conditions are congenital cataracts, microphthalmia, and persistent pupillary membranes. Congenital cataracts and microphthalmia may affect vision, and referral to a veterinary ophthalmologist for surgical evaluation is recommended.

Persistent pupillary membranes vary in appearance and are named based on the structures with which they associate (ie, iris-to-iris, iris-to-lens, iris-to-cornea). In addition, persistent pupillary membranes may simply appear as a cluster of pigment on the anterior lens capsule without overt pigment strands; this type of persistent pupillary membrane is common in dogs, especially cocker spaniels. The most common type of persistent pupillary membrane in cats is iris-to-cornea, and a corneal opacity is usually present at the endothelial attachment point.

French bulldogs appear to be predisposed to ocular dermoids. Clinically, dermoids are typically located on the eyelids, conjunctiva, or limbus of the cornea. The most common complication is corneal irritation, and surgery to remove the dermoid is often recommended.

Serum total calcium (tCa) exists in 3 fractions: protein-bound (primarily albumin), ionized (iCa), and complexed. iCa is the most clinically relevant fraction of tCa for evaluating calcium homeostasis; however, methods for measuring iCa in clinical practice are not always readily available. Although formulas to adjust tCa to correct for serum protein concentration have been evaluated, these formulas are not designed for and do not predict iCa in the general population. These formulas were hypothesized to be predictive of iCa in patients with hypoalbuminemia but not hyperphosphatemia, which can affect the complexed fraction of calcium. A retrospective review of 262 dogs with serum albumin concentration ≤2.5 g/L and serum phosphorus concentration ≤5 mg/dL calculated adjusted calcium concentration (aCa) using the formula aCa = tCa (mg/dL) – serum albumin concentration (g/dL) + 3.5 (g/dL). Results demonstrated that low aCa was useful for accurate detection of ionized hypocalcemia in this population of dogs.

Although hip dysplasia is a malformation of the hip joint, the consequent degenerative joint disease (DJD) is largely caused by the dynamic and abnormal articulation of the femoral head within the acetabulum. Hip joint laxity can lead to abnormal acetabular contact with the femoral head, which can exacerbate the disease. DJD is the primary reason for medical intervention in older dogs, as pain and decreased range of motion typically impact daily activities, particularly exercise and mobility, posturing to urinate and defecate, overall engagement, and advanced exercises (eg, agility, detection/law enforcement work, guide dog work).  

This study details the PennHIP scoring system for detecting congenital hip dysplasia and suggests that quantifying hip laxity is a key factor in improving hip joint quality scores. PennHIP evaluations are performed by PennHIP specialists to measure passive hip joint laxity of the pelvis under compression or distraction, which changes the femoral head displacement from the center of the acetabulum. The measured distance is then divided by the radius of the femoral head, resulting in a unitless measure of joint laxity (ie, the distraction index [DI]), which is more accurately predictive of DJD risk than subjective methods (eg, the Orthopedic Foundation for Animals [OFA] system—a 7-point scoring system that describes nondysplastic hips as excellent, good, or fair and dysplastic hips as mild, moderate, or severe).^1,2 The PennHIP index is most useful in patients <24 months of age and in females not in estrus, as hormonal changes have been shown to directly correlate with hip laxity.³ 

Key pearls to put into practice:

DJD is the most common reason military working dogs >5 years of age are discharged.⁴ Attention to multimodal pain management, including joint restorative therapies, is important in these patients.

When screening for hip dysplasia, it is key to obtain quality radiographs taken with the patient under sedation. The positive predictive value of standard OFA positioning may be enhanced by the addition of DI values to OFA hip joint scores.

Limitations exist when screening young dogs for hip dysplasia. Environmental factors, estrus, breed, body weight, frame size, history of strenuous activity, and poor muscle mass can contribute to joint laxity. It is thus important to educate pet owners about the specific needs of their dog when deciding whether radiography is warranted to evaluate hip integrity.

Hyperlipidemia is a disturbance of lipid metabolism that results in increased serum lipids (ie, triglycerides, cholesterol, or both). Hyperlipidemia in a fasted state is abnormal and indicates accelerated synthesis or reduced degradation of lipoproteins. Hyperlipidemia due to a lipid disorder is primary (ie, a defect of lipoprotein metabolism) or secondary (ie, characterized by increased lipoproteins, decreased lipoprotein catabolism, or both). 

This randomized, crossover, double-blinded study evaluated the effects of 3 high-starch diets (ie, dietary peas/barley, peas/barley/rice, corn) in 12 dogs with stable diabetes and a history of hyperlipidemia. Dogs were fed a basal diet (9% fat on a dry-matter basis) for 60 days, then randomized to be fed each of the test diets for 60 days. The test diets had similar percentages of crude protein, fat, fiber, and ash but differed in sources of starch (ie, peas and barley vs corn). At the end of the test period, plasma triglyceride and cholesterol curves were measured over 10 hours.

Mean plasma triglyceride levels were significantly lower after the pea and barley diet trial as compared with the basal diet trial at fasting and 8 hours postprandial and as compared with the corn diet trial 4 hours postprandial. Mean, minimum, and maximum plasma cholesterol levels were significantly lower after the pea and barley diet as compared with the corn diet at all time points except during fasting; there were no differences as compared with the basal diet. 

Feeding a lower-fat diet is considered critical for hyperlipidemia management. The results of this study suggest that dietary ingredients may also play an important role. Although dogs fed the pea and barley diet had lower cholesterol at several time points as compared with dogs fed the corn diet, hypercholesterolemia in dogs is believed to be less clinically important than hypertriglyceridemia. In addition, a complete dietary analysis of the diets was not specified, making it challenging to interpret the results. Barley contains β-glucans (ie, polysaccharides found in the bran of cereal grains that have several reported health benefits in humans^1,2) and has been evaluated in humans for its cholesterol and lipid-lowering effects.³ Pea protein has been found to reduce triglyceride and cholesterol levels in some species.^4-8 Although the mechanism is not fully understood, the benefit of pea protein may be due to increased hepatic activity of low-density lipoproteins, resulting in increased clearance of low-density lipoprotein cholesterol, decreased synthesis of fatty acids, and increased excretion of bile acids in feces.^4-7

Key pearls to put into practice:

Hyperlipidemia in a fasted dog or cat is abnormal and should be managed.

Dietary and drug interventions can decrease the morbidity associated with hyperlipidemia.

Dietary ingredients, fiber, and several nutrients (eg, β-glucans), in addition to reduced dietary fat, may play an important role in management of patients with hyperlipidemia.

Although other analgesic drugs have increased in popularity, opioids continue to be extensively used for pre-, intra-, and postoperative analgesic periods in veterinary medicine.¹ Opioid analgesic drugs are classified according to the opioid receptor(s) at which they exert agonistic action.² μ-opioid analgesic drugs include morphine, hydromorphone, methadone, and fentanyl; buprenorphine is classified as a partial μ agonist. Mixed agonist/antagonist drugs include butorphanol and nalbuphine; these are κ agonists and predominately μ antagonists. 

Morphine and butorphanol are commonly used in veterinary practice, but nalbuphine (a noncontrolled, human opioid drug³) is not. Butorphanol and nalbuphine have similar pharmacologic and adverse effects in dogs and cats. However, there is conflicting evidence as to whether nalbuphine has equal or greater sedative and analgesic effects as compared with butorphanol or morphine, and extensive analgesic studies involving nalbuphine in veterinary medicine are lacking.⁴ Butorphanol as an analgesic in small animals is less effective than μ agonists, partial μ agonists, and NSAIDs, primarily because of its short duration of action and ability to control only mild to moderate degrees of pain.⁵ As compared with morphine, neither butorphanol nor nalbuphine have been shown to reduce the minimum alveolar concentration of inhalant anesthetics.⁶ In addition, butorphanol should be used judiciously in patients with the multidrug sensitivity gene (MDR1 gene, also known as ABCB1 gene).⁷

This study compared the analgesic effects of intra- and postoperative nalbuphine (either 0.5 mg/kg or 1 mg/kg), butorphanol, and morphine administered with acepromazine for premedication in dogs undergoing ovariohysterectomy. The authors believed that morphine would provide the most effective analgesia as compared with nalbuphine and butorphanol and that nalbuphine would provide a dose-dependent degree of analgesia. The number of rescue doses of propofol needed to maintain an adequate level of anesthesia was used to assess intraoperative analgesia. The dynamic and interactive visual analog scale and the modified Glasgow composite measure pain scale were used to assess postoperative pain. No difference in the degree of analgesia was observed among the 3 opioids, and the effects of a higher and lower dose of nalbuphine were similar. All 3 opioids, when combined with acepromazine, provided insufficient analgesia for all dogs during the surgical procedure. In addition, none of the 4 premedication protocols provided acceptable analgesia within the first 6 hours postoperatively. The authors speculated that the morphine dose (0.2 mg/kg IV) may have been insufficient to provide adequate analgesia; however, the butorphanol and nalbuphine doses were comparable with those in other studies.

Key pearls to put into practice:

This study did not fully illustrate the antinociceptive advantages of morphine, butorphanol, and nalbuphine. However, opioid drugs are valuable analgesics for surgical procedures and should be administered pre-emptively to help control surgical nociception.

Increasing the dose of nalbuphine or butorphanol may not provide increased analgesia because of their ceiling effects. Increasing the dose of morphine (0.4-0.5 mg/kg) can increase analgesia but may also increase adverse effects. μ-agonist opioids (eg, morphine, hydromorphone) or partial μ-agonist opioids (eg, buprenorphine) may provide better analgesia for surgical patients as compared with butorphanol or nalbuphine.

Administering maropitant prior to μ-agonist opioid drugs can decrease the incidence of vomiting in dogs and may provide additional analgesia.^8,9

Butorphanol and nalbuphine are κ agonists and μ antagonists; therefore, either can be used as a nonemergent, μ-opioid–reversing drug.

Immunosurveillance helps identify infected or abnormal cells. Signaling molecules, collectively referred to as immune checkpoint molecules, on T lymphocytes help regulate immunosurveillance and can be either activating or inhibitory. Inhibitory immune checkpoint molecules, which suppress T lymphocyte activation, are aberrantly expressed in many human cancers. Suppression may allow tumors to evade the host immune surveillance, allowing more aggressive clinical behavior. 

Two inhibitory immune checkpoint molecules often expressed in human tumors are programmed death ligand-1 (PD-L1) and cytotoxic T-lymphocyte associated protein-4 (CTLA-4)^1,2; these molecules are associated with more aggressive behavior and worse prognosis, and measuring their expression on tumors may help provide a more accurate prognosis.^3,4 A variety of canine tumors express PD-L1 and CTLA-4, which have been shown to be prognostic in canine high-grade B-cell lymphoma.⁵ PDL-1 is detected more frequently in malignant than benign mammary gland tumors,^6,7 but association with prognosis has not been reported.

This study investigated the immunostaining and gene expression of PDL-1 and CTLA-4 in 41 histologically malignant and 12 benign canine mammary gland tumors with known outcomes. The goal was to determine whether PDL-1 and CTLA-4 immunostaining and gene expression are correlated with biologic behavior and clinical outcome. Metastasized malignant mammary gland tumors had significantly higher immunostaining scores and gene expression for both PDL-1 and CTLA-4 than nonmetastasized malignant tumors. 

On multivariate analysis, PDL-1 and tumor grade were independent prognostic indicators of survival; CTLA-4, tumor size, and tumor emboli were not independent prognostic indicators of survival.

Key pearls to put into practice:

Canine malignant mammary gland tumors are a heterogeneous group of tumors with biological behavior that can be difficult to predict.

Different prognostic factors, including histologic subtype, tumor grade, and stage, have been evaluated, but additional factors likely play a role in the aggressive behavior of a tumor.

Results of this study show PDL-1 and CTLA-4 immunostaining of mammary gland tumors may allow better prognostication in dogs and could lead to development of future therapeutics.

NSAIDs are commonly prescribed in veterinary medicine, but there are concerns regarding safety profiles of these drugs.^1-3 Reported adverse effects include anorexia; lethargy; vomiting; gastric irritation, ulceration, and perforation; renal insufficiency; and idiosyncratic hepatotoxicity.   In this retrospective study, medical records of 81 dogs with laboratory evaluations conducted in advance of NSAID therapy were reviewed. Of these, 56% had an elevation in at least one renal (ie, BUN, creatinine) or hepatic (ie, ALP, ALT, AST) value, which are often reflective of renal perfusion, hepatocellular injury, and cholestasis.   Dogs with elevated hepatic blood values were less likely to have an NSAID administered, although this was not the case for an elevated renal parameter in isolation. This variation in administration may be due to the relatively low number of dogs with an elevated renal parameter, as opposed to a lack of concern for renal elevation. Results also suggested that dogs <8 years of age were less likely to have an elevated renal or hepatic blood value questioning screening utility in young, healthy, euvolemic patients. Other associations pertaining to patient history, physical examination, or onset of illness were not significant.

Key pearls to put into practice:

Patients with compromised circulating volume (eg, dehydration, hypotension, GI losses, ascites, congestive heart failure) are at increased risk for adverse effects secondary to NSAID administration.

Although risk factors for idiosyncratic, life-threatening hepatotoxicity are unknown, there is concern that NSAID administration may exacerbate pre-existing underlying hepatitis.⁴

Regardless of physical examination and serum chemistry profile findings, pet owners should be informed of the possible adverse effects prior to an NSAID being administered and guided to seek medical care if adverse effects occur.

This registry-based retrospective study examined 6,150 units of blood from 1,914 active canine blood donors in order to estimate and predict positivity to transmittable blood-borne pathogens. Of the 1,779 units tested for antibodies, 10 (0.56%) were positive for antibodies against Anaplasma phagocytophilum and A platys, and none had antibodies against Ehrlichia canis or E ewingii. After excluding the antibody-positive units, 1.1% of 6,140 units were found to be PCR-positive for A phagocytophilum, Bartonella spp, Brucella canis, Candidatus Mycoplasma haematoparvum, Mycoplasma haemocanis, or a combination thereof. Units from the first blood collection were more likely to test PCR-positive for pathogens than were units from subsequent collections. The prevalence of transmittable pathogens is low but represents a risk to transfusion recipients, highlighting the importance of screening blood donors, especially those donating for the first time.

Separation anxiety is common in dogs, especially those adopted as adults. This study assessed whether high-arousal departures and greetings can lead to or be associated with separation anxiety. Many veterinary behaviorists suggest minimizing greetings and departures as part of a treatment plan for dogs with separation anxiety, and excessive greeting has been previously reported as a risk factor for separation anxiety.¹ The first half of this study compared the behavior of shelter dogs after a high-arousal situation (ie, being played with, petted, and spoken to) versus a low-arousal situation (ie, receiving a calm and brief greeting, receiving a short petting interaction, then being ignored) before being left alone in an unfamiliar room. Heart rate, activity, and vocalizations were measured across 10 trial sessions. Initially, the heart rate and activity were higher in dogs after a high-arousal situation, but values decreased across sessions. Of note, these dogs were in a relatively barren room (not a home) and had no prior relationship with the human who interacted with them; thus, this may not be a particularly good measure of separation anxiety.

The second half of this study involved a more clinically applicable experiment in which a questionnaire for dog owners was posted on multiple dog-related Facebook groups, including a group focused on separation anxiety. Owners were asked how they originally greeted and departed from their dog, whether this has changed over time, and, if changed, how they now greet and depart from their dog. Responses from owners of dogs with (n = 978) and without (n = 1,012) separation anxiety were compared. Owners of dogs with separation anxiety reported engaging in low-arousal greetings and departures both when they initially acquired the dog and presently. Owners scored their dogs for separation-anxiety–related behaviors (eg, barking, destructiveness); these scores were not correlated with the intensity of greetings or departures. The authors concluded that high-arousal greetings and departures were not risk factors for separation anxiety; however, further research—including video-recorded observation of newly adopted dogs when owners leave and return—is warranted.

Key pearls to put into practice:

Separation anxiety may be more prevalent in dogs adopted after the sensitive period for socialization (7-16 weeks); owners of these dogs should be instructed to begin leaving their dog alone for short periods to habituate them to being alone.

Based on the results of this study, intensity of departures and greetings may not be correlated with separation anxiety, and it may not be necessary to advise owners to ignore their dog when leaving and returning home; however, further research is needed.

Prevention and treatment options for FIP, a virulent pathotype of feline enteric coronavirus, are limited. Feline recombinant interferon omega is the most commonly available antiviral treatment, but its efficacy against FIP virus has not been well-demonstrated. ERDRP-0519 (ERDRP), a nonnucleoside inhibitor that targets RNA polymerase, is effective against in vitro and in vivo morbilliviruses. This study examined the in vitro efficacy of ERDRP against FIP virus. Results demonstrated significant inhibition of FIP virus replication in a dose-dependent manner, confirming ERDRP is highly effective against a coronavirus in vitro. Further study is needed to assess suitability of ERDRP in treatment of FIP virus in vivo.

Surgical site infection (SSI) is an important cause of morbidity in dogs. Previous studies based on older guidelines from the Centers for Disease Control and Prevention have reported SSI rates of <5% for the lateral fabellar nylon suture technique, a procedure used for cranial cruciate ligament (CCL) repair.^1,2 

This study examined SSI rates and contributing variables for lateral suture surgery of the stifle joint in dogs; 150 surgical procedures in 130 dogs were evaluated, and the SSI rate was found to be 17.3%. Of these, infected joints were found in 73.1% of dogs; 53% of affected dogs required implant removal. All infections were Staphylococcus spp, with only 10.5% of isolates being methicillin resistant. Although all dogs received perioperative β-lactam antibiotics, only 13.3% received a postoperative antibiotic course. Postoperative antibiotics have been associated with reduced SSI in some CCL studies.^3,4

Variables significantly associated with SSI included increased body weight and use of propofol instead of alfaxalone as an anesthetic induction agent. For each 2.2-lb (1-kg) increase in body weight, the SSI rate increased 4%. Use of propofol was associated with a 3.6-fold increase.

Key pearls to put into practice:

Heavier dogs have a higher risk for postoperative infection of the stifle joint after lateral fabellotibial nylon suture surgery for CCL rupture.

Dogs receiving alfaxalone as an anesthetic induction agent for lateral fabellotibial nylon suture repair may have lower risk for SSI than when propofol is used.

If SSI occurs after extracapsular suture repair for CCL rupture, the lateral suture may need to be removed in ≈50% of cases.

Following are the author's top 5 signs of patient stress and excitement on clinical pathology.

A stress leukogram is a common set of leukocyte responses caused by the release of endogenous corticosteroids that result from stress-related disease and hospitalization. Possible changes include segmented neutrophilia, lymphopenia, monocytosis, and eosinopenia, but all abnormalities are not always present,¹ and it is unusual for alterations to vary >2 to 3 times the reference values.² Lymphopenia is most common, and segmented neutrophilia is usually present.³ Monocytosis and eosinopenia are possible in dogs; however, they are more variable and frequently not present in cats. 

Neutrophilia is caused by decreased adherence to the vascular endothelium from receptor downregulation, which inhibits margination of cells and therefore increases the proportion of cells in the circulating pool inside blood vessels.⁴ Prolonged circulation time may cause neutrophils to appear hypersegmented,⁵ and increased release of neutrophils from bone marrow is possible.⁴ The segmented neutrophil count can double in dogs and triple in cats due to a larger number of cells in the marginating pool.⁶ Neither a left shift to band neutrophils or toxic changes are expected due to lack of inflammatory response.

Instead of entering circulation, lymphocytes become redistributed to and retained in lymphocytic tissue (eg, lymph nodes).⁶ It is suspected that monocytes increase in concentration due to mechanisms similar to those of neutrophils (eg, decreased margination), although this has not been definitively proven. Eosinopenia can be difficult to detect because eosinophils are rare and only a few may be present in circulation at baseline. 

The stress leukogram is transient, and cell dynamics return to normal when increased stress is resolved.³ The changes observed in a stress leukogram can also occur with consistently increased cortisol concentrations in patients with hyperadrenocorticism. Stressed patients with underlying illness may have a co-occurring inflammatory leukogram as suggested by the presence of a left shift and neutrophil toxicity; these do not occur with a stress response alone.

Leukocytosis can be caused by fear, exercise, or excitement; is mediated by increased catecholamine concentrations (eg, epinephrine, norepinephrine); and should be considered a transient physiologic response. Catecholamine hormones can cause cells from the marginating pool to shift to the circulating pool in the vasculature.^5,7 This effect may double the total WBC concentration within minutes but is temporary, and, at least in horses, cell counts return to baseline values after 30 minutes.⁸ In addition, splenic contraction induced by catecholamine hormones can expel leukocytes into the peripheral circulation. 

Leukocytosis is usually characterized by segmented neutrophilia without a left shift. Lymphocytosis may be present, especially in kittens and young cats. The effect in cats is often considered a prominent lymphocytosis, which can be up to twice the upper reference value.^5,6

Transient erythrocytosis occurs when catecholamines from excitement or stress cause splenic contraction, resulting in expulsion of stored erythrocytes into circulation.⁹ Transient erythrocytosis is most common in young horses, less frequent in dogs, and unusual in cats—possibly because the feline spleen is nonsinusoidal—but can occur under experimental conditions.^5,10 RBC concentration (ie, hematocrit) only slightly increases in most small animals, and the effect may not be appreciated because values may remain within reference intervals. In a study, the hematocrit of racing greyhounds increased immediately postrace, presumably due to catecholamine-induced splenic contraction, although decreased plasma volume may have also been a contributing factor.¹¹

Transient stress hyperglycemia, or physiologic hyperglycemia, is particularly common in cats and is most likely due to catecholamine release in acute cases, resulting in glycogenolysis and suppression of insulin release.¹² An increase in glucose and lactate concentrations has been correlated with epinephrine and norepinephrine, but not cortisol, concentrations.¹² 

Stress hyperglycemia should be differentiated from diabetes mellitus, but this can be challenging, especially in cats, as blood glucose can become increased with stress alone. Diabetes mellitus is unlikely if repeat sampling for hyperglycemia is negative. In patients with chronic stress, endogenous corticosteroids may be more likely to cause hyperglycemia.¹³ Catecholamines and corticosteroids can be contributing factors for transient hyperglycemia in hospitalized patients. 

Measuring fructosamine concentration can also help discern stress-related hyperglycemia from diabetes mellitus.¹⁴ In dogs, infusion of a combination of glucagon, epinephrine, and cortisol (ie, stress hormones) more effectively induced hyperglycemia than individual hormones.¹⁵ Glucosuria may occur with stress-related hyperglycemia, particularly in cats, if the renal threshold is exceeded.

Chronic stress in dogs can cause long-term increase of endogenous corticosteroids, which may result in increases in serum ALP activity. Increased activity is initially due to an increase in the liver ALP isoenzyme; corticosteroid-induced ALP (C-ALP) activity begins to increase after 7 days.¹⁶ Evidence indicates that hepatocytes upregulate a gene that generates C-ALP when exposed to corticosteroids.¹⁷ Cats do not have C-ALP. 

Enzymatic activity may remain increased for several weeks after stress has resolved due to the prolonged half-life of the hormones. C-ALP activity can be used to screen for hyperadrenocorticism, but screening can be challenging in stressed patients. Although C-ALP can be measured specifically, only total ALP activity is typically reported. It is thus important to consider the impact of stress when investigating liver disease.¹⁸

Patient stress and excitement may interfere with routine laboratory data interpretation. It is important to consider these factors so the most accurate conclusions are drawn and the patient is managed appropriately. 

Belinda, a 9-lb (4-kg), 5-year-old spayed domestic shorthair cat, was returned to an animal shelter approximately one year after adoption with a recurring mass on the upper left eyelid (Figure 1). The conjunctiva and periocular tissue around the left eye were thickened and inflamed; periocular alopecia was also present. Belinda had been acting normally at home, and the surrendering owner had no other concerns.

An incisional biopsy of the mass had been performed one year prior, and a cutaneous mast cell tumor (MCT) was diagnosed; at the time, histopathology showed the mast cells extended to the surgical margins, which is expected with incisional biopsy, and no mitotic figures were seen.

On physical examination, Belinda was bright, alert, and responsive. Her vital parameters were within normal limits. The entire upper left eyelid and periocular skin around the medial canthus and extending to the medial lower eyelid exhibited moderate to severe diffuse thickening and alopecia. The left mandibular lymph node was mildly enlarged. The remainder of the physical examination was within normal limits.

There were no significant abnormalities on CBC and serum chemistry profile. Premedication with diphenhydramine (2 mg/kg IM) was administered prior to fine-needle aspiration of the mass and mandibular lymph node. Cytology of the mass was highly cellular and composed predominantly of variably granulated mast cells (Figure 2). There was mild to moderate anisocytosis and mild anisokaryosis. Binucleated cells were frequent. 

Left mandibular lymph node aspirate showed frequent, well-granulated mast cells distributed individually and in groups among a population of lymphocytes, including predominantly small lymphocytes with fewer medium and large lymphocytes and scattered plasma cells (Figures 3 and 4). Given the cytologic findings from the mass and lymph node, abdominal ultrasonography was performed. No abnormalities were seen on ultrasound, but a fine-needle aspirate of the spleen revealed an increased concentration of mast cells scattered individually and in small groups among normal splenic lymphoid and hematopoietic tissue (Figure 5).

Surgery was not pursued because of the presence of metastatic disease. Belinda was placed in palliative care in a permanent foster home. She was prescribed diphenhydramine (12.5 mg PO every 12 hours), famotidine (10 mg PO every 24 hours), and prednisolone (7.5 mg PO every 24 hours). Periodic attempts were made to decrease the prednisolone dose; however, increased swelling, erythema, and pruritus with self-injury were consistently noted, and the initial prescribed dose (7.5 mg PO every 24 hours) was determined to be the appropriate maintenance dose.

Belinda continued to do well for 15 months, at which time she was returned for evaluation of moderate, focal, cranial abdominal pain with apparent nausea and vomiting. She weighed 9.72 lb (4.41 kg). CBC and serum chemistry profile were unremarkable, and imaging was considered but declined. Maropitant (4.4 mg SC every 24 hours for 3 days), lactated Ringer’s solution (100 mL SC), and buprenorphine (0.044 mg via buccal oral transmucosal route every 8 hours for 3 days) were administered. Famotidine, prednisolone, and diphenhydramine were continued at the previously determined doses. One month later, Belinda was again stable and maintaining a good quality of life.

Cutaneous MCTs are the second most common skin neoplasm in cats. Although most feline cutaneous MCTs are benign, ≈10% are aggressive regardless of histologic type.¹ MCTs most frequently arise on the head and neck, followed by the trunk and limbs. There can be a solitary lesion, clusters of lesions, or widespread distribution of lesions ranging from papules and plaques to discrete nodules in the skin or subcutis. Cats may exhibit pruritus, erythema, or edema of the affected area.¹

The mean age for development of MCTs is ≈10 years,¹ but periorbital MCTs are more common in younger cats.² There is no sex predisposition. Siamese cats may be more predisposed, especially when young, but MCTs in these patients often regress spontaneously within 24 months.³

MCTs generally exfoliate readily via fine-needle aspiration techniques. Mast cells are large round cells with a centralized purple nucleus often obscured by numerous dark purple granules that fill the abundant cytoplasm. The granules, especially in feline MCTs, can stain poorly with quick stains commonly used in many clinics, making in-clinic diagnosis challenging.^1,4

Histologically, feline MCTs are divided into mastocytic (more common) and atypical (less common; previously classified as histiocytic) forms. The mastocytic form is further subdivided into well-differentiated and pleomorphic forms.¹ A well-differentiated MCT is typically composed of morphologically normal-appearing mast cells that have minimal anisocytosis and anisokaryosis.¹ Mitotic figures can be present but are uncommon. Small lymphocyte clusters can also be present. Spindle cell infiltrates can be seen in MCT aspirates but are less common in feline tumors as compared with canine tumors.¹ Mast cells in pleomorphic tumors exhibit more variability (including anisocytosis and anisokaryosis) and eosinophilic infiltrates.¹ The cytology of atypical MCTs more closely resembles histiocytes, as opposed to mast cells, and can also contain lymphocytic and eosinophilic infiltrates.¹ The cytologic features seen in pleomorphic and atypical MCTs do not correlate with malignant behavior.¹

The most important prognostic factor for feline cutaneous MCTs is mitotic index (MI). Low MI (ie, <1 per 10 high-power fields [HPFs]) is associated with a better prognosis. High MI (ie, >5 per 10 HPFs) is associated with a poorer prognosis. Other factors associated with poor prognosis include multiple (>5) simultaneous cutaneous tumors, spread to local lymph nodes, low or moderate cytoplasmic granularity, and a high Ki67 index.¹

The treatment of choice for a solitary cutaneous MCT is surgical removal. Studies demonstrate that tumor recurrence is low regardless of whether complete surgical excision is obtained.^2,3 Multiple de novo cutaneous MCTs occur in a significant number of cats, and pet owners should be advised of this possibility.¹ Additional clinical staging should be considered for all cats with cutaneous MCTs, but cats with any factors for poor prognosis (eg, high mitotic tumor index, >5 simultaneous cutaneous tumors, others as mentioned previously) and cats with visceral MCTs should be fully staged with an evaluation that includes CBC, serum chemistry profile, urinalysis, lymph node aspiration, abdominal ultrasonography with splenic aspiration, thoracic radiography, and possibly bone marrow aspiration. Mastocytemia is more common in cats with MCTs as compared with dogs, and ≈10% of cats with a single cutaneous MCT have mastocytemia.¹

Medical treatment for feline cutaneous MCTs may include diphenhydramine (2-4 mg/kg PO every 12 hours), famotidine (1 mg/kg PO every 12 hours), and prednisolone (1-2 mg/kg PO every 24 hours to start).^5-7,8 Other potential treatment options may include chemotherapy (eg, lomustine), small molecule inhibitors (eg, imatinib mesylate [tyrosine kinase inhibitor]), and radiation therapy. These therapies may increase survival in some cats; consultation with a veterinary medical oncologist is therefore strongly recommended.^8-10

• Infiltrative disease
  • Neoplasia 
    • Hemangiosarcoma (may be focal enlargement/mass as opposed to diffuse splenomegaly)
    • Lymphoma
    • Mast cell tumor
    • Plasma cell neoplasia
    • Histiocytic sarcoma (diffuse or focal enlargement) 
    • Other sarcomas (eg, leiomyosarcoma, fibrosarcoma; often focal enlargement) 
    • Leukemia 
  • Amyloidosis 
• Infectious disease 
  • Bacterial
    • Brucellosis
    • Rickettsial (ie, ehrlichiosis, anaplasmosis)
    • Salmonellosis 
    • Tularemia
  • Viral
    • Infectious canine hepatitis
  • Fungal
    • Histoplasmosis
  • Protozoal 
    • Babesiosis
    • Hepatozoonosis
• Reactive/hyperplastic changes (often cause focal enlargement) 
  • Lymphoid hyperplasia
  • Nodular hyperplasia 
    • Splenic
    • Complex
    • Lymphoid 
  • Extramedullary hematopoiesis (eg, bone marrow failure [myelofibrosis, myelophthisis, toxicity, immune-mediated disease, radiation], tissue inflammation or injury, hypoxia, hemolytic anemia, splenic hematoma, splenic thrombosis, lymphoid hyperplasia) 
  • Hematoma 
• Congestion 
  • Anesthesia/sedation
  • Right-sided congestive heart failure
  • Portal hypertension
  • Splenic vein thrombosis 
  • Splenic torsion

Amputation is generally performed at the metacarpophalangeal or metatarsophalangeal joints, especially in patients with neoplasms or osteomyelitis. More distal amputations are reserved for patients with traumatic or degenerative diseases that only affect the distal phalanges. Amputation of the second or fifth digit does not affect limb function; however, amputation of the third or fourth digits, which are weight-bearing, may affect function or result in mechanical lameness.²

The surgical principles of proximal and distal interphalangeal joint amputation and metacarpophalangeal and metatarsophalangeal joint amputation are similar.^1,2 The digital pad is preserved in proximal and distal interphalangeal joint amputation but is removed in metacarpophalangeal and metatarsophalangeal joint amputation, most frequently performed for digit amputation.^1,2 If the location is distal (second or third phalanx) and the condition is benign, amputation at the interphalangeal joints can be performed. 

Malignant lesions usually require soft tissue and bone margins (wide surgical excision) for cancer-free excision at the surgical margin. Distal malignant lesions are thus usually excised at the metacarpophalangeal or metatarsophalangeal joints. Ring block or regional analgesia can be performed using longer-lasting anesthetics (eg, bupivacaine, liposome-encapsulated bupivacaine).

• #15 scalpel blade  
• Rongeur
• Electrocautery tool (recommended)
• Metzenbaum scissors
• Monofilament nonabsorbable suture (4-0 or 3-0)
• Monofilament absorbable suture (4-0 or 3-0) 
• Needle holder
• Bandage materials 
• Esmarch tourniquet
  • Adherent wrap
  • Scissors

To exsanguinate the limb, tightly apply an Esmarch bandage from the most distal aspect of the toes to 2 to 3 cm proximal to the carpus or the tarsus. Tightly secure the bandage at the proximal aspect of the limb to prevent blood from flowing into the limb during surgery. Cut the bandage from distal to proximal to expose the surgical site (up to the carpus or tarsus), leaving the most proximal aspect of the tourniquet intact. Be careful not to cut the skin.

Beginning on the dorsal aspect of the affected digit, make an inverted Y-shaped skin incision along the sides of the digit that meets on the palmar aspect.⁴

Ligate or cauterize arteries and veins that are <1 to 2 mm in diameter and located axially or abaxially at the dorsal (dorsal common digital vasculature) and ventral (palmar common digital vasculature) aspects of the digit.⁵

Transect the tendons of the superficial and deep digital flexor (palmar), as well as the common digital extensor (dorsal, thoracic limb) or long digital extension (dorsal, pelvic limb) at the level of the proximal phalanx and the metacarpal (or metatarsal) bone.⁵

Carefully transect the joint capsule at the level of the phalanx and the corresponding metacarpal (or metatarsal) bone to be amputated. Avoid direct mechanical damage to the cartilage,⁵ and remove the digit. Perform a condylectomy if needed to allow cosmetic closure of the skin.

Remove the tourniquet.

Suture subcutaneous tissue with a simple interrupted pattern using a 3-0 or 4-0 monofilament absorbable suture (A). Suture the skin with a cruciate pattern using a 3-0 or 4-0 monofilament nonabsorbable suture (B).

Provide postoperative multimodal pain management with injectable analgesics (ie, mu agonist opioids) for the first 12 to 24 hours and oral analgesics (eg, NSAIDs, gabapentin, tramadol) after the patient recovers and has normal deglutition. 

Use a soft, padded bandage for 1 to 2 weeks (if tolerated by the patient) to prevent trauma to the incision while walking. Restrict exercise for 3 weeks until the wound heals.

To exsanguinate the regional distal area of the limb, tightly apply an Esmarch bandage from the most distal aspect of the toes to 2 to 3 cm proximal to the carpus or the tarsus. Tightly secure the bandage at the proximal aspect of the limb to prevent blood from flowing into the limb during surgery. Cut the bandage from distal to proximal to expose the surgical site (up to the carpus or tarsus), leaving the most proximal aspect of the tourniquet intact. Be careful not to cut the skin.

Make a skin incision that encircles the nail (around the ungual process), sparing the digital pad. Continue the incision proximally and dorsally (over the phalangeal bone) to expose the distal interphalangeal joint or the proximal interphalangeal joint depending on the determined level of amputation. 

Sharply dissect soft tissue away from the bone and transect the extensor tendons (dorsal), flexor tendons (palmar), and collateral ligaments (lateral). 

Disarticulate the joint.

Suture the subcutaneous tissue with an appositional, interrupted knot-burying pattern to maximize wound healing and prevent wound dehiscence in a high-motion area. Create a Y-shaped pattern by pulling the digital pad over the cut end of the bone and suturing (both sides) laterally and dorsally.

Suture the skin with a simple interrupted pattern using a 3-0 or 4-0 monofilament nonabsorbable suture, which can typically be removed 2 to 3 weeks postoperatively.

Provide postoperative multimodal pain management with injectable analgesics (ie, mu agonist opioids) for the first 12 to 24 hours and oral analgesics (eg, NSAIDs, gabapentin, tramadol) after the patient recovers and has normal deglutition.

Use a soft, padded bandage for 1 to 2 weeks (if tolerated by the patient) to prevent trauma to the incision when the patient walks. Restrict exercise for 3 weeks until the wound heals.