April 2018   |   Volume 16   |   Issue 4

Top 5 Potential Heartworm Treatment Challenges

in this issue

in this issue

Isoxazolines

Nutritional Assessment in a Dog with Chronic Enteropathy

Corneal & Conjunctival Cytology

Top 5 Muscle & Tendon Injuries in Lame Patients

Splenectomy: Hilar Ligation Technique

Top 5 Causes of Splenomegaly in Dogs

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Top 5 Complications During & After Heartworm Treatment

Jennifer Anne Sidley, DVM, DACVIM (Cardiology), CVCA Cardiac Care for Pets, Alexandria, Virginia

Cardiology

|Peer Reviewed

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Top 5 Complications During & After Heartworm Treatment
Radiograph from a dog with severe heartworm disease illustrating severe pulmonary arterial dilation, right heart enlargement, diffuse bronchointerstitial infiltrate, and focal region of pulmonary consolidation from embolized heartworms

Treatment complications can make heartworm disease particularly challenging. Following are the most common complications the author has encountered from heartworm treatment, as well as strategies to minimize them. 

1

Pulmonary Emboli

Embolized worms are one of the most dangerous risks following melarsomine therapy. As worms die, they decompose, leaving fragments that become lodged in the distal pulmonary artery and capillary beds and block blood flow (Figure 1). The higher the worm burden and heartworm classification, the higher the risk for life-threatening complications. Clinical signs are most common 10 to 21 days postinjection but can occur as early as 2 days postinjection or as late as 30 days postinjection.1 Sudden coughing, hemoptysis, dyspnea, lethargy, and anorexia are hallmark signs. Pale mucous membranes, pulmonary crackles, fever, leukocytosis, and thrombocytopenia are common. Strict cage confinement, oxygen (if needed), and tapering anti-inflammatory doses of prednisone (0.5 mg/kg q12h for 1 week, 0.5 mg/kg q24h for the second week, then 0.5 mg/kg q48h for 1-2 weeks) are recommended if signs develop.2

Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM
Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 1 Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM

Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM
Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 1 Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 1 Radiographs before (A) and 11 days after (B) melarsomine injection showing increased overall pulmonary infiltrate with focal region of pulmonary consolidation from embolized worms (black arrow). A progressive increase in cranial pulmonary artery size can be seen (gray arrow). Images courtesy of Clarke E. Atkins, DVM, DACVIM

Before treatment, patients should be stabilized to maximize lung function and improve their ability to handle dying worms. Anti-inflammatory doses of prednisone 7 to 14 days before treatment should be given to patients with significant pulmonary infiltrate or respiratory signs (eg, coughing, tachypnea); right-sided heart failure should be treated and stabilized.

Exercise increases blood flow to damaged, blocked vessels and leads to worsening lung injury, increased pulmonary vascular resistance, pulmonary hypertension, and, potentially, right-sided heart failure. Therefore, strict exercise restriction is essential to minimize the severity of cardiopulmonary damage.3,4 Restriction should begin the day of diagnosis and extend throughout the entire treatment and recovery period, with the most extreme restriction lasting 4 to 6 weeks after each melarsomine injection.2 Restriction may vary depending on patient and owner needs but ideally involves cage confinement or restriction to a single room with just short leash walks to eliminate, particularly for more severe cases. 

A split 3-dosage protocol can reduce the severity of complications from dying worms.5 The first injection kills approximately 50% of worms, then the lungs are able to recover for one month before the other half of the worms are killed. If the lungs have not fully healed at this point, the second and third injections can be delayed until signs have resolved.6

2

Rapid Microfilarial Death

Rapid microfilarial death (Figure 2) can cause signs ranging from mild lethargy, ptyalism, inappetence, and nausea to more severe hypotension, tachycardia, tachypnea, and collapse. If these signs develop, supportive care with IV fluids and soluble glucocorticoids (eg, dexamethasone sodium phosphate [0.25 mg/kg IV slowly over 2-4 minutes]) is indicated. Rapid microfilaricidal treatment with high-dose (ie, 50 μg/kg) ivermectin is no longer recommended by the American Heartworm Society2; instead, a combination of doxycycline (10 mg/kg q12h for 4 weeks) with a monthly macrolide preventive is recommended to kill microfilariae at a slower rate with less potential for complications.2 Within 5 to 9 months, most dogs will become amicrofilaremic. Because milbemycin oxime kills microfilariae much more rapidly than do ivermectin, selamectin, and moxidectin, the latter 3 have a lower risk for microfilarial death complications and are preferred in dogs that are microfilaremic.6 In microfilaremic dogs, administration of glucocorticoids (eg, prednisolone [1 mg/kg PO], dexamethasone [0.25 mg/kg IV]) with or without antihistamines (eg, diphenhydramine [1 mg/kg IV or IM]) is recommended one hour before, and possibly again 6 hours after, administration of the first dose of preventive; patients should be monitored for potential adverse effects for the first 8 to 12 hours.2,6

Single microfilaria in a blood smear
Single microfilaria in a blood smear

FIGURE 2 Single microfilaria in a blood smear

FIGURE 2 Single microfilaria in a blood smear

3

Incomplete Adulticide Efficacy

Closing the gap in treatment so that all stages present are susceptible can help prevent persistent heartworm infection postadulticide therapy. Melarsomine kills adults and mature L5 larvae that are at least 4 months postinfection. Macrolide preventives reliably kill L3 and L4 larvae that are present up to 2 months postinfection; thus, there is a 2-month gap when immature L5 larvae are not sensitive to either preventive or melarsomine and can later develop into adult heartworms. Allowing 2 to 3 months to lapse after preventive treatment before administering melarsomine can help close this gap and allow all stages present to be sensitive to melarsomine and prevent treatment failure.2,6 

Melarsomine is not 100% effective, and not all worms are killed in every patient. The extended 3-dose treatment protocol has a higher efficacy than the 2-dose protocol.6,7 The American Heartworm Society recommends the 3-dose protocol for all dogs treated for heartworms, regardless of stage, because of its higher efficacy and lower risk for pulmonary complications.2 This may involve greater cost for the owner and a longer period of exercise restriction, but the potential benefit for the patient outweighs this added cost and inconvenience.

Improved sensitivity of tests over time has allowed clinicians to detect smaller worm numbers (as few as 1-3 female worms). Typically, the worm burden is still significantly reduced in persistently positive animals. The decision for retreament should be made on a case-by-case basis, depending on patient age, activity level, worm burden, and history. A geriatric, low-energy dog would likely tolerate a few persistent worms better than would a young, active dog, and the latter would benefit more from retreatment.

4

Injection Site Reactions

Significant irritation can occur at the injection site, causing pain, swelling, tenderness, seroma formation, and reluctance to move. Care should be taken to follow the recommended technique and inject deep in the muscle belly to avoid superficial or subcutaneous injection and leakage. Administering butorphanol before the injection can help reduce discomfort, and the sedation may also help ensure proper technique. Hypersalivation, panting, vomiting, diarrhea, anorexia, and weakness have also been reported following injection.6,8

5

Caval Syndrome

When large numbers of worms mature over a short period of time, the right heart chambers and vena cava can become engorged with worms (ie, caval syndrome), leading to severe right-sided heart dysfunction, pulmonary hypertension, intravascular hemolysis, hemoglobinuria, disseminated intravascular coagulation, shock, and multiple organ failure (Figures 3 and 4).

Gross image of a dog with caval syndrome. Image courtesy of Clarke E. Atkins, DVM, DACVIM
Gross image of a dog with caval syndrome. Image courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 3 Gross image of a dog with caval syndrome. Image courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 3 Gross image of a dog with caval syndrome. Image courtesy of Clarke E. Atkins, DVM, DACVIM

Echocardiogram of a dog with caval syndrome showing large worm burden (arrow) in the right ventricle, severe right ventricular hypertrophy, and septal flattening. Image courtesy of Clarke E. Atkins, DVM, DACVIM
Echocardiogram of a dog with caval syndrome showing large worm burden (arrow) in the right ventricle, severe right ventricular hypertrophy, and septal flattening. Image courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 4 Echocardiogram of a dog with caval syndrome showing large worm burden (arrow) in the right ventricle, severe right ventricular hypertrophy, and septal flattening. Image courtesy of Clarke E. Atkins, DVM, DACVIM

FIGURE 4 Echocardiogram of a dog with caval syndrome showing large worm burden (arrow) in the right ventricle, severe right ventricular hypertrophy, and septal flattening. Image courtesy of Clarke E. Atkins, DVM, DACVIM

Prompt extraction of the worms to remove the obstruction is essential for survival and typically involves referral to a specialist with proper tools (eg, long alligator forceps, horsehair catheter, basket retrieval device).9 During extraction, care must be taken to avoid excessive intracardiac or vessel damage, as well as laceration to the worms themselves, which can cause sudden antigenic release from macerated heartworms and fragment emboli. Without prompt worm retrieval, most dogs live only a few days; with worm retrieval, survival rates up to 60% to 71% have been reported, although outcomes are likely highly dependent on the clinician’s expertise.10 Melarsomine therapy is usually needed to kill the remaining worms.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Nutritional Assessment in a Dog with Chronic Enteropathy

Nutritional Assessment in a Dog with Chronic Enteropathy

Linda Toresson, DVM, Evidensia Specialist Animal Hospital, Helsingborg, Sweden

Gregg K. Takashima, DVM, WSAVA Global Nutrition Committee Series Editor

Kara M. Burns, MS, MEd, LVT, VTS (Nutrition), Olathe, Kansas

Nutrition

|Peer Reviewed

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Nutritional Assessment in a Dog with Chronic Enteropathy

THE CASE

A 4.5-year-old intact female shar-pei was presented for chronic recurrent diarrhea, which was either watery or mucoid, of more than a year’s duration. Vomiting and hyporexia developed the month before presentation and was associated with mild weight loss. The dog was the only pet in the household and was up-to-date on vaccinations and flea/tick preventives; heartworm prevention was unnecessary, as there is no heartworm disease in Sweden or northern Europe, where this dog lives.

Physical Examination

The patient had to be sedated for physical examination due to temperament. BCS was 4/9, with a muscle condition score showing mild muscle atrophy and a dull hair coat. Despite chronic diarrhea, no signs of dehydration were observed. All other vital parameters were within normal limits. Rectal palpation was painful despite sedation.

Dietary History

Several therapeutic diets labeled intestinal, including a high-fiber diet, had been tried throughout the last year without clinical improvement. The protein sources of those diets included chicken, egg, and turkey, and the owners sometimes gave treats such as cold cuts and table scraps. Water intake remained the same throughout the year. Metronidazole had been prescribed on several occasions; diarrhea would cease with metronidazole but would recur each time after discontinuation of therapy.

Diagnostic Results

Diagnostics included screening for intestinal parasites, CBC, serum chemistry profile, urinalysis, and a GI panel, including trypsin-like immunoreactivity, cobalamin, and folate. No intestinal parasites were detected. Subnormal serum concentrations of folate, cobalamin, and cholesterol were detected (Table). CBC and serum chemistry profile were otherwise unremarkable.

Endoscopy of the stomach and small and large intestine were performed. Histopathology of biopsies of the small and large intestine revealed a moderate lymphocytic-plasmacytic enteritis, with a moderate degree of villous atrophy, and moderate lymphocytic-plasmacytic colitis.

TABLE

SUBNORMAL SERUM CHEMISTRY RESULTS

Test Reference Interval Baseline 9 Weeks After Baseline 5 Months After Baseline
Cobalamin 251-908 ng/L (185 - 670 pmol/L) 231 ng/L (170 pmol/L) 705 ng/L (520 pmol/L) 250 ng/L (184 pmol/L)
Folate 7.7-24.4 µg/L (17.4 - 55.3 nmol/L) 3.5 µg/L (7.9 nmol/L) 35 µg/L (79.3 nmol/L) 25 µg/L (56.6 nmol/L)
Cholesterol 158-282 mg/dL (4.09 - 7.30 mmol/L) 124 mg/dL (3.21 mmol/L) 189 mg/dL (4.90 mmol/L) N/A

DIAGNOSIS:

CHRONIC ENTEROPATHY

Treatment & Follow-Up

The dog’s diet was changed to a commercial lamb and rice novel single-source protein diet, and folate supplementation (5 mg PO q24h) was initiated. Treatment with prednisolone was initiated (initial dose, 1.5 mg/kg q24h) and slowly tapered over 6 months (maintenance dose, 0.2 mg/kg q48h). Several attempts to further taper the dose were made but would cause diarrhea to relapse. Four weekly cobalamin injections (800 µg) were administered according to Texas A&M University Gastrointestinal Laboratory recommendations (see Suggested Reading). 

At follow-up 4 weeks after the last cobalamin injection, the dog’s stool had normalized, vomiting had stopped, and appetite returned. Serum cobalamin concentration, cholesterol, and folate had normalized (Table). Folate and cobalamin supplementation was stopped and prednisolone was further tapered to 0.5 mg/kg q48h.

At follow-up 3 months later, the dog had experienced 2 recurrences of diarrhea, and serum cobalamin concentrations had decreased to subnormal levels. A new parenteral cobalamin maintenance supplementation protocol was recommended; however, the owners were not interested in a new series of injections but were instead interested in oral cobalamin supplementation. 

Oral cobalamin supplementation has been proven to be effective in humans with cobalamin deficiency,1-5 and recent studies have confirmed its efficacy in dogs and cats with chronic enteropathy and hypocobalaminemia.6-9 It offers an alternative to parenteral supplementation and may suit some owners better, as oral administration may be an easier and more cost-effective alternative to monthly injections, particularly for patients requiring long-term maintenance supplementation. Because oral supplementation in dogs with hypocobalaminemia had not been studied at the time of this case, the potential for failure of this therapy was carefully discussed with the owners before supplementation (1 mg PO q24h) was initiated. 

At follow-up 2 months later, serum cobalamin concentration was higher than after the first series of injections and the dog was clinically stable. The dog has been on successful oral cobalamin maintenance therapy for 8 years.

ASK YOURSELF…

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Quiz: Nutritional Assessment in a Dog with Chronic Enteropathy

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Changing the diet to a novel protein is most likely to be successful in patients with chronic enteropathy if:

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Which of the following statements regarding cobalamin is true?

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What is the most likely mechanism behind the cobalamin deficiency in this patient?

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In which breeds has congenital cobalamin malabsorption been reported?

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A middle-aged intact female cocker spaniel with a history of lethargy and reduced appetite of 2 months’ duration has a subnormal serum cobalamin concentration. The dog has been fed a homemade diet due to hyporexia for 6 weeks. How should the cobalamin deficiency be interpreted?

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Diet in Disease is a series developed by the WSAVA, the Academy of Veterinary Nutrition Technicians, and Clinician’s Brief.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Corneal & Conjunctival Cytology

Leah Moody, BSc, Mississippi State University

Caroline Betbeze, DVM, MS, DACVO, Mississippi State University

Ophthalmology

|Peer Reviewed

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Corneal & Conjunctival Cytology
Figure 1 Mucopurulent ocular discharge, hyperemic conjunctiva, and elevation of the nictitating membrane in a dog. Signs of stromal ulcerative keratitis, including an obvious corneal defect and superficial corneal vascularization and cellular infiltration of the axial cornea, are present. Corneal and conjunctival cytology were performed.

An initial ocular examination with basic diagnostic testing (eg, direct and indirect ophthalmoscopy, fluorescein stain, Schirmer tear test, tonometry) is indicated for most patients presented with corneal and/or conjunctival diseases, which are common in domestic animals. Ulcerative keratitis (Figure 1) is particularly common and often resolves in 5 to 7 days with appropriate treatment.1 With complicated corneal ulcers and other progressive or persistent corneal diseases, investigation beyond basic diagnostics may be necessary.

Cytology can have a variety of applications, including: 

  • Immediate characterization of inflammatory or neoplastic cells or infectious organisms, including cases in which culture and susceptibility testing or PCR may be indicated
  • Allowing for direction of empiric therapy while awaiting culture and susceptibility results
  • Diagnosing many infectious and inflammatory diseases (eg, ulcerative or fungal keratitis, feline eosinophilic conjunctivitis or keratitis, bacterial conjunctivitis) 
  • Facilitating prompt and appropriate medical therapy 2 
  • Characterizing cells of a proliferative corneal or conjunctival mass
  • In patients with corneal ulcers that are progressing in depth or do not respond to initial treatment within 5 to 7 days because a common cause of progression is infection3

Corneal cytology is contraindicated in patients that have severe ulcers with an exposed Descemet’s membrane (ie, descemetocele) or with corneal perforation. Because these patients require surgical treatment, cytology is unnecessary and could cause further injury to the eye.1,3 Conjunctival cytology is rarely contraindicated; however, it may not be of much diagnostic value in patients with conjunctival lesions without an ulcerated or easily exfoliated surface. Cases in which conjunctival cytology may not be diagnostic include conjunctival thickening or nodules (eg, nodular granulomatous episcleritis), certain infectious organisms (eg, mycobacterial, fungal), and some types of neoplasia (eg, squamous cell carcinoma).4 In addition, conjunctival cytology, although not contraindicated, has minimal diagnostic utility in corneal ulceration.

Culture and susceptibility testing can be performed in combination with cytology if bacterial or fungal disease is suspected. If both procedures will be performed, culture samples should be taken before cytology collection.3,4

Microscopic evaluation of the corneal cytology sample collected from the patient in Figure 1 revealed moderate neutrophilic inflammation and squamous epithelial cells. No infectious agents were found; however, neutrophilic inflammation supports the diagnosis of infectious keratitis.
Microscopic evaluation of the corneal cytology sample collected from the patient in Figure 1 revealed moderate neutrophilic inflammation and squamous epithelial cells. No infectious agents were found; however, neutrophilic inflammation supports the diagnosis of infectious keratitis.

Figure 2 Microscopic evaluation of the corneal cytology sample collected from the patient in Figure 1 revealed moderate neutrophilic inflammation and squamous epithelial cells. No infectious agents were found; however, neutrophilic inflammation supports the diagnosis of infectious keratitis.

Figure 2 Microscopic evaluation of the corneal cytology sample collected from the patient in Figure 1 revealed moderate neutrophilic inflammation and squamous epithelial cells. No infectious agents were found; however, neutrophilic inflammation supports the diagnosis of infectious keratitis.

Corneal or conjunctival cytology can be used to identify the number, morphology, and staining characteristics of inflammatory cells and infectious organisms present in the disease. Neoplastic cells may also be identified in the sample.4 Normal corneal samples should include noncornified epithelial cells, few lymphocytes and neutrophils, and rare bacteria; moderate neutrophilic inflammation can be identified in keratitis cases, including ulcerative keratitis (Figure 2).5 Conjunctival samples are normally composed of squamous and columnar epithelial cells, goblet cells, melanin, and occasional bacteria; inflammatory cells can be visualized in conjunctivitis cases (Figure 3). Lymphocytes, neutrophils, monocytes, and plasma cells are rarely observed. 

Microscopic evaluation of the conjunctival cytology sample collected from the patient in Figure 1 also revealed neutrophilic inflammation with no infectious agents, which indicates secondary conjunctivitis.
Microscopic evaluation of the conjunctival cytology sample collected from the patient in Figure 1 also revealed neutrophilic inflammation with no infectious agents, which indicates secondary conjunctivitis.

Figure 3 Microscopic evaluation of the conjunctival cytology sample collected from the patient in Figure 1 also revealed neutrophilic inflammation with no infectious agents, which indicates secondary conjunctivitis.

Figure 3 Microscopic evaluation of the conjunctival cytology sample collected from the patient in Figure 1 also revealed neutrophilic inflammation with no infectious agents, which indicates secondary conjunctivitis.

With bacterial disease, neutrophils predominate, may be degenerate or nondegenerate, and may contain intracellular bacteria. Even if bacteria are not visualized, presence of neutrophilic inflammation suggests infection of the cornea.1 Identification of fungal hyphae is suggestive of mycotic disease.3 Presence of eosinophils or mast cells is an abnormal finding in a corneal or conjunctival cytology sample and is suggestive of eosinophilic keratitis or allergic conjunctivitis, respectively.4,6

Successful treatment of corneal and conjunctival disease requires appropriate and immediate therapy, as vision loss can occur rapidly.3 Referral to an ophthalmologist should be considered for patients with complicated corneal ulcers and other progressive ocular diseases.

STEP-BY-STEP

CORNEAL & CONJUNCTIVAL CYTOLOGY


WHAT YOU WILL NEED

Clinician's Brief
  • Topical anesthetic (eg, proparacaine, tetracaine)
  • Glass slides
  • Kimura spatula
  • #15 scalpel blade (sterile)
  • Microapplicator to collect cytology 
  • Romanowsky-type stain
  • Microscope

STEP 1

Using a damp cotton ball or piece of ocular gauze, gently wipe away any ocular surface debris, mucus, or excess ointment. Traditional 4-by-4 (10.16 cm x 10.16 cm) gauze may be used to clear periocular debris but should never come in contact with the corneal or conjunctival surface.


STEP 2

Apply 1 to 2 drops of topical anesthetic to the eye, waiting approximately 30 seconds between each drop. Allow approximately 5 minutes for the topical anesthetic to achieve maximal effect; cytology supplies can be collected during this time.

Author Insight

Most patients require only topical anesthesia, and sedation is not usually necessary; however, fractious or excited patients may require chemical sedation to reduce the risk for injury during the procedure. If required, sedation may cause the globe to rotate ventrally, and small-toothed forceps (eg, Bishop-Harmon) will be needed to gently grasp the bulbar conjunctiva to position the globe for cytology collection. 


STEP 3

Restrain or have an assistant properly restrain the patient by placing one hand on the back of the head and the other hand under the chin, being careful not to squeeze the muzzle too tightly.

Hold the eyelids open using the thumb and forefinger of the nondominant hand. Rest the dominant hand on the patient’s head. This position will ensure that, if the patient moves, the instruments move with the patient, which can decrease the chance of ocular injury. Be careful not to touch the eyelids with the instrument, as this may contaminate the sample.

Clinician's Brief

STEP 4

Using a microapplicator, Kimura spatula, or the blunt end of a sterile #15 scalpel blade, gently scrape the cornea or conjunctiva 5 to 7 times. The scraping movement can be up to 3 to 5 mm in length, depending on the size of the area of cellular infiltration. For the cornea, sampling the area surrounding the ulceration or any area that has a cellular appearance is recommended (A). For conjunctiva (palpebral or bulbar), any diseased tissue should suffice (B). An ideal sample is collected with minimal patient discomfort and provides an adequate monolayer of intact corneal or conjunctival epithelial cells.

Clinician's Brief
Clinician's Brief

Author Insight

The margin of the ulcerative defect, plaque, or raised inflammatory lesions will have the highest chance of containing causative organisms, inflammatory infiltrate, or diagnostic cells.


STEP 5

Transfer the sample from the collection instrument to a glass slide by gently tapping the instrument or rolling the brush on the slide, being careful not to smear or crush the cells. Preparing several slides from repeat sampling and multiple samples can increase the chances of collecting an adequate diagnostic sample, but the risks of collecting more than one sample must be evaluated based on the severity and depth of the lesion.

Clinician's Brief

STEP 6

Stain the slides using a Romanowsky-type stain (eg, Diff-Quik) and Gram stain. Slides can also be submitted to a diagnostic laboratory that is familiar with veterinary ophthalmologic diseases. The authors suggest evaluating at least one slide in-house to quickly initiate proper patient therapy.


STEP 7

Evaluate a sample under oil immersion using a microscope, ensuring evaluation of multiple high-power fields.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Frequency of Urinary Tract Infection in Dogs Treated with Oclacitinib

William Oldenhoff, DVM, DACVD, Madison Veterinary Specialists in Monona, Wisconsin

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Frequency of Urinary Tract Infection in Dogs Treated with Oclacitinib

In the Literature

Simpson AC, Schissler JR, Rosychuk RAW, Moore AR. The frequency of urinary tract infection and subclinical bacteriuria in dogs with allergic dermatitis treated with oclacitinib: a prospective study. Vet Dermatol. 2017;28(5):485-e113.


FROM THE PAGE …

Several drugs used to treat chronic skin diseases in dogs can predispose patients to UTI and bacteriuria. These sequelae have been established in dogs that receive glucocorticoids and cyclosporine,1-3 but it has not been established whether oclacitinib also predisposes dogs to UTI. Approximately 0.5% to 11.3% of allergic dogs treated with oclacitinib have had clinical signs described as cystitis; however, quantitative urine cultures were not performed.4-6 In addition, there were previously no studies that investigated the frequency of UTI or subclinical bacteriuria in dogs receiving oclacitinib in the absence of other predisposing urinary or metabolic concerns. The purpose of this study* was to evaluate the frequency of UTI and subclinical bacteriuria in dogs receiving oclacitinib.

Fifty-five dogs were included in the study. All were at least 24 months of age and had a history of allergic dermatitis and no apparent history of urinary tract disease or predisposition to UTI. Dogs with bacteriuria or positive urine culture and susceptibility results within the previous 24 months were excluded from the study. Steroids, antibiotics, cyclosporine, and lokivetmab were withdrawn for suitable periods before the study and were not allowed during the study. Forty-seven of the 55 dogs received oclacitinib for over 180 days and had follow-up urinalyses and quantitative urine cultures. The remaining dogs were withdrawn early due to need for systemic antimicrobials (n = 6), decreased efficacy of oclacitinib over time (n = 1), or urinary incontinence (n = 1); follow-up cultures were performed earlier in these dogs.

None of the study patients developed positive urine cultures during the study. A small number of dogs (n = 7) developed microscopic hematuria; however, in 6 of these dogs, this occurrence was suspected to be iatrogenic from cystocentesis. Granular casts, crystalluria, and pyuria were noted in 3 dogs, 9 dogs, and 1 dog, respectively. These developments were deemed not clinically significant because of lack of lower urinary tract signs and negative bacterial cultures.

*This study was supported in part by a Zoetis Excellence in Dermatology Research Grant.

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Oclacitinib was not associated with increased risk for UTI or subclinical bacteriuria. Routine urine cultures are not warranted if a dog is receiving only oclacitinib.

 

2

If a patient receiving oclacitinib has a prior history of UTI or suffers from a condition predisposing to UTI, routine urinalysis with culture is warranted.

 

3

No novel nonurinary adverse events were reported. Consistent with previous reports,4,7 GI events, which were noted in 7.3% of study patients, were the most common adverse event.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Prognostic Markers in Feline Hepatic Lipidosis

Faith I. Buckley, DVM, DACVIM (SAIM), Bulger Veterinary Hospital, North Andover, Massachusetts

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Prognostic Markers in Feline Hepatic Lipidosis

In the Literature

Kuzi S, Segev G, Kedar S, Yas E, Aroch I. Prognostic markers in feline hepatic lipidosis: a retrospective study of 71 cats. Vet Rec. 2017;181(19):512.


FROM THE PAGE …

Hepatic lipidosis is a common liver disease in cats that is associated with high morbidity and mortality. Aggressive therapy to reverse the catabolic state and hepatic failure resulting from prolonged anorexia is required.1-3 Anorexia may be precipitated by comorbidities (eg, GI disease, pancreatitis, cholangiohepatitis) or may be primary (ie, decreased food intake in a healthy animal due to stress-related environmental events or food refusal).

In this study, clinical and laboratory parameters were evaluated in 71 cats diagnosed with hepatic lipidosis (based on liver cytology or histopathology) to identify those associated with mortality. Cats with hepatic lipidosis were older than those in the control group, and female cats were overrepresented.1-3 Primary idiopathic hepatic lipidosis resulting from stress-related anorexia accounted for 20% of cases, which emphasizes the importance of educating pet owners about prevention.

Severity of hepatobiliary enzyme elevation was not associated with survival, whereas markers of hepatic dysfunction (eg, hypoalbuminemia, hyperbilirubinemia, hypocholesterolemia, hyperammonemia) had greater impact on survival, regardless of whether they were observed at time of presentation or developed during hospitalization. Hypokalemia, hyponatremia, hypochloremia, and hypophosphatemia were associated with death, although these are correctable and may be indicative of unbalanced fluid therapy and/or overhydration.2

Recovery from hepatic lipidosis has been best predicted by a 50% progressive decrease in bilirubin concentration during the first 7 to 10 days of reinstitution of nutrition.2 Overall mortality in this study was 38%.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Aggressive therapy is often necessary to increase the chance of patient survival and complete recovery; early reintroduction of nutrition remains vital.

 

2

Close monitoring of electrolytes (ie, sodium, chloride, potassium, phosphorous) during hospitalization and aggressive correction of abnormalities are recommended to limit mortality.

 

3

The underlying cause of the anorexic event leading to hepatic lipidosis is not a prognostic factor.

 

4

Cats of all BCSs—not just obese cats—can develop hepatic lipidosis.

 

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Patellar Luxation & Cranial Cruciate Ligament Disease

Jason Bleedorn, DVM, DACVS, University of Wisconsin–Madison

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Patellar Luxation & Cranial Cruciate Ligament Disease

In the Literature

Fauron AH, Bruce M, James DR, Owen MA, Perry KL. Surgical stabilization of concomitant canine medial patellar luxation and cranial cruciate ligament disease. Vet Comp Orthop Traumatol. 2017;30(3):209-218.


FROM THE PAGE …

Cranial cruciate ligament (CCL) rupture occurs commonly in combination with medial patellar luxation (MPL) in dogs, with higher MPL grades increasing the risk for CCL rupture.1 Despite many surgical option combinations and studies describing these techniques, little (if any) objective clinical trial data comparing various surgical approaches exist.

This multi-institutional retrospective study compared clinical outcomes and complications following tibial tuberosity transposition-advancement (TTTA) against extracapsular stabilization and tibial tuberosity transposition (ECS+TTT) for correction of CCL rupture and/or MPL instability in dogs. A total of 72 stifles were evaluated in 66 dogs; over a 10-year period, 40 were stabilized using TTTA and 32 using ECS+TTT. Overall, complications occurred 2.7 times more often with ECS+TTT (46.9%) as compared with TTTA (17.5%). Major complications occurred only in the ECS+TTT group (5/32) and included premature implant failure, reluxation, and infection necessitating surgical revision or implant removal. Minor complications that occurred were predominantly wound-related. Dogs of greater weight were more likely to have TTTA performed over ECS+TTT; however, greater weights did not correspond with higher complication rates. Reluxation rate was similar in both groups (TTTA, 20%; ECS+TTT, 15.6%). The performance of a femoral sulcoplasty also reduced risk for a poor outcome.

The results of this study suggest that surgical stabilization using TTTA may be a safer approach for correction of concomitant CCL rupture and MPL as compared with ECS+TTT. The overall complication rates in both groups were higher than previously reported for each individual procedure alone; this higher rate could possibly be related to case contributions from many surgeons with varying experience levels. Despite the high rate of complications, the outcome was good to excellent in most cases.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Thorough examination for CCL instability in dogs with MPL is important.

 

2

Surgical stabilization of concurrent CCL and MPL may be associated with a higher complication rate than either procedure individually.

 

3

Surgeons already proficient in tibial tuberosity advancement (TTA) may consider a combination of this approach with tibial tuberosity transposition (TTT) to be a superior option for concurrent MPL/CCL rupture; however, this combination (ie, TTTA) should only be reserved for those surgeons who have mastered the TTA technique.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Biomarkers & Slow-Kill Protocol for Heartworm Disease

Amara Estrada, DVM, DACVIM (Cardiology), University of Florida

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Biomarkers & Slow-Kill Protocol for Heartworm Disease

In the Literature

Yoon WK, Kim YW, Suh SI, Hyun C. Evaluation of cardiopulmonary and inflammatory markers in dogs with heartworm infection treated using the slow kill method. Vet Parasitol. 2017;244:35-38.


FROM THE PAGE …

The therapeutic protocol for treatment of canine heartworm disease recommended by the American Heartworm Society consists of 3 intramuscular injections of melarsomine, with steroid and antithrombotic agents as needed. This regimen has long been the basis for heartworm adulticidal therapies and is safe and effective when used as directed; however, melarsomine periodically has limited availability and is unavailable in many countries. Thus, many slow-kill protocols have been circulated as possible alternatives when melarsomine is unattainable. Critics of these techniques have argued that dogs with high worm burdens would be at greater risk for complications (eg, pulmonary and systemic inflammation, pulmonary thromboembolic events, myocardial ischemia) related to their worm burden. In addition, it is assumed that dogs with a higher worm burden would be more resistant to effective long-term elimination of disease with a slow-kill protocol.

This study looked at a small population of shelter dogs with heartworm disease and assessed cardiac, hemostatic, and inflammatory biomarkers to try to correlate worm burden with changes in biomarkers during a course of a slow-kill protocol. The slow-kill protocol consisted of 4-week administration of doxycycline (10 mg/kg PO q24h) and 6-month administration of ivermectin (6-10 µg/kg PO every 15 days). All dogs survived and tested negative for microfilariae at the 6-month recheck; however, 4 of the 12 treated dogs that had higher worm burdens were still positive for heartworm antigen at the end of treatment, and 3 of the 4 remained positive at the end of the study. All biomarkers tested were initially higher (and pathologically abnormal) in dogs with higher worm burdens. Dogs with higher worm burdens and clinical signs had higher elevations in all biomarkers before therapy, and these elevations decreased during the course of therapy.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

The slow-kill method does not appear to be an effective protocol for managing heartworm disease, particularly in dogs with higher worm burdens; current American Heartworm Society recommendations for adulticide therapy should continue to be followed.

2

Use of biomarkers as a tool to provide additional or supplementary prognostic information when other tools (eg, echocardiography) are not available may be helpful in identifying dogs with higher worm burdens. Clinical signs and radiographic or echocardiographic evaluation remain the gold standard for such investigation.

3

The slow-kill method appears to reduce biomarkers associated with cardiac, systemic, and pulmonary inflammation but not such that it would be recommended as initial therapy in an attempt to reduce possible complications from adulticide therapy.

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Research Note: Urinary Effects of Allopurinol in Dogs with Leishmaniasis

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Allopurinol is a parasitistatic drug used for long time periods (≥6 months) in the treatment of canine leishmaniasis. Reports indicate that prolonged allopurinol therapy is associated with xanthinuria and xanthine urolithiasis. The purpose of this retrospective study was to describe the most common urinary adverse effects associated with allopurinol use in the treatment of canine leishmaniasis. Medical records of 320 dogs diagnosed with leishmaniasis in endemic areas were reviewed. All dogs received anti-Leishmania spp treatment with meglumine antimoniate once or twice daily for 4 weeks and allopurinol twice daily. Median duration of treatment with allopurinol until diagnosis of xanthinuria, renal mineralization, and/or urolithiasis was one year (range, 3 weeks to 9 years). Forty-two dogs (13.1%) developed adverse urinary effects defined by presence of xanthinuria: 9 of the 42 dogs (21.4%) developed xanthinuria alone; 9 (21.4%) had xanthinuria with urolithiasis; 11 (26.2%) showed xanthinuria with renal mineralization; and 13 (31%) developed xanthinuria, renal mineralization, and urolithiasis. Clinical signs associated with the urinary tract (eg, urinary obstruction, dysuria) developed in 19 of the 42 dogs (45.2%). No other adverse effects associated with allopurinol were reported. The authors concluded that xanthine urolithiasis and renal mineralization can occur in dogs secondary to allopurinol therapy, warranting monitoring for development of urinary adverse effects from the beginning of treatment.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Subcutaneous Administration of Synthetic B-Type Natriuretic Peptide in Dogs

Ashley E. Jones, DVM, DACVIM (Cardiology), Veterinary Specialty Center, Buffalo Grove, Illinois

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Subcutaneous Administration of Synthetic B-Type Natriuretic Peptide in Dogs

In the Literature

Oyama MA, Solter PF, Thorn CL, Stern JA. Feasibility, safety, and tolerance of subcutaneous synthetic canine B-type natriuretic peptide (syncBNP) in healthy dogs and dogs with stage B1 mitral valve disease. J Vet Cardiol. 2017;19(3):211-217.


FROM THE PAGE …

Several natriuretic peptides have been identified, and their use as adjunctive heart failure therapy is under investigation. B-type natriuretic peptide (BNP) has been studied most extensively in cats and dogs. It is normally released by atrial tissue; in heart disease, it is also released from ventricular tissue.1 BNP binds to natriuretic peptide receptors, which results in activation of the secondary messenger molecule cGMP. Ultimately, BNP blocks the harmful effects of the renin-angiotensin-aldosterone system, inducing diuresis and natriuresis; these effects become blunted with advanced heart disease.2 Administration of BNP in humans has been shown to be beneficial in acute congestive heart failure therapy.3

The primary goal of this study* was to evaluate the feasibility, tolerance, and safety of subcutaneous administration of synthetic canine BNP (syncBNP) in healthy dogs and dogs with mild heart disease. Pilot data were also collected for markers of biologic activity, particularly neurohormonal activity.

Six client-owned dogs were divided into 2 groups. The first group was given 2.5 µg/kg SC syncBNP followed by 5 µg/kg SC syncBNP 2 hours later. After no major adverse effects were observed, the second group was given 5 µg/kg SC syncBNP followed by 10 µg/kg SC syncBNP. Blood and urine samples were obtained from all dogs at baseline, 45, and 120 minutes after administration of the 5 µg/kg dose to evaluate for natriuresis, neurohormonal activity, and effects on renal function. 

Overall, syncBNP was well tolerated in all patients. There was a significant increase in plasma cGMP concentration at both 45 and 120 minutes following subcutaneous administration of 5 µg/kg syncBNP, which suggests active binding of syncBNP to natriuretic peptide receptors. There was no significant change in any of the other blood and urine variables assessed, although there was a trend toward decreased plasma renin activity and increased fractional sodium excretion.

*This study was funded by Virbac Corporation.

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Natriuretic peptides are released in higher concentrations in patients with heart disease and are beneficial for antagonizing the harmful effects of renin-angiotensin-aldosterone system while promoting diuresis and natriuresis.

2

Effects of natriuretic peptides become blunted with chronicity and progression of heart disease.

 

3

Administration of syncBNP may be a promising therapy for congestive heart failure; it has been shown to be beneficial in humans with congestive heart failure and to be well tolerated in healthy dogs and dogs with mild heart disease.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Pyrexia in Cats

Garret E. Pachtinger, VMD, DACVECC, VETgirl; Veterinary Specialty and Emergency Center, Levittown, Pennsylvania

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Pyrexia in Cats

In the Literature

Spencer SE, Knowles T, Ramsey IK, Tasker S. Pyrexia in cats: retrospective analysis of signalment, clinical investigations, diagnosis and influence of prior treatment in 106 referred cases. J Feline Med Surg. 2017;19(11):1123-1130.


FROM THE PAGE …

In animals with fever, the hypothalamic set point is elevated, typically by infection, inflammation, neoplasia, or drug administration.1 This retrospective study of 106 cats with persistent fever (≥102.6°F) evaluated common causes and effective treatment options for feline pyrexia. 

Unlike previous studies that have shown immune-mediated disease to be a common cause of pyrexia in dogs,2-4 this study showed immune-mediated disease to be an uncommon cause in cats (5.7%); infectious disease was the most common cause (38.7%), followed by inflammatory conditions (17.9%) and neoplasia (12.3%). The most common infectious disease identified was feline infectious peritonitis (20.8%); others included cellulitis and/or otitis media, pyothorax, pyelonephritis and/or UTI, Mycoplasma felis infection, cholangiohepatitis, and abscess. The average length of hospitalization was 5 days. Survival outcome (67%) was comparable to that in a canine study (70%).1 These results emphasize the importance of infectious disease over immune-mediated disease as a cause of pyrexia in cats.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

The hospital in this study actively participates in feline infectious peritonitis research, which could have led to its overrepresentation. Nevertheless, infectious disease remains the most likely cause for feline pyrexia, thereby warranting evaluation.

2

Treatment before referral was not associated with temperature at presentation or outcome. Importantly, the study supports use of broad-spectrum antimicrobial therapy versus antipyretics, which can increase the risk for side effects, including worsening of infectious disease.

3

Targeted diagnostics, rather than a myriad of tests (ie, the wide-net approach), should be considered. The initial database should be tailored to the patient’s localizing signs (eg, cytology in cats with effusion, MRI for neurologic signs).

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Research Note: Signalment & Heat Stress in Dogs

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Dogs rely on an increased respiratory rate to initiate the necessary cooling when overheated; as such, brachycephalic dogs are particularly susceptible to hyperthermia when heat stressed. This study demonstrated that brachycephalic dogs have a decreased capacity for thermoregulation but that BCS appears to be a more important factor than breed. When considering heat stress situations, including air travel, both factors should be taken into account.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Research Note: Babesiosis Vaccine Antigens

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Existing commercial vaccines against babesiosis contain soluble parasite antigens (SPAs) from in vitro culture supernatants of Babesia canis. This study identified and characterized the specific antigen in SPA serum that confers immunity in vaccinated dogs (ie, canine Babesia antigen [CBA]) and sequenced the gene that encodes it. The gene was then cloned and expressed in Escherichia coli. The recombinant CBA (rCBA) was found to protect against challenge infection in rCBA-vaccinated dogs. The rCBA antigen could replace existing SPA vaccines, thereby eliminating the need for dog blood and serum for production of vaccine.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Top 5 Muscle & Tendon Injuries in Lame Patients

Mary Sarah Bergh, DVM, MS, DACVS, DACVSMR, Iowa State University

Orthopedics

|Peer Reviewed

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Top 5 Muscle & Tendon Injuries in Lame Patients

Muscles and tendons are essential parts of the musculoskeletal system that allow standing, ambulating, and flexion and extension of joints. Injuries can be caused by external trauma (eg, vehicular accident), internal trauma from fracture fragments, or, most commonly, repetitive fatigue and/or application of supraphysiologic forces.

A good working knowledge of musculoskeletal anatomy is important to understand the clinical impact of injuries to the muscle–tendon unit (ie, strains). Strains are common in small animals and should be included in the differential list for any type of lameness or decrease in working or sporting performance. Clinicians should always take a complete history, perform a thorough examination, and obtain radiographs of the affected region to evaluate bony structures. Ultrasonography, CT, and MRI offer more complete evaluation of the muscle–tendon unit and can aid in diagnosis and guide treatment. 

Following are the author’s most common muscle and tendon injuries to consider in the lame patient.

1

Biceps Tenosynovitis

Biceps tenosynovitis is a common cause of forelimb lameness that most frequently affects medium- and large-breed dogs secondary to repetitive fatigue. It is characterized by inflammation of the biceps brachii tendon and the synovial sheath that envelops it in the shoulder joint (Figure 1).1,2 Clinical presentation often consists of a chronic progressive forelimb lameness that is worsened by exercise. The severity of lameness can vary from mild to nonweight-bearing, and atrophy of the supraspinatus and infraspinatus muscles is often present (Figure 2). Pain may be elicited during the biceps test, in which pressure is applied on the biceps tendon in the intertubercular groove when the shoulder is flexed and the elbow extended (Figure 3).1,2 Additional diagnostics (eg, ultrasonography, MRI, arthroscopy) are often needed to confirm diagnosis.1-3 Medical management (eg, rest, NSAIDs, physiotherapy) often results in resolution of mild lesions.1-3 Some dogs may require biceps tendon release or tenodesis to resolve pain and lameness.1-3

2

Achilles Tendon Strain

The Achilles tendon consists of 3 tendons: the superficial digital flexor tendon, the gastrocnemius tendon, and the combined tendon of the gracilis, semitendinosus, and biceps femoris muscles. Injury can occur secondary to acute trauma (ie, laceration, avulsion) or secondary to chronic degeneration, and clinical presentation depends on the severity of the injury and the tendons that have been injured.4,5 Mild strains may result only in lameness, pain, and swelling. If all 3 tendons have been severely compromised, the patient will walk with a complete plantigrade stance (Figure 4A); if only the gastrocnemius tendon has been injured, the patient will walk with a partial plantigrade stance (ie, increased flexion of the tarsus) with a noticeable flexion of the digits due to increased tension on the superficial digital flexor tendon (Figure 4B).4-6 Mild strains can be treated with medical management (eg, rest, NSAIDs, physiotherapy, orthotics); however, if a gait abnormality is present, surgical repair of the muscle–tendon unit is recommended.4-6

Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).
Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).

FIGURE 4 Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).

Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).
Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).

FIGURE 4 Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).

FIGURE 4 Two clinical presentations of Achilles tendon injury. A complete plantigrade stance with relaxed toe position, with complete rupture of the 3 components of the Achilles tendon (A), is present. Increased flexion angle of the tarsus with curling or flexion of the digits is present when the gastrocnemius tendon is ruptured and the superficial digital flexor tendon is intact (B).

3

Iliopsoas Muscle Strain

The iliopsoas muscle consists of the iliacus and psoas major muscle groups, which originate along the lumbar spine and ilium and insert on the lesser trochanter of the femur. Its main function is to flex and externally rotate the hip. Injury can occur secondary to an acute excessive force or repetitive use and/or trauma, resulting in a mild-to-severe pelvic limb lameness.7-10 Pain often can be elicited on examination by extension and internal rotation of the hip joint, abduction of the femur, and direct palpation of the muscle–tendon junction near the lesser trochanter.7-10 Because the femoral nerve runs through the iliopsoas muscle, some dogs that strain this muscle may also develop a peripheral neuropathy from compression of the nerve.8,9 Standard radiography can identify mineralization in the tendon, whereas ultrasonography, CT, and MRI are helpful for identifying early and subtle lesions and can help direct therapy (Figures 5 and 6).8-10 Mild-to-moderate acute lesions can often be treated with medical management (eg, rest, NSAIDs, physiotherapy, platelet-rich plasma injections).10 If the lesion is severe and results in fibrosis or contracture of the muscle, a partial tenectomy may be indicated.8,10

4

Contracture of the Infraspinatus Muscle

Contracture of the infraspinatus muscle is most commonly seen in medium- and large-breed hunting dogs.11-14 Patients frequently have an initial forelimb lameness associated with an acute strain that resolves over several weeks. A characteristic forelimb gait abnormality then develops as the muscle irreversibly contracts.11-14 Because the infraspinatus muscle runs from the infraspinous fossa to the lateral aspect of the greater tubercle of the humerus, contracture results in the inability to extend the shoulder completely, and the limb is externally rotated and held in an abducted position.11-14 When walking, the limb is circumducted with the elbow partially flexed. This unique gait abnormality is easily observed when the patient walks up or down stairs (Figure 7). Surgical treatment is required and consists of a partial tenectomy of the infraspinatus muscle, which results in immediate improvement in gait abnormality and provides an excellent prognosis.11-14

Characteristic gait abnormality in a patient with infraspinatus muscle contracture. The limb is held in an abducted and externally rotated position and is circumducted with the elbow partially flexed when ambulating.
Characteristic gait abnormality in a patient with infraspinatus muscle contracture. The limb is held in an abducted and externally rotated position and is circumducted with the elbow partially flexed when ambulating.

FIGURE 7 Characteristic gait abnormality in a patient with infraspinatus muscle contracture. The limb is held in an abducted and externally rotated position and is circumducted with the elbow partially flexed when ambulating.

FIGURE 7 Characteristic gait abnormality in a patient with infraspinatus muscle contracture. The limb is held in an abducted and externally rotated position and is circumducted with the elbow partially flexed when ambulating.

5

Luxation of the Superficial Digital Flexor Tendon

The superficial digital flexor tendon extends distal to the calcaneus, gliding over a bursa and the calcaneal tuber as it is supported by retinaculum on either side. Traumatic injury resulting in rupture of the retinaculum and medial or lateral displacement of the tendon has been reported in dogs and a cat.15,16 In Shetland sheepdogs, a hereditary basis has been established, and luxation is almost always lateral and caused by varying degrees of flattening of the lateral aspect of the calcaneal tuber.17 Depending on the inciting cause, clinical signs can include acute or chronic intermittent pelvic limb lameness and swelling around the calcaneal tuber.15-17 In some cases, the tendon can be luxated and reduced manually, with the tarsus held in extension.15,16 Medical management is ineffective for this condition.15-17 Prognosis is good to excellent following surgical treatment directed at repairing the torn retinaculum, imbrication of redundant retinaculum, and, in some cases, deepening the groove between the medial and lateral processes of the calcaneal tuber.15-17

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Isoxazolines

Isoxazolines

Craig Datz, DVM, MS, DABVP (Canine & Feline), DACVN, University of Missouri

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Isoxazolines

Isoxazolines kill fleas and are indicated for the treatment and prevention of flea infestations, as well as the treatment and control of various tick infestations.1-6

OVERVIEW

  • The isoxazoline drug class was launched in the United States in 2014 with afoxolaner, followed shortly by oral fluralaner, sarolaner, topical fluralaner, and lotilaner.

MECHANISM OF ACTION

  • Isoxazolines are absorbed systemically; fleas and ticks must bite the animal to be killed. 
    • Isoxazolines work by selective inhibition of GABA- and glutamate-gated chloride channels, leading to hyper-excitation and death of the flea or tick.7-10 
    • Because GABA channels in mammals have much a lower sensitivity to isoxazolines and mammals lack anion-inhibitory glutamate channels, there is low toxicity potential.8
  • For fleas, the onset of action for all products is reported to be 2 to 4 hours, with nearly 100% of fleas killed within 8 hours1-6; for ticks, the onset of action for >90% tick control is 4 to 8 hours, although study protocols often assess tick control at 48 hours after administration.1-6

CLINICAL APPLICATION

  • Several studies have shown that isoxazolines can reduce the risk for tick-borne disease transmission. 
    • Afoxolaner and sarolaner each prevented Borrelia burgdorferi infection (ie, Lyme disease) in controlled laboratory studies.11,12 
    • In other laboratory studies, afoxolaner, fluralaner, and lotilaner each prevented transmission of Babesia canis.13-16 
    • Ixodes holocyclus, the Australian paralysis tick, was controlled by afoxolaner, fluralaner, and sarolaner.17,18 
    • In a comparative laboratory study, transmission of Ehrlichia canis was prevented by permethrin–imidacloprid and prevented in some but not all dogs by either afoxolaner or fluralaner.19

ADMINISTRATION & DOSING

  • Fluralaner and lotilaner chewables should be administered with food, whereas afoxolaner and sarolaner may be given with or without food.1-3,6
  • Labeled ages, body weights, and dosing intervals vary (see Isoxazolines at a Glance).
    • Collies with the multidrug sensitivity gene (MDR1 gene, also known as ABCB1 gene) mutation (ivermectin-sensitive) were treated with up to 10 times the label dose of afoxolaner or 3 times the label dose of fluralaner with no adverse effects noted.20,21 
  • Fluralaner has been shown to be well tolerated with concurrent use of milbemycin–praziquantel and deltamethrin collars in dogs and emodepsid–praziquantel in cats.22-24
  • Extra-label use of isoxazolines for other ectoparasites has been reported. 
    • In one study of generalized demodicosis in 8 adult dogs, a single dose of fluralaner resulted in elimination of Demodex canis mites and resolution of dermatologic signs.25 
    • Afoxolaner, sarolaner, and lotilaner at label doses were also shown to be effective in dogs with generalized demodicosis.26-29 
    • In dogs with Sarcoptes scabiei var canis, 2 doses of afoxolaner (on days 0 and 28) or sarolaner (on days 0 and 30) or a single dose of fluralaner eliminated mites and resulted in skin improvement within 4 weeks.30-33 
    • Dogs with ear mites (Otodectes cynotis) have been successfully treated with afoxolaner, fluralaner, and sarolaner; topical fluralaner is effective in cats with ear mites.28,34,35

TABLE

ISOXAZOLINES AT A GLANCE1-5

Drug Species Product Minimum Age Minimum Body Weight Dosing Interval
Afoxolaner Dog Chew 8 weeks 4 lb (1.8 kg) 1 month
Fluralaner Dog Chew 6 months 4.4 lb (2 kg) 12 weeks*
Sarolaner Dog Chew 6 months 2.8 lb (1.3 kg) 1 month
Lotilaner Dog Chew 8 weeks 4.4 lb (2 kg) 1 month
Fluralaner Dog Topical solution 6 months 4.4 lb (2 kg) 12 weeks*
Fluralaner Cat Topical solution 6 months 2.6 lb (1.2 kg) 12 weeks*

 

*The dosing interval is every 8 weeks for Amblyomma americanum (lone star) ticks.2,4

SAFETY & ADVERSE EFFECTS

  • Vomiting, diarrhea, lethargy, and decreased appetite were occasionally observed in safety studies in puppies 8 to 9 weeks old (in both treated and control groups) at 1 time, 3 times, and 5 times the maximum oral label dose and in field studies.1-4,6,9,36-38 
    • Neurologic signs (eg, tremors, seizures) were noted in some puppies treated with sarolaner at 3 to 5 times the label dose.3 
    • Fluralaner topical solution was similarly studied in dogs and cats; other than cosmetic changes at the application sites, no treatment-related adverse effects were observed.4,5 
    • In the feline field study, neurologic signs were seen with topical fluralaner in 2 of 224 cats5; this drug should be used with caution in cats with a history of neurologic disease.5
  • Safety in breeding, pregnant, or lactating dogs has not been evaluated for afoxolaner, sarolaner, or lotilaner.1,3,6 
    • Oral fluralaner was studied at up to 3 times the maximum label dose at 8-week intervals in male and female beagles through breeding, pregnancy, and lactation. 
      • No treatment-related effects were observed in the adult dogs or on reproductive performance. 
      • In litters from 2 of 10 dams, abnormalities (eg, limb deformity, cleft palate) were noted in some puppies on gross examination.2
  • In uncontrolled, open-label field studies, all drugs were effective in reducing or resolving signs of flea allergy dermatitis in dogs.39-43

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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Splenectomy: Hilar Ligation Technique

W. Alex Fox-Alvarez, DVM, DACVS-SA, University of Florida

J. Brad Case, DVM, MS, DACVS, University of Florida

Surgery, Soft Tissue

|Peer Reviewed

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Splenectomy: Hilar Ligation Technique

The spleen has a diverse set of functions, including hematopoiesis, RBC filtration and storage, and immune surveillance. Despite its many functions, removal of the spleen is commonly performed in dogs and cats with rarely observed long-term adverse sequelae. Splenectomy is indicated in cases of splenic neoplasia, trauma, torsion, and infiltrative disease and, occasionally, as treatment for immune-mediated disorders. It is also commonly performed on an emergency basis for hemoabdomen of splenic origin.

Spleen Anatomy

Clinicians should have an understanding of the splenic and regional vascular anatomy before performing splenectomy. The spleen is located on the left side of the body. The head of the spleen is the craniodorsal-most portion and is attached to the greater curvature of the stomach via the gastrosplenic ligament, in which the short gastric arteries and veins are located. The tail of the spleen is the larger, caudal, more mobile portion that sweeps across the ventral midline, with a loose terminal attachment to the greater omentum. 

The main blood supply to the spleen comes from the splenic branch of the celiac artery. This splenic artery runs along the left limb of the pancreas, giving off pancreatic branches before spreading into the vessels supplying the splenic parenchyma. It is important to avoid ligating the splenic vessels proximal to these pancreatic branches to avoid damaging pancreatic blood supply. 

Splenic and regional vascular anatomy showing the splenic artery (A), gastroepiploic artery (B), short gastric arteries (C), and omental arteries (D)
Splenic and regional vascular anatomy showing the splenic artery (A), gastroepiploic artery (B), short gastric arteries (C), and omental arteries (D)

FIGURE Splenic and regional vascular anatomy showing the splenic artery (A), gastroepiploic artery (B), short gastric arteries (C), and omental arteries (D)

FIGURE Splenic and regional vascular anatomy showing the splenic artery (A), gastroepiploic artery (B), short gastric arteries (C), and omental arteries (D)

The head of the spleen is supplied by the short gastric arteries, which arise from the dorsal branch of the splenic artery and anastomose with the branches of the left gastric artery. The majority of the spleen is supplied by the ventral branch of the splenic artery and its numerous intermediate branches into the hilus. The ventral splenic artery continues as the left gastroepiploic artery supplying the greater curvature and fundic portion of the stomach. Ideally, this continuation should be preserved; however, it was shown that sacrifice of the left gastroepiploic vessel did not compromise gastric blood flow or the integrity of the gastric wall in healthy dogs.1 At the terminal portion of the tail of the spleen, the vessels continue as branches to the omentum.

Surgical Approach

The least complicated anatomic approach to splenectomy that ensures no inadvertent ligation of the pancreatic or left gastroepiploic vessels is the hilar ligation technique. With this technique, the vessels are ligated as they terminate into the spleen. The speed of this technique varies depending on the manner of ligation used, with the use of a vessel-sealing device being the fastest, followed by a staple or clip device, and lastly suture ligation. Some devices can seal vessels up to 7 mm in diameter, whereas hemostatic clips are appropriate for vessels up to 3 mm in diameter. With the appropriate size and material, hand ligation with suture can be used in any size vessel for splenectomy. The following describes the hilar approach to splenectomy. 

Of note, one study evaluating the relationship between gastric dilatation volvulus and previous splenectomy found dogs with a previous splenectomy to be 5.3 times more likely to develop gastric dilatation volvulus than were dogs without splenectomy.2 Other studies have reported development of gastric dilatation volvulus in atypical breeds (eg, bichon frise, beagle) after splenectomy, which suggests splenectomy may be a potential predisposing factor.3 Thus, some surgeons may recommend prophylactic gastropexy be performed in dogs undergoing splenectomy.

STEP-BY-STEP

SPLENECTOMY: HILAR LIGATION TECHNIQUE


WHAT YOU WILL NEED

  • Standard general surgery pack including needle holders, thumb forceps, Metzenbaum scissors, suture scissors, and hemostatic forceps (8-12 inches [20-30 cm])
  • Balfour retractor 
  • Abdominal laparotomy sponges 
  • Suction device and Poole suction tip 
  • Electrosurgery handpiece (helpful, but not required)
  • Suture for ligation (generally 2-0 to 3-0 size, depending on patient and pedicle size) 
  • +/- Hemostatic clip or staple applicator (optional alternative or supplement to sutures)
  • +/- Vessel sealing device (optional alternative or supplement to sutures)

STEP 1

Position the patient in dorsal recumbency (A), and prepare the abdomen with a standard aseptic technique. Drape the patient from xiphoid to pubis (B). In male dogs, maintain the penis out of the sterile field.

Clinician's Brief
Clinician's Brief

STEP 2

Make a ventral midline abdominal incision from the xiphoid to 2 to 3 cm caudal to the umbilicus (A). The incision can be extended caudally if the size of the mass requires. Using electrosurgical instruments or ligation, remove the falciform fat en bloc to improve exposure (B). In rare cases, extension from midline into a paracostal incision may be indicated for removal of larger splenic masses.

Clinician's Brief
Clinician's Brief

STEP 3

Perform a methodical exploration of the abdomen. If hemoabdomen is present, use suction to remove the hemorrhage and improve visualization. Carefully inspect the liver and the remaining abdominal viscera to monitor for presence of gross metastasis. A liver biopsy is indicated in cases of suspected malignancy regardless of gross appearance (see Liver Biopsy). Gently manipulate the spleen out of the body and onto moistened laparotomy sponges. A diseased spleen is often friable and should be carefully handled to prevent rupture. If the omentum is adhered to a splenic mass, divide the adhesions using electrosurgical devices or ligation. Digital dissection is not recommended, as rupture of the splenic mass may occur.


STEP 4

The hilar vessels can be visualized as they enter the splenic parenchyma (A). Using hemostatic forceps, bluntly isolate the vessels (B). Using 3-0 absorbable suture, circumferentially double ligate the hilar pedicles (C and D). Before transecting the vessel, place hemostatic forceps on the pedicle close to the spleen (E); this will help prevent splenic bleeding. Repeat this step for all vessels along the splenic hilus until the spleen is removed (F).

Author Insights

As an alternative to suture ligation, splenic hilar vessels can be ligated using a vessel-stapling apparatus or a vessel-sealing device.4

To speed up splenectomy, a surgical assistant can work on isolating the splenic hilar vessels using hemostatic forceps while the surgeon ligates and divides the isolated vessels.

One veterinary study demonstrated no difference in clinical outcome between splenectomy performed using a vessel-sealing device versus a stapler; however, the sealing device yielded significantly shorter procedure times.5 Another study found the bursting strength of the sealing device to be greater than 300 mm Hg (ie, ≈3 times systolic pressure).6


STEP 5

After removing the spleen, biopsy any other grossly abnormal tissue. Check the splenic pedicles and biopsy sites for appropriate hemostasis, then gently lavage with warm sterile saline and evacuate the fluid. Perform routine abdominal closure. 

Submit the spleen and tissue for histopathologic evaluation. 


Postoperative Care & Monitoring

IV fluids should be continued postoperatively and matched to meet the patient’s needs. Ongoing monitoring should include serial packed cell volume checks, continuous ECG for assessment of changes in heart rate and rhythm, twice-daily urine output assessment, body weight monitoring, and serial venous blood gas and lactate monitoring. IV opioid analgesics should be administered for at least 24 to 48 hours before weaning or switching to oral analgesic medications. Perioperative antibiotics should not be required for longer than 24 hours unless splenectomy was performed for splenic abscess, in which case antibiotics should be chosen based on results of culture and susceptibility testing and administered for 10 to 14 days.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


Top 5 Causes of Splenomegaly in Dogs

Todd Archer, DVM, MS, DACVIM, Mississippi State University

Alyssa Sullivant, DVM, MS, DACVIM, Mississippi State University

Internal Medicine

|Peer Reviewed

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Top 5 Causes of Splenomegaly in Dogs

The spleen is a complex organ composed of 2 distinct parenchymal areas (red pulp and white pulp), each with important hematologic and immunologic functions.

The red pulp filters blood and removes senescent or damaged blood cells, aids in the metabolism and subsequent recycling of iron, and serves as a site for hematopoiesis, producing leukocytes, platelets, and RBCs when demand is increased. Regions of white pulp consist of lymphoid tissue that produces and stores immune cells (eg, lymphocytes, macrophages), which provide immune surveillance of blood for “foreign” material (eg, cells harboring infectious organisms, antibody-coated cells that are targeted for destruction and removal from circulation). The spleen also acts as a reservoir of blood, storing up to 20% of the total RBC mass and up to 30% of the platelet mass in the body. The spleen releases RBCs and platelets readily to meet physiologic demand. 

Splenic disorders are common in middle-aged and older dogs, with clinical signs ranging from vague signs of illness to life-threatening hemoabdomen. In these disorders, splenomegaly is often present, regardless of disease severity. Splenomegaly is typically caused by discrete nodule(s) or diffuse enlargement.1 Although splenomegaly can be present in the absence of clinical signs, patients with chronic splenic disease may exhibit lethargy, inappetence, vomiting, abdominal enlargement, and weight loss. Patients presented with hemoabdomen are often collapsed and in hypovolemic shock. Arrhythmias are common with splenic diseases, especially hemangiosarcoma.2 Splenomegaly may be detected on abdominal palpation or through imaging modalities such as radiography, ultrasonography, or advanced imaging. Imaging is useful for differentiating a splenic mass from diffuse splenomegaly and is important in narrowing the possible causes of splenomegaly. 

The “two-thirds/two-thirds”2 and “fifty/fifty”3 rules are often cited regarding the incidence of splenic malignancy. In a study of 325 dogs, 66% of dogs with splenomegaly were diagnosed with splenic malignancy, and 65% of those malignancies were hemangiosarcoma.2 An earlier study of 1480 dogs found that approximately 50% of splenic samples represented malignancy, with hemangiosarcoma accounting for approximately 50% of malignancies.3 However, in a study of 105 dogs with nonruptured splenic masses, 70.5% had benign splenic lesions and 29.5% had malignant neoplasia, with hemangiosarcoma accounting for 58% of malignancies.4 Although splenic neoplasia is a common cause of splenomegaly, it is impossible to differentiate between malignant and benign lesions grossly. A definitive diagnosis should be obtained before considering euthanasia. Fine-needle aspiration of the spleen is safe, and cytologic diagnoses correspond to histologic diagnoses in at least 50% of cases.5-7 Submission of the entire spleen for histopathology is recommended to increase the likelihood of distinguishing between benign and malignant processes, particularly between hemangiosarcoma and hematoma.1 

Following are the authors’ top 5 causes of splenomegaly seen most often in veterinary practice. 

1

Hemangiosarcoma

Hemangiosarcoma is the most common malignant disease of the spleen, representing one-half to two-thirds of all malignant splenic tumors. It is more prevalent in older medium- and large-breed dogs (eg, German shepherd dogs, golden retrievers, Labrador retrievers, standard poodles).2,8 Hemangiosarcoma arises from the vascular endothelium and often develops into a large cavitary mass in the spleen (Figure 1). Approximately 25% of dogs with splenic hemangiosarcoma may have concurrent hemangiosarcoma affecting the right side of the heart.9 Clinical signs are typically related to anemia, which may be mild to severe and life-threatening, and include pale mucous membranes, tachycardia, lethargy, and abdominal distention.8 Intra- and extrasplenic hemorrhage may occur and can cause marked hemoabdomen and acute anemia with subsequent hypovolemia and collapse. Although hematomas and, less commonly, other benign splenic lesions may cause hemoabdomen, hemangiosarcomas are more likely to cause hemoabdomen.8 Blood study findings can include schistocytosis, thrombocytopenia, and, possibly, disseminated intravascular coagulation.

Hemangiosarcomas are the most common splenic malignancy in dogs.3 Lesions are often cavitary, and hemoabdomen is common.
Hemangiosarcomas are the most common splenic malignancy in dogs.3 Lesions are often cavitary, and hemoabdomen is common.

FIGURE 1 Hemangiosarcomas are the most common splenic malignancy in dogs.3 Lesions are often cavitary, and hemoabdomen is common.

FIGURE 1 Hemangiosarcomas are the most common splenic malignancy in dogs.3 Lesions are often cavitary, and hemoabdomen is common.

Initial testing and staging should include CBC, serum chemistry profile, coagulation testing (prothrombin time and partial thromboblastin time), 3-view thoracic radiography, abdominal ultrasonography, and cardiac ultrasonography. Splenic aspirates may disclose malignant cells or evidence of nonspecific hemorrhage only, and a definitive diagnosis requires histopathology. Dogs with Stage I hemangiosarcoma have a solitary primary tumor less than 5 cm in diamter, and dogs with Stage II have a primary tumor that is ruptured, is greater than 5 cm in diameter, or has lymph node involvement.8 Stage III dogs have splenic rupture or lymph node involvement and evidence of distant metastasis.8 Survival times do not differ markedly between stages.8 Splenectomy alone yields a median survival time of 86 days, whereas dogs receiving adjunctive doxorubicin-based chemotherapy have a longer median survival time of 172 days if no evidence of gross disease is present after surgery.10

2

Extramedullary Hematopoiesis

Extramedullary hematopoiesis (EMH; ie, hematopoiesis occurring outside the bone marrow) causes diffuse uniform symmetric enlargement of the spleen (because of “work hypertrophy”) with increased activity of the mononuclear phagocytic system and increased blood cell production.10 Hypoxia is the main stimulus for splenic EMH in an adult animal11 and can be seen with any disease that undermines the ability of the bone marrow to function properly. 

Because EMH is a benign condition that occurs in response to an underlying hematologic abnormality, diagnostic efforts are directed at the disease process driving the EMH. Mild EMH occurs with many splenic and nonsplenic disorders11 and can be seen with both immune-mediated hemolytic anemia and immune-mediated thrombocytopenia, as the spleen is a major site of removal and destruction of antibody-coated cells and a site for extramedullary production of blood cells. EMH can also be associated with a variety of splenic neoplasms. In patients with EMH, ultrasonography typically shows focal or diffuse, heterogenous nodules or masses within the spleen.4,6

Fine-needle aspiration of lesions yields a predominance of small lymphocytes.11 Myeloid and erythroid precursors may be seen, particularly in anemic patients (Figure 2).10 A concurrent CBC analysis is recommended to determine which hematologic abnormality is responsible for splenic EMH.11 Frequently, increased numbers of immature cells (eg, nucleated RBCs) may be seen in the circulation due to splenic EMH.11

Erythroid (arrow) and myeloid (arrowhead) precursors are common cytologic findings in splenic extramedullary hematopoiesis, particularly in response to anemia.11 Lymphocytes (asterisk) are also commonly seen.
Erythroid (arrow) and myeloid (arrowhead) precursors are common cytologic findings in splenic extramedullary hematopoiesis, particularly in response to anemia.11 Lymphocytes (asterisk) are also commonly seen.

FIGURE 2 Erythroid (arrow) and myeloid (arrowhead) precursors are common cytologic findings in splenic extramedullary hematopoiesis, particularly in response to anemia.11 Lymphocytes (asterisk) are also commonly seen.

FIGURE 2 Erythroid (arrow) and myeloid (arrowhead) precursors are common cytologic findings in splenic extramedullary hematopoiesis, particularly in response to anemia.11 Lymphocytes (asterisk) are also commonly seen.

3

Multicentric Lymphoma

Lymphoma is a systemic disorder of uncontrolled proliferation of neoplastic lymphoid cells. Multicentric lymphoma is the most common form of lymphoma in dogs, and the liver and/or spleen are frequently involved (Stage IV).12 Infiltration of neoplastic lymphoid cells often causes a diffuse enlargement of the spleen that results in a characteristic “honeycomb” or “moth-eaten” appearance on ultrasonography (Figure 3),13 which has a sensitivity of 100%, specificity of 23.3%, positive predictive value of 64.7%, negative predictive value of 100%, and accuracy of 68.1% for diagnosis of splenic lymphoma.13

Numerous, variably sized, sharply defined, hypoechoic nodules with a “honeycomb-like” appearance are characteristic of splenic lymphoma.
Numerous, variably sized, sharply defined, hypoechoic nodules with a “honeycomb-like” appearance are characteristic of splenic lymphoma.

FIGURE 3 Numerous, variably sized, sharply defined, hypoechoic nodules with a “honeycomb-like” appearance are characteristic of splenic lymphoma.

FIGURE 3 Numerous, variably sized, sharply defined, hypoechoic nodules with a “honeycomb-like” appearance are characteristic of splenic lymphoma.

In one study, fine-needle splenic aspirate findings confirmed lymphoma in all multicentric lymphoma patients with a moth-eaten appearance of the spleen.13 Further differentiating lymphoma type (B-cell vs T-cell) using flow cytometry helps with prognosis. Treatment with chemotherapy is considered standard of care and is associated with 80% to 90% remission rates with median survival times of 10 to 12 months, depending on the chemotherapy protocol used.12

4

Nodular Hyperplasia/ Hematoma

Nodular hyperplasia and hematoma are thought to be a continuum of the same process, which starts as nodular hyperplasia and possibly results in formation of a hematoma.10 Hyperplastic nodules are benign masses that typically cause discrete abnormal areas in the spleen. During ultrasonography, hyperplastic nodules appear as focal or diffuse discrete hyperechoic, hypoechoic, or isoechoic masses—which may or may not cause shadowing—in the spleen. They may cause an irregular splenic border, but rarely do hyperplastic nodules distort, or bulge, the splenic capsule. These nodules cannot be distinguished from neoplasia by ultrasonography alone.14,15 They consist of a benign accumulation of cells normally found in the spleen, including lymphoid, hematopoietic, and plasmacytic cellular infiltrates, and develop in response to antigenic stimulation from a variety of inflammatory or neoplastic conditions.11 One study suggested that a hematoma may develop when blood flow (out of the spleen) is disrupted by hyperplastic nodules.3 

Hematomas consist of hemorrhage and organized fibrin and are the most common benign splenic lesion (Figure 4).2,3 Although uncommon, some hyperplastic nodules, especially large hyperplastic nodules, may distort or bulge the splenic capsule. Hemoabdomen may also occur, but the incidence is markedly lower than in hemangiosarcoma.2 Surgical excision is indicated for hematomas and hyperplastic nodules large enough to cause splenomegaly, with excision being curative. Because hematomas may develop in neoplastic tissue, submission of the entire spleen for histopathology is crucial to minimize the risk for misclassifying a malignant neoplasm as a hematoma.16

Splenic hematomas are the most common benign splenic mass. They may be quite large and are grossly indistinguishable from hemangiosarcoma.
Splenic hematomas are the most common benign splenic mass. They may be quite large and are grossly indistinguishable from hemangiosarcoma.

FIGURE 4 Splenic hematomas are the most common benign splenic mass. They may be quite large and are grossly indistinguishable from hemangiosarcoma.

FIGURE 4 Splenic hematomas are the most common benign splenic mass. They may be quite large and are grossly indistinguishable from hemangiosarcoma.

5

Congestion

Splenic congestion has numerous causes, including sedation, anesthesia, thrombosis, right-sided congestive heart failure, splenic torsion, and portal hypertension. Splenic congestion may cause severe splenomegaly and clinical signs, as the spleen is capable of pooling up to 30% of blood volume.10 Smooth muscle relaxation may be responsible for drug-induced splenic congestion, which is transient and may be limited to certain drugs (eg, phenothiazine sedatives, ultrashort-acting barbiturates).17 Administration of acepromazine, thiopental, or propofol produces marked splenomegaly.18 Severe hepatic disease may lead to portal hypertension and subsequent splenomegaly. Increased systemic hydrostatic pressure from right-sided congestive heart failure or increased splenic vein hydrostatic pressure because of thrombosis may cause splenic congestion.

Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.
Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.

FIGURE 5 Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.

Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.
Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.

FIGURE 5 Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.

FIGURE 5 Splenic torsion appears as a large soft-tissue opacity that displaces the GI tract caudally and peripherally (A). The splenic head is obscured caudal to the left margin of the stomach (B). The metallic opacity seen in the stomach and intestines is caused by recent barium administration.

Treatment of the underlying disease in these conditions may relieve or reduce splenomegaly. In cases of splenic torsion (Figures 5 and 6), splenectomy is the recommended treatment, with approximately 90% of dogs surviving to discharge.19

The spleen is markedly enlarged, hypoechoic, and lacy, with hyperechoic patches surrounding the hilus. A perivenous hyperechoic triangle at the splenic hilus is continuous with the mesentery, and no flow is present on Doppler. These findings are often associated with splenic torsion.20
The spleen is markedly enlarged, hypoechoic, and lacy, with hyperechoic patches surrounding the hilus. A perivenous hyperechoic triangle at the splenic hilus is continuous with the mesentery, and no flow is present on Doppler. These findings are often associated with splenic torsion.20

FIGURE 6 The spleen is markedly enlarged, hypoechoic, and lacy, with hyperechoic patches surrounding the hilus. A perivenous hyperechoic triangle at the splenic hilus is continuous with the mesentery, and no flow is present on Doppler. These findings are often associated with splenic torsion.20

FIGURE 6 The spleen is markedly enlarged, hypoechoic, and lacy, with hyperechoic patches surrounding the hilus. A perivenous hyperechoic triangle at the splenic hilus is continuous with the mesentery, and no flow is present on Doppler. These findings are often associated with splenic torsion.20

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

All Clinician's Brief content is reviewed for accuracy at the time of publication. Previously published content may not reflect recent developments in research and practice.

Material from Digital Edition may not be reproduced, distributed, or used in whole or in part without prior permission of Educational Concepts, LLC. For questions or inquiries please contact us.


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