November / December 2022   |   Volume 20   |   Issue 8

Therapy Options for Vestibular Dysfunction in a Geriatric Dog

Dog laying on bed

in this issue

in this issue

Vestibular Dysfunction in a Geriatric Dog

Pruritus in a Hyperthyroid Cat

Abdominal Palpation in Dogs & Cats

Top 5 Causes of Erythrocytosis in Dogs & Cats

Differential Diagnosis: Elevated ALT

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Abdominal Palpation in Dogs & Cats

Alice Defarges, DVM, MSc, DACVIM, University of Guelph

Allison Collier, DVM, DVSc, University of Guelph

Internal Medicine

|Peer Reviewed

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Abdominal Palpation in Dogs & Cats

Abdominal palpation can help identify and localize abdominal pain during physical examination. Pathology (eg, abdominal masses, organomegaly) may be identified via palpation before development of clinical signs. Palpation should be learned through practice, ideally with a mentor, and repeated if abnormalities are missed on palpation but subsequently identified on imaging.

Distance Examination

Prior to palpation, the contour of the abdomen can be visually assessed (Figure 1). An abnormal contour (eg, disappearance of the flank or abdominal tuck) can indicate abdominal enlargement; differential diagnoses include obesity, pregnancy, organomegaly, and ascites.

Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)
Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)

FIGURE 1 Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)

Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)
Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)

FIGURE 1 Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)

FIGURE 1 Normal abdominal contour (A); abnormal abdominal contour and abdominal enlargement caused by ascites (B)

Assessing position and demeanor can also be beneficial. Patients with abdominal pain may be unwilling to roll onto their back, and patients with cranial abdominal pain may demonstrate prayer position (ie, lowered cranial half of the body and raised caudal half; Figure 2).

Prayer position, which often indicates cranial abdominal pain
Prayer position, which often indicates cranial abdominal pain

FIGURE 2 Prayer position, which often indicates cranial abdominal pain

FIGURE 2 Prayer position, which often indicates cranial abdominal pain

Palpation Technique

Abdominal palpation can be performed using the PALPATE (ie, position, anatomy, level, pressure, assessment, thorough systematic approach, extra-abdominal assessment) technique.1


STEP-BY-STEP

ABDOMINAL PALPATION


STEP 1

Position

Provide a comfortable, safe position for the clinician and patient (ie, table for small dogs or cats, floor for large dogs) in a quiet, calm environment. If palpation is challenging (eg, patient is obese, tense, painful, or stressed), try placing the patient in lateral recumbency.

Author Insight

An assistant should be present to restrain the patient.


STEP 2

Anatomy

Visualize the 3D orientation of abdominal organs (see Approximate Location of Organs in the Abdominal Cavity).

APPROXIMATE LOCATION OF ORGANS IN THE ABDOMINAL CAVITY

  • Cranial abdomen
    • Stomach
    • Liver
    • Spleen
    • Pancreas
  • Mid-abdomen
    • Spleen
    • Kidneys (dorsal)
    • Adrenal glands (dorsal)
    • Small intestine
  • Caudal abdomen
    • Urinary bladder
    • Prostate
    • Uterus
    • Colon
    • Small intestine
Clinician's Brief
Clinician's Brief
Clinician's Brief

Author Insight

Abdominal organ location varies among normal patients (A), patients with hepatomegaly (indicated by the liver extending beyond the costal margin; B), and patients with an abdominal mass (C). Understanding which organs are normally palpable or nonpalpable can help identify abnormalities (see Palpable & Nonpalpable Organs on Normal Abdominal Palpation).

PALPABLE & NONPALPABLE ORGANS ON NORMAL ABDOMINAL PALPATION

  • Palpable
    • Intestines, colon
    • Bladder (if full)
    • Both kidneys (cats); ± caudal pole of left kidney (dogs)
    • Tail of spleen
  • Nonpalpable
    • Liver
    • Pancreas
    • Stomach
    • Adrenal glands
    • Uterus (except with pregnancy or pyometra)
    • Ovaries
    • Lymph nodes

STEP 3

Level

Avoid superficial palpation that only detects abdominal wall musculature and deep palpation that can cause pain.


STEP 4

Pressure

Apply gentle, progressive pressure on the abdomen. To appreciate organ shape and size in medium and large dogs, hold the abdomen between both hands (ie, 2-handed technique; A). For cats and small dogs, hold the abdomen between the thumb and fingers of one hand (ie, one-handed technique; B).2,3 Bring the fingers together with a light but forceful touch, and move the fingers in a dorsal to ventral direction.

Clinician's Brief
Clinician's Brief

Author Insight

Gentle palpation is recommended in postoperative patients and those with either suspected hemoabdomen or urethral obstruction to avoid hemorrhage from a mass or bladder rupture, respectively.


STEP 5

Assessment

Use the fingertips to sense the size and shape of organs and detect abnormalities (eg, masses, pain, abdominal distension, organomegaly, foreign objects).

Liver

Palpate the cranial abdominal cavity beneath the costal arch; hepatomegaly is commonly indicated if margins of the liver extend beyond the rib cage.

Clinician's Brief
Spleen

Palpate the mid-abdomen, usually on the left side. The tail of the spleen may be felt on the ventral abdominal floor in a normal dog in a recumbent position.

Kidneys

Palpate the dorsal abdomen.

Author Insight

Only the caudal poles of the kidneys are palpable in dogs. In some dogs, the entire right kidney is in the rib cage, and in other dogs, neither caudal pole may be palpable because of surrounding musculature and adipose tissue. Both kidneys are palpable in cats and are more mobile than in dogs, allowing assessment of shape, contour, and symmetry. Because feline kidneys can be incorrectly palpated as one large kidney, one hand should be kept still while the other hand is moved to separate the kidneys.

Intestines

Place the fingers on either side of the mid-abdomen, press the fingers toward each other, and move them in a dorsal to ventral direction; loops of intestines may be felt slipping through the fingers. Assess the intestines for thickening, masses, intussusception, and foreign objects. 

Palpate the dorsal abdomen; the colon may be felt as a tubular structure if filled with feces. Fecal material is typically compressible; do not confuse fecal material with an abdominal mass.

Clinician's Brief

Author Insight

Although characterization of an abdominal mass via palpation can raise suspicion for differential diagnoses, palpation is rarely diagnostic. Imaging studies are usually required to better locate and characterize a mass.

Bladder

Palpate the caudal abdomen for a fluid-filled balloon-like structure; the urinary bladder is often pear-shaped in dogs and spherical in cats. Assess size and firmness; the bladder is often firm and round in patients with urethral obstruction. Palpate gently if an obstruction is suspected to avoid bladder rupture.

Clinician's Brief

STEP 6

Thorough Systematic Approach

Use a consistent technique (eg, cranial to caudal, dorsal to ventral) to ensure all areas of the abdomen are evaluated and none are missed, which could result in unidentified lesions and inaccurate diagnoses.


STEP 7

Extra-Abdominal Assessment

Palpate the back for pain that may confound abdominal palpation findings. Evaluate the abdominal wall for hernias, lipomas, masses, evidence of skin disease, and evidence of dermatologic lesions (eg, petechiae and ecchymoses, both of which may be indicative of coagulopathy and warrant more gentle palpation).


Fluid Wave Technique

Assessing for abdominal fluid during abdominal palpation is important, as a fluid wave can suggest ascites.

STEP-BY-STEP

FLUID WAVE TO ASSESS FOR ABDOMINAL FLUID


STEP 1

Place one hand on either side of the abdomen.


STEP 2

Perform gentle ballottement of the abdomen with one hand, keeping the other hand in a fixed position on the opposite side of the abdomen for at least 3 to 5 seconds to allow the impulse to be transmitted through the abdominal fluid (if a fluid wave is present) and perceived (ie, tap; Video).

VIDEO

Author Insight

A minimum of 30 to 40 mL/kg of peritoneal fluid is necessary for detection of a fluid wave.4 Lack of a fluid wave thus does not rule out ascites, and presence of a fluid wave does not indicate the cause of ascites.

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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Pruritus in a Hyperthyroid Cat

Antonia Ioannou, BVMS, MRCVS, Cummings School of Veterinary Medicine at Tufts University

Orla Mahony, MVB, DACVIM & DECVIM, Tufts University Cummings School of Veterinary Medicine

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Pruritus in a Hyperthyroid Cat

Figure Facial excoriations

Fleur, a 12-year-old spayed domestic shorthair cat, is presented for a one-week history of worsening pruritus. She was diagnosed with hyperthyroidism 6 weeks prior, and treatment with methimazole (2.5 mg/cat PO every 12 hours) was initiated at that time.

History

Fleur is an indoor-only cat. Her appetite is mildly decreased, but she eats regularly. She has no recent history of vomiting, diarrhea, coughing, sneezing, polyuria, or polydipsia. As a kitten, she was diagnosed with ocular keratitis secondary to feline herpesvirus type 1 infection.

Physical Examination

On physical examination, Fleur is bright, alert, and responsive. Temperature, pulse, and respiration are within normal limits. BCS is 4/9. There is a palpable thyroid slip, right-sided thyroid nodule, and grade II/VI parasternal heart murmur. She has bilateral hair loss and facial excoriations with no obvious signs of fleas or other ectoparasites (Figure).

How would you diagnose and treat this patient?

Treatment & Outcome

Methimazole is a thyroid peroxidase inhibitor that inhibits thyroid hormone synthesis by interfering with iodine incorporation into tyrosyl residues of thyroglobulin. The primary differential diagnosis for pruritus and facial excoriations in this patient was an adverse effect of methimazole treatment. Other methimazole-related idiosyncratic reactions were assessed via CBC to rule out blood dyscrasias and serum chemistry profile to rule out hepatopathy and evaluate changes in renal function. Urinalysis can help assess renal function but was not performed prior to CBC because of concerns for methimazole-induced thrombocytopenia.  

Methimazole administration adjustments (eg, switching to transdermal methimazole, reducing the amount of oral methimazole) can be considered in patients with GI upset secondary to methimazole; however, methimazole should be discontinued if facial excoriations, blood dyscrasias, or hepatopathy occur, as these adverse effects are not related to the dose.  

Methimazole was discontinued, and pruritus and facial excoriations resolved. Successful control of hyperthyroidism was achieved via radioactive iodine treatment administered after one month.

Suggested Reading

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.

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Corticotropin-Releasing Hormone Test to Differentiate Hyperadrenocorticism in Dogs

Thomas Schermerhorn, VMD, DACVIM (SAIM), Kansas State University

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Corticotropin-Releasing Hormone Test to Differentiate Hyperadrenocorticism in Dogs

In the literature

Tanaka S, Suzuki S, Sato A, et al. Utility of a corticotropin-releasing hormone test to differentiate pituitary-dependent hyperadrenocorticism from cortisol-producing adrenal tumors in dogs. J Vet Intern Med. 2022;36(1):29-38. doi:10.1111/jvim.16336


FROM THE PAGE...

Corticotropin-releasing hormone is produced in the hypothalamus and is a component of the hypothalamic–pituitary–adrenal axis. This hormone stimulates the release of ACTH from the pituitary gland, targeting the adrenal cortex and stimulating a hormonal response that includes release of cortisol and related glucocorticoid hormones. Although some tests (eg, ACTH stimulation, dexamethasone suppression) that evaluate the hypothalamic–pituitary–adrenal axis may be familiar, others (eg, corticotropin-releasing hormone test) are infrequently used in the clinical setting.

This study evaluated the usefulness of a corticotropin-releasing hormone test for distinguishing pituitary-dependent hyperadrenocorticism (PDH) from hyperadrenocorticism caused by a cortisol-producing adrenal tumor (ie, adrenal-dependent hyperadrenocorticism [ADH]). Plasma ACTH was measured before and 30 minutes after IV injection of 1.5 µg ovine corticotropin-releasing factor. 

Postinjection values increased significantly from baseline in all study groups (ie, control, PDH, ADH), demonstrating that ovine corticotropin-releasing hormone stimulated ACTH release. Baseline and postinjection ACTH were higher in the PDH group compared with the control and ADH groups. There was no difference in postinjection concentrations between the control and ADH groups. 

Baseline and postinjection ACTH had moderate sensitivity (83.87%) and high specificity (96.97%) to distinguish between dogs in the PDH and control groups. Baseline ACTH had moderate sensitivity (90.62%) and specificity (87.50%) and postinjection ACTH had high sensitivity (100%) and moderate to low specificity (66.67%) to distinguish between dogs in the PDH and ADH groups.

...TO YOUR PATIENTS

Key pearls to put into practice:

1

The corticotropin-releasing hormone test is not appropriate for initial diagnosis of hyperadrenocorticism in dogs. Diagnosis in dogs with appropriate clinical signs requires one or more clinically useful screening tests (eg, low-dose dexamethasone suppression, ACTH stimulation).

2

Common tests to differentiate PDH from ADH include high-dose dexamethasone suppression, endogenous ACTH concentration, and adrenal imaging. The corticotropin-releasing hormone test is clinically useful and an alternative differentiation test option. Overall sensitivity and specificity of the corticotropin-releasing hormone test are comparable with other differentiation tests.

 

3

Time needed for the corticotropin-releasing hormone test (ie, 30 minutes) is comparable to that needed for adrenal ultrasonographic examination and is significantly shorter than the 8-hour period required for the high-dose dexamethasone suppression test.

4

Lack of familiarity and experience with corticotropin-releasing hormone preparations and incomplete details regarding cost of testing may inhibit use. Further studies are needed before the corticotropin-releasing hormone test can be recommended for routine clinical practice.

5

Test performance, cost, logistics (eg, sampling times, availability of reagents and equipment), and convenience for the pet owner and veterinary staff should be considered when selecting a test to differentiate PDH from ADH.

Author Information

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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Albuterol Toxicosis in Dogs

Alex Blutinger, VMD, DACVECC, Veterinary Emergency Group, White Plains, New York

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Albuterol Toxicosis in Dogs

In the literature

Crouchley J, Bates N. Retrospective evaluation of acute salbutamol (albuterol) exposure in dogs: 501 cases. J Vet Emerg Crit Care (San Antonio). 2022. doi:10.1111/vec.13182


FROM THE PAGE …

Albuterol (ie, salbutamol) is a selective beta-2–adrenoreceptor agonist commonly used in human medicine as a bronchodilator and in the management of premature labor. Although albuterol has been used as a bronchodilator in dogs and cats, use in veterinary medicine is not common.1 High doses of albuterol result in diminished beta-2 selectivity and activation of beta-1 adrenergic receptors, causing cardiovascular stimulation.2 Systemic hypotension in response to albuterol-induced peripheral and coronary vasodilation can also contribute to increased heart rate.3 Hypokalemia may develop due to stimulation of sodium/potassium-ATPase via beta-2 adrenergic receptors.4,5

Clinical signs of toxicosis are based on beta-agonist actions on adrenoreceptors in various organs. Most organs are affected, but the cardiovascular system, musculoskeletal system, and CNS are primarily affected. Clinical signs include tachycardia, tachypnea, lethargy, vomiting, muscle tremors, ataxia, agitation, and polydipsia. Most dogs develop clinical signs within several hours of exposure.  

This retrospective study evaluated onset and duration of common clinical signs, treatment, and outcome in 501 dogs with acute, accidental exposure to albuterol. Clinical signs developed in 471 dogs (94%) following albuterol exposure. Tachycardia was the most common clinical sign (404 dogs [80.6%]); median onset and duration were 2.5 and 13.3 hours, respectively. Tachypnea, dullness/lethargy, and vomiting were also common. Blood potassium concentration was measured in 142 dogs, and hypokalemia was reported in 106 dogs (median onset and duration were 2.4 and 13 hours, respectively). Beta-blockers, IV fluids, potassium supplementation, and sedation were the most common treatments. Survival rate among dogs with clinical signs was 99.6%.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Most dogs exposed to albuterol develop rapid-onset clinical signs but generally recover within 24 hours, and death is uncommon. Early assessment is recommended for all dogs with accidental exposure.

2

Beta-blockers are recommended in dogs with severe or prolonged tachycardia or with signs of reduced cardiac output/hypoperfusion (eg, pale mucous membranes, cold extremities, weak pulses, dull mentation) following albuterol exposure.

3

Serum potassium levels should be evaluated in all patients with clinical signs of toxicosis, and potassium supplementation should be considered in patients that are hypokalemic and have clinical signs (eg, muscle weakness, flaccid paralysis, hypoventilation) or ECG changes associated with hypokalemia (eg, prolonged QT interval, U waves, ST segment depression, increased P-wave amplitude and duration, bradycardia, AV block, cardiac arrest).

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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Gel Fingernail Polish & Viable Bacteria Counts in Small Animal Surgery

Lisa Corti, DVM, DACVS, CCRP, North Shore Veterinary Surgery, Andover, Massachusetts, North Shore Community College, Danvers, Massachusetts

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Gel Fingernail Polish & Viable Bacteria Counts in Small Animal Surgery

In the literature

Anderson SL, Wisnieski L, Achilles SL, Wooton KE, Schaffer CL, Hunt JA. The impact of gel fingernail polish application on the reduction of bacterial viability following a surgical hand scrub. Vet Surg. 2021;50(7):1525-1532. doi:10.1111/vsu.13703


FROM THE PAGE...

Because sterile gloves are commonly punctured during surgical procedures, hand disinfection is essential to lower the rate of surgical site infections1-4; however, the area underneath the fingernails harbors bacteria and can be difficult to clean.4,5 Nail polish has traditionally been thought to harbor microbes and increase the risk for transferring bacteria to patients.6,7 Studies in both human and veterinary medicine have evaluated whether nail polish influences the bacterial load on fingernails, with variable results.4,5,7-10

This randomized controlled trial evaluated the effect of gel nail polish on the number of viable bacteria present before and after a surgical hand scrub 1 day and 14 days after a manicure from a licensed cosmetologist. A total of 40 veterinary students and faculty participated and washed their hands and fingernails with chlorhexidine gluconate 4% as part of the manicure. Nails from both hands were trimmed and filed to <2 mm in length and randomly assigned to receive or not receive gel polish.

On days 1 and 14, fingernails were sampled for culture with sterile toothpicks and phosphate-buffered, saline-soaked cotton swabs before and after a standard 5-minute presurgical hand scrub consisting of a chlorhexidine gluconate 4% sterile brush and sponge with a plastic pick to clean under the fingernails. Culture samples were taken from the cuticle, nail plate, and underside of each nail and placed on agar plates. The number of colony-forming units per mL (ie, viable bacteria) were counted.

No significant difference in the number of viable bacteria detected from nails with or without gel polish after the standard surgical scrub was found; however, longer fingernail length was significantly correlated with a higher number of postscrub viable bacteria.

...TO YOUR PATIENTS

Key pearls to put into practice:

1

Applying gel or acrylic nail polish does not increase risk for presence of viable bacteria after a surgical hand scrub.5,7,9,10

2

Fingernail length is a risk factor for postscrub viable bacteria. Nail length <2 mm is recommended when scrubbing into surgical procedures.4,5,8,10

 

3

Because sterile gloves are commonly punctured during surgery,1-3 presurgical hand cleaning heavily impacts development of surgical site infections.4,7,11,12 One standard surgical preparation uses a sterile chlorhexidine gluconate 4% sponge and brush with a fingernail pick.5,11,12 The pick is used to remove debris from under the fingernails, then the brush is used to scrub the nails. A 5-minute scrub with the sponge is performed, cleaning each side of the fingers, hands, and forearms up to the elbows.5,11 Alcohol-based hand rubs are popular in human and veterinary medicine and may be superior to chlorhexidine and povidone-iodine scrubs when manufacturer recommendations are followed.4,7,11,12

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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Vitality of Discolored Teeth in Dogs

Kendall Taney, DVM, DAVDC, FAVD, Center for Veterinary Dentistry & Oral Surgery, Gaithersburg, Maryland

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Vitality of Discolored Teeth in Dogs

In the literature

Feigin K, Bell C, Shope B, Henzel S, Snyder C. Analysis and assessment of pulp vitality of 102 intrinsically stained teeth in dogs. J Vet Dent. 2022;39(1):21-33. doi:10.1177/08987564211060387


FROM THE PAGE...

Intrinsically stained teeth are a common finding in dogs and exhibit discoloration within tooth hard tissues, unlike extrinsically stained teeth, which have discoloration on the tooth surface. Causes of intrinsic staining include amelogenesis imperfecta, dentinogenesis imperfecta, tetracycline ingestion during tooth development, dental fluorosis, tooth resorption, hyperbilirubinemia, pulp necrosis, injury, and aging.1 

Intrinsic staining can indicate pathology or injury that may affect tooth health or vitality. Determining appropriate treatment can be challenging, as many patients do not have radiologic or clinical signs that can definitively predict tooth vitality.

This prospective study analyzed clinical, radiographic, and histopathologic characteristics of 102 intrinsically stained teeth. There was no evidence of coronal injury (eg, fracture, displacement, mobility) in 55 (53.9%) out of 102 teeth. On histopathologic analysis, 85 (87.6%) of 97 intrinsically stained teeth were nonvital. Radiographic evidence of endodontic disease and periodontal disease was present, respectively, in 58 (57%) and 49 (48%) of 102 intrinsically stained teeth; 29 (28%) had evidence of tooth resorption. Only 19 (18.6%) of 102 intrinsically stained teeth were radiographically normal. All teeth with radiographic evidence of periapical lucency had pulp necrosis. Incisor teeth were most commonly affected, but all tooth types (ie, incisors, canines, premolars, molars) were discolored. 

A previous study found that 92.2% of intrinsically discolored teeth were nonvital based on gross appearance of the pulp.2 The current study is the first to histopathologically confirm pulp death, and results verify that a high percentage of intrinsically discolored teeth are nonvital; however, normal contralateral teeth were not histologically evaluated for comparison.

...TO YOUR PATIENTS

Key pearls to put into practice:

1

Tooth discoloration is a common posttraumatic complication caused by pulpal hemorrhage. Hemolysis of RBCs follows pulpal hemorrhage, and more profound discoloration can occur when hemolyzed RBCs combine with putrefying pulpal tissue.3 Transillumination can help demonstrate increased opacity of an intrinsically stained tooth, but subtle changes can be difficult to detect with the naked eye.

2

Intrinsically stained teeth are likely nonvital. In this study, most (87.6%) intrinsically stained teeth were histopathologically confirmed to be nonvital, which is consistent with results of a previous study.2

3

Nonvital teeth are likely to develop endodontic and periodontal disease and should be treated quickly with exodontics or endodontics.

 

4

Radiographic signs may support a diagnosis of nonvitality but are not definitive.3,4 All teeth with radiographic evidence of periapical lucency also had pulp necrosis in this study.

 

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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Chronic Enteropathy & Canine Metabolomic Profiles

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Walker HK, Boag AM, Ottka C, et al. Serum metabolomic profiles in dogs with chronic enteropathy. J Vet Intern Med. 2022;1-8. doi:10.1111/jvim.16419

Diagnosis and prognostication of canine chronic enteropathy (CE) can be challenging with current diagnostic approaches, but measuring serum metabolic biomarkers may be a noninvasive method of diagnosis. This method has improved accuracy, as well as better prediction and monitoring of treatment response; however, few of these biomarker measurements are used clinically. Metabolomic profiles in dogs with CE and healthy dogs are not well characterized, and comprehensive studies are lacking.

This study* sought to compare metabolomic profiles of dogs with histopathologically confirmed CE (n = 55) with those of healthy controls (n = 240). A canine-specific proton nuclear magnetic resonance (ie, 1H NMR) spectroscopy analytical platform was used to measure 99 serum metabolites. Differences in 19 metabolites and 18 lipoprotein composition indexes were identified; this may prompt further research into diagnostic and prognostic approaches to canine CE, as well as therapeutic trials.

*This study was partially supported by PetBIOMICS.

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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Vertebral Left Atrial Size in Dogs with Preclinical Myxomatous Mitral Valve Disease

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

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Vertebral Left Atrial Size in Dogs with Preclinical Myxomatous Mitral Valve Disease

In the literature

Lee D, Yun T, Koo Y, et al. Change of vertebral left atrial size in dogs with preclinical myxomatous mitral valve disease prior to the onset of congestive heart failure. J Vet Cardiol. 2022;42:23-33. doi:10.1016/j.jvc.2022.05.003


FROM THE PAGE...

Vertebral left atrial size (VLAS) is a radiographic measurement that objectively estimates left atrial size and can help determine whether cardiac enlargement is present in dogs with suspected or diagnosed myxomatous mitral valve disease (MMVD). VLAS can be useful when other imaging modalities (eg, echocardiography, thoracic-focused point-of-care ultrasonography) cannot be performed (eg, due to financial constraints, lack of availability, lack of technical expertise). Increase in vertebral heart size (VHS) prior to onset of congestive heart failure (CHF) and rate of change in VHS over time (VHS/month) can help predict possible occurrence of CHF.1-3 Additional studies in dogs with MMVD have reported VLAS ranges for each stage of disease.4-6

This retrospective study investigated whether VLAS can help determine if dogs with preclinical MMVD are at higher or lower risk for developing CHF. Dogs (n = 41) were assigned to 2 groups based on whether or not CHF developed within 180 days of initial diagnosis of MMVD. Radiographic and echocardiographic parameters, including VLAS and rate of change in VLAS over time (VLAS/month), at 3 time points (ie, first visit, 1-180 days postdiagnosis, 181-360 days postdiagnosis) were compared between groups. Results demonstrated no significant difference in VLAS between the groups at the first visit; however, VLAS and change in VLAS over time were significantly higher in the group that developed CHF within 180 days of initial diagnosis of MMVD.

...TO YOUR PATIENTS

Key pearls to put into practice:

1

Not all patients in the current retrospective study received pimobendan; results should thus be interpreted with caution. Pimobendan is administered to most dogs with stage B2 MMVD based on the ACVIM consensus statement and EPIC clinical trial results.7,8 A follow-up study of this cohort of dogs found that VHS consistently decreased during the first several months of treatment; this decrease was associated with a better outcome, longer preclinical time period, and reduced risk for developing CHF within 6 months.

2

Owners of dogs with MMVD should be instructed on home resting respiratory rate monitoring. Effective monitoring and accurate measurement of resting respiratory rate at home is an effective way to monitor patients between visits to the clinic. Small changes can be communicated to clinicians, allowing phone consultations and possible initiation of a furosemide trial to help avoid emergency clinic visits during an episode of CHF.

3

A cut-off VLAS value of >2.95 was specific for identifying dogs with impending (ie, within 180 days) CHF, but sensitivity was low, indicating that a large number of dogs with VLAS >2.95 will not develop CHF within 6 months; however, this measurement can help identify dogs at greater risk.

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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Once-Weekly Insulin Therapy in Dogs

Andrew Bugbee, DVM, DACVIM, University of Georgia

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Once-Weekly Insulin Therapy in Dogs

In the literature

Hulsebosch SE, Pires J, Bannasch MJ, et al. Ultra-long-acting recombinant insulin for the treatment of diabetes mellitus in dogs. J Vet Intern Med. 2022;36(4):1211-1219. doi:10.1111/jvim.16449


FROM THE PAGE...

Canine diabetes mellitus is traditionally managed with twice-daily insulin injections, but an intensive daily treatment schedule can negatively impact pet owner quality of life and perceived well-being of their pet. 

This study* of 5 client-owned dogs evaluated once-weekly administration of a novel ultra-long-acting (ULA) insulin as an alternative to twice-daily insulin. All dogs were previously diagnosed with diabetes, had been treated with twice-daily insulin therapy for ≥2 months, and demonstrated moderate to good glycemic control. After enrollment in the study, dogs were maintained on a twice-daily insulin protocol and monitored with an implantable flash glucose monitoring system for 10 to 14 days. On day 0, dogs were transitioned to once-weekly ULA insulin, and the flash glucose monitoring system was continued. Weekly evaluation continued for 8 weeks and included full physical examination and measurement of serum drug concentration and antidrug antibody levels; ULA insulin was adjusted as needed based on glycemic monitoring, body weight, and clinical signs. 

ULA insulin therapy maintained a similar level of glycemic and clinical control as compared with twice-daily insulin protocols. Serum ULA insulin concentrations associated with good glycemic control were achieved in all dogs following the second injection, with peak levels reached in week 3. Occurrence of hypoglycemia was not significantly different between baseline and study exit, with biochemical hypoglycemia (<70 mg/dL) occurring in 4.2% of all glucose readings, and a single episode of potential clinical hypoglycemia observed by an owner during the ULA insulin treatment phase.

By week 6, one dog developed antidrug antibodies to ULA insulin and required twice-daily insulin during the final week to achieve glycemic control. The dog remained responsive to prestudy twice-daily insulin, but an attempt to restart ULA insulin after a 2-week washout period yielded no response, suggesting continued presence of antidrug antibodies. In addition, one dog had an incomplete response to ULA insulin therapy after 8 weeks and required intermittent administration of a porcine zinc (lente) insulin with meals.

Once-weekly (ie, ULA) insulin protocols offer a less rigorous treatment schedule for dogs with diabetes mellitus, but other factors—including treatment costs, effective monitoring of long-term therapy, and frequency of potential adverse effects (eg, treatment failure) in a larger population—should be evaluated.

...TO YOUR PATIENTS

Key pearls to put into practice:

1

A novel once-weekly insulin therapy maintained a similar level of diabetic control as compared with traditional twice-daily insulin injections in a small population of dogs. Efficacy of the novel insulin as a first-line therapy in uncontrolled diabetic dogs is unknown and was not evaluated.

2

Hypoglycemia was uncommon during the study period; however, some dogs managed with ULA insulin may require intermittent supplemental conventional insulin therapy to control postprandial hyperglycemia. ULA insulin alone may not be adequate for all dogs to achieve good glycemic control.

3

The once-weekly insulin was designed to be nonimmunogenic, but 1 out of 5 dogs formed antidrug antibodies and required supplemental twice-daily insulin in the final week of the study, warranting evaluation in a larger population of dogs.

*This study was funded by Akston Biosciences.

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

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Intrathoracic Wooden Skewers Migrating from the Stomach & Duodenum in Dogs

Travis Lanaux, DVM, DACVECC, University of Florida

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Intrathoracic Wooden Skewers Migrating from the Stomach & Duodenum in Dogs

In the literature

Garcia-Pertierra S, Das S, Burton C, et al. Surgical management of intrathoracic wooden skewers migrating from the stomach and duodenum in dogs: 11 cases (2014-2020). J Small Anim Pract. 2022;63(5):403-411. doi:10.1111/jsap.13474


FROM THE PAGE...

When ingested, wooden skewers (eg, toothpicks, kebab sticks) can migrate from the GI tract to other parts of the body, creating diagnostic and therapeutic challenges and possibly leading to severe or life-threatening complications. 

This retrospective study reviewed clinical presentation, management, and outcome of 11 dogs in which ingested wooden skewers migrated from the cranial GI tract to the thorax. Clinical signs included anorexia/hyporexia, vomiting/regurgitation, lethargy, pyrexia, and gait abnormalities/lameness. Median time from development of clinical signs to referral presentation was 14 days (range, 2-112 days). 

The most common hematologic and serum chemistry abnormalities were neutrophilia with a left shift, thrombocytopenia, mild ALP elevation, and mild hypoalbuminemia. CT was more sensitive than other imaging modalities (ie, radiography, ultrasonography, MRI) for detecting skewers in the thorax, allowing for definitive diagnosis in all dogs that underwent CT. The stomach was the most common site of migration; only one dog had a skewer that originated from the duodenum. 

The authors recommend laparotomy with diaphragmotomy as the initial surgical approach unless the skewer is in the cranial thorax, in which case a median sternotomy or lateral thoracotomy is preferred. 

Although these were complex cases managed at referral clinics, overall short- and long-term prognoses were good.


...TO YOUR PATIENTS

Key pearls to put into practice:

1

Dogs with intrathoracic wooden skewers migrating from the cranial GI tract can have diverse clinical signs with widely variable duration.

 

2

CT is the preferred imaging modality for detecting migrating wooden skewer foreign bodies in the thorax.

 

3

Surgical management of intrathoracic wooden skewers migrating from the cranial abdomen typically results in a good prognosis.

 

Suggested Reading & Author Information

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Respiratory & GI Disease in Brachycephalic Dog Breeds

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Petchell WHR, Noble P-JM, Broome HAO, Burrow R. Incidence of alimentary and respiratory disease in brachycephalic dogs presenting to primary care veterinary practices participating in the SAVSNET project. Vet Rec. 2022;191(7):e1685. doi:10.1002/vetr.1685

Dogs with brachycephalic obstructive airway syndrome, particularly French bulldogs, have a high incidence of GI disease. This study analyzed records of 750 French bulldogs (n = 260), pugs (n = 252), and bulldogs (n = 238) to determine the incidence of respiratory and GI disease among brachycephalic breeds. French bulldogs had a higher incidence of esophageal, gastric, and intestinal disease compared with pugs and bulldogs, and pugs had the highest incidence of respiratory tract and miscellaneous (ie, exercise intolerance, syncope) diseases. These results demonstrate significant breed-specific differences in the incidence of respiratory and GI disease among brachycephalic dogs.

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Differential Diagnosis: Elevated ALT

Marie Chartier, DVM, DACVIM (Internal Medicine), VCA Roberts Animal Hospital, Hanover, Massachusetts

Internal Medicine

|Peer Reviewed

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Differential Diagnosis: Elevated ALT

Following are differential diagnoses for patients presented with elevated ALT.

  • Hepatocyte damage
    • Hypoxia (eg, anemia, cardiopulmonary disease, thromboembolic disease, seizures, ischemic myopathy [cats])
    • Portosystemic shunt
    • Portal vein hypoplasia 
    • Hepatic lipidosis (cats)
    • Diabetes mellitus
    • Hyperthyroidism
    • Hyperadrenocorticism (usually only mild to moderate elevation, less common than ALP elevation) 
    • Neoplasia
    • Inflammatory (eg, copper storage disease, chronic hepatitis)
    • Infectious (eg, leptospirosis, bacterial cholangiohepatitis, FIP, histoplasmosis, canine infectious hepatitis [adenovirus type 1])
    • Drugs (eg, acetaminophen, azathioprine, carprofen, tetracyclines, methimazole, trimethoprim–sulfonamides, amiodarone, chronic phenobarbital administration) 
    • Toxicity (eg, blue-green algae, Amanita spp mushrooms, aflatoxin, xylitol, sago palm, azole antifungals) 
    • Reactive hepatopathy (eg, enteritis, chronic enteropathy) 
    • Pancreatitis
    • Trauma 
    • Muscular dystrophy (dogs) 
  • Induction (independent from toxicity) 
    • Phenobarbital 
    • Glucocorticoids
  • Other
    • Liver lobe torsion

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Top 5 Causes of Erythrocytosis in Dogs & Cats

Elizabeth Flaherty, DVM, Companion Care Vets, Redhill, Surry, United Kingdom

Lisa M. Pohlman, DVM, MS, DACVP, Kansas State University

Internal Medicine

|Peer Reviewed

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Top 5 Causes of Erythrocytosis in Dogs & Cats

Erythrocytosis (ie, polycythemia) is an increase in erythrocytes in the peripheral blood; is characterized by increased hematocrit, hemoglobin, and RBC concentration; and can be relative or absolute (Figure).

Approach to classifying erythrocytosis1,6
Approach to classifying erythrocytosis1,6

FIGURE Approach to classifying erythrocytosis1,6

FIGURE Approach to classifying erythrocytosis1,6

Relative erythrocytosis is an increased hematocrit not caused by an increase in total body RBC mass.1 Examples include hemoconcentration secondary to dehydration and redistribution caused by epinephrine-induced splenic contraction.2,3

Absolute erythrocytosis is caused by an absolute increase in total body RBC mass and can be primary or secondary.1,4 Primary absolute erythrocytosis is present when there is increased RBC proliferation in the absence of increased erythropoietin and is most indicative of a neoplastic myeloproliferative condition (ie, polycythemia vera) in veterinary patients.4 Secondary absolute erythrocytosis results from increased concentrations of erythropoietin that stimulate erythroid hyperplasia in bone marrow and increase RBC production and can be appropriate, inappropriate, or endocrinopathy-associated.1,2,4-6 Secondary appropriate absolute erythrocytosis is induced by tissue hypoxia. Secondary inappropriate absolute erythrocytosis is due to uncontrolled erythropoietin secretion, not induced by tissue hypoxia.1,2,4,5 

Clinical signs of erythrocytosis are secondary to hyperviscosity caused by increased RBC mass and depend on the degree and duration of hematocrit increase. Signs may include erythematous to cyanotic mucous membranes, dark-colored blood, dilated episcleral vessels, increased capillary refill time, tachycardia, tachypnea, neurologic disturbances secondary to hypoxic injury from increased blood viscosity (eg, weakness, lethargy, ataxia, seizures, blindness, behavior changes), vomiting, abdominal or lumbosacral pain, thrombosis, microvascular injury, polyuria, polydipsia, and bleeding (eg, melena, epistaxis, hematochezia, hematuria, hematemesis) as a result of decreased blood flow and consequential sludging of blood in small vessels that can lead to congestion, distention, and ultimately thrombosis, tissue hypoxia, and vessel rupture.6-11

Following are causes of erythrocytosis listed in order of most to least common, according to the authors.

Top 5 Causes of Erythrocytosis in Dogs & Cats

  1. Dehydration & Splenic Contraction (Relative Erythrocytosis)
  2. Hypoxemia (Secondary Appropriate Absolute Erythrocytosis)
  3. Erythropoietin-Secreting Neoplasms (Secondary Inappropriate Absolute Erythrocytosis)
  4. Endocrinopathy-Associated Erythrocytosis (Secondary Absolute Erythrocytosis)
  5. Myeloproliferative Neoplasia (ie, Polycythemia Vera; Primary Absolute Erythrocytosis)
1

Dehydration & Splenic Contraction (Relative Erythrocytosis)

Dehydration

Dehydration causes hemoconcentration and decreased total intravascular fluid volume without decreased erythrocytes,7 resulting in an artifactual increase in hematocrit due to hemoconcentration.1 

Clinical evidence of dehydration during physical examination can help identify erythrocytosis due to dehydration. Uncomplicated cases may have concurrent prerenal azotemia with urine specific gravity that indicates urine is concentrated and there is increased serum total protein.7 Sodium and chloride may also be increased, depending on the tonicity of the fluid lost.1 

Erythrocytosis due to dehydration can be treated with fluids to correct the volume deficit. Type and route of fluid administration should be based on the degree of dehydration, the underlying condition causing dehydration, and other metabolic abnormalities.4

Splenic Contraction

Pain, fear, and exercise cause epinephrine release, resulting in contraction of splenic smooth muscle and release of erythrocyte-rich splenic blood into the peripheral circulation.1 Peripheral blood (normal hematocrit, ≈35%-50%, depending on species) mixes with high-hematocrit splenic blood (hematocrit, 70%-80%) to cause erythrocytosis.1 Splenic contraction is a normal, short-term, physiologic response to epinephrine that abates when the stimulus is removed and the patient is calm. Erythrocytosis due to splenic contraction is most common in dogs because dogs have a muscular spleen; however, in experimental conditions, cats showed a 25% increase in hematocrit from splenic contraction.1 Unlike erythrocytosis due to hemoconcentration, serum total protein is in the reference interval in patients with splenic-contraction–induced erythrocytosis.1,2,4 Other signs of catecholamine release (eg, excitement leukogram [ie, mature neutrophilia with concurrent lymphocytosis]) are possible.4

2

Hypoxemia (Secondary Appropriate Absolute Erythrocytosis)

Tissue hypoxia (eg, as a result of adjustment to high altitude, chronic pulmonary disease, cardiac disease, hemoglobin disorders, cardiac shunts, venoarterial shunts) stimulates increased release of erythropoietin, which may lead to secondary appropriate absolute erythrocytosis.1,4,7-9,12,13 This type of erythrocytosis is characterized by erythrocytosis with chronic hypoxemia, which is most often induced by partial pressure of oxygen <60 mm Hg.4,7

3

Erythropoietin-Secreting Neoplasms (Secondary Inappropriate Absolute Erythrocytosis)

Secondary inappropriate absolute erythrocytosis can occur due to increased production of erythrocytes induced by an erythropoietin-secreting neoplasm; this is an inappropriate response because erythropoietin production is increased in the absence of systemic hypoxia.4,7 Most erythropoietin or erythropoietin-like substance-releasing tumors are renal in origin and may include primary renal lymphoma, renal sarcoma, nephroblastoma, renal cell carcinoma, fibrosarcoma, or adenocarcinoma.4,9,13-15 Erythropoietin may also be secreted by tumors of other tissues, including nasal fibrosarcoma, hepatocellular carcinoma, schwannoma, and cecal leiomyosarcoma.2,5,16 Renal tumors may lead to erythrocytosis via paraneoplastic processes that release erythropoietin or an erythropoietin-like substance from tumor cells or via damage to blood flow in the renal parenchymal microvasculature with subsequent erythropoietin release due to local hypoxia.4,7,9,14,15 

Renal tumors should be confirmed because other renal injuries, including pyelonephritis, can also lead to inappropriate secondary erythrocytosis.7 Erythrocytosis related to renal tumors is generally mild to moderate but has been reported as severe in some cases.13 Erythropoietin or an erythropoietin-like substance produced by these tumors can be confirmed with immunohistochemistry detection of erythropoietin mRNA in the tumor cells using reverse-transcriptase PCR.5,16 Treatment includes removal of the erythropoietin-secreting neoplasm and management of erythrocytosis using therapeutic phlebotomy and fluid support with IV crystalloids.13 Myelosuppression with hydroxyurea may be recommended if erythrocytosis is severe enough to require phlebotomies more frequently than every 4 weeks.13

4

Endocrinopathy-Associated Erythrocytosis (Secondary Absolute Erythrocytosis)

Hormones (eg, cortisol in dogs, thyroxine and growth hormone in cats) can directly or indirectly stimulate erythropoiesis. It is important, however, to note that endocrinopathy-associated erythrocytosis is generally mild if present and alone is insufficient to result in clinical signs.6

5

Myeloproliferative Neoplasia (ie, Polycythemia Vera; Primary Absolute Erythrocytosis)

Polycythemia vera, the cause of primary absolute erythrocytosis, is a chronic myeloproliferative disease characterized by an increase in hematocrit or packed cell volume >65%, no increase in erythropoietin concentration, normal blood volume, and normal arterial partial pressure of oxygen.2,10,11 Polycythemia vera most commonly affects middle-aged to older dogs; no sex or breed predisposition has been reported.10 Pathogenesis includes rapid production of an increased number of erythrocytes with normal to prolonged half-life in the blood. In some dogs, a mutant oncogene JAK2 sequence with 2 amino acid changes (ie, V617F, C618L) controls the autoregulation of kinase activity and leads to constitutively active kinase and an increase in erythrocyte production in the absence of erythropoietin.3,10,11 Treatment includes therapeutic phlebotomy and IV hydration with crystalloids to reduce blood viscosity, as well as myelosuppressants (most commonly, hydroxyurea) to lower hematocrit to a normal range.10,11 

Mean survival time is ≈5 months in dogs treated only with phlebotomies.10 Survival time can increase to between 8 and 33 months in dogs treated with hydroxyurea following reduced hematocrit (ie, <60%) via phlebotomy and fluid replacement.6,10 Initial administration of hydroxyurea in dogs should be 30 mg/kg PO once every 24 hours (or divided and given every 12 hours) for 1 to 2 weeks, then every 48 hours and tapered to the lowest effective frequency.6,10,17 Intervals longer than 48 hours were found to be insufficient for management of polycythemia vera in dogs in a report.10 Adverse effects of hydroxyurea may include anorexia, vomiting, alopecia, sloughing of nails, and bone marrow hypoplasia. 

A similar administration schedule is reported in cats, with a suggested maintenance dosage of 22 mg/kg PO every 48 hours.17 Cats given large doses of hydroxyurea are likely to develop methemoglobinemia and Heinz body hemolytic anemia in addition to adverse effects; lower doses should thus be considered, and patients should be monitored carefully.6

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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Vestibular Dysfunction in a Geriatric Dog

Mark Troxel, DVM, DACVIM (Neurology), Massachusetts Veterinary Referral Hospital, Woburn, Massachusetts

Neurology

|Peer Reviewed

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Vestibular Dysfunction in a Geriatric Dog

A 12-year-old spayed rottweiler crossbreed is presented for emergency evaluation following sudden onset ataxia in all limbs. She is ambulatory without support but veers and stumbles to the right and occasionally falls to the right when walked on a leash. She also compulsively circles to the right when not on a leash in the examination room.

On neurologic examination, she is quiet and alert but appears disoriented and has a mild head tilt to the right. Cranial nerve examination reveals a resting horizontal nystagmus with fast phase to the left. When placed on her back, there is a positional rotary nystagmus with fast phase to the left. The remainder of the cranial nerve examination is normal. General proprioception and hopping are normal in all limbs. Patellar reflexes are normal bilaterally, and withdrawal reflexes are normal in all limbs. There is no evidence of hyperesthesia.

Neurologic examination results suggest right peripheral vestibular disorder. Differential diagnoses include idiopathic vestibular disease (ie, old dog vestibular, geriatric dog vestibular), otitis interna, hypothyroidism, aural neoplasia (eg, squamous cell carcinoma, ceruminous gland adenocarcinoma), trauma, ototoxicity, and other less common disorders. 

CBC, serum chemistry profile, and total thyroxine (tT4) results are within normal limits. Otoscopic examination is attempted, but a large amount of hair in the horizontal ear canal obstructs visualization of the tympanic membrane. 

Presumptive diagnosis is idiopathic vestibular disease, as there is no history suggestive of otitis media/interna (eg, head shaking, pawing/scratching ears or sides of face, rubbing side of head on objects), no recent use of ototoxic medications or topical cleaning agents, and no recent trauma.

Which of the following drugs would be appropriate for this patient?

Do Not Use Proceed with Caution Safe

The following represents the best responses based on drug metabolism, pharmacokinetics, species, diagnostic differentials, clinical and laboratory data, and other pertinent findings.

MAROPITANT

Correct ResponseSafe1 mg/kg SC or IV over 1-2 minutes every 24 hours or 2-8 mg/kg PO every 24 hours) is FDA-approved for use as an antiemetic in dogs and cats and is indicated for prevention and treatment of acute vomiting in dogs and cats, as well as prevention of vomiting due to motion sickness in dogs and cats ≥4 months of age.1 Although maropitant is often used to improve appetite and reduce nausea and vomiting in patients with vestibular dysfunction, there is no peer-reviewed evidence to specifically support this treatment. Maropitant is a neurokinin receptor antagonist that acts in the CNS to inhibit the binding of substance P (ie, the primary neurotransmitter involved in vomiting); peripheral and central causes of vomiting may therefore be suppressed.1

Maropitant is generally well tolerated. The most commonly reported adverse effects are pretravel vomiting and hypersalivation in patients given the higher motion sickness dose and pain or swelling at the injection site with subcutaneous administration.2,3 Other reported adverse effects include depression, lethargy, inappetence, diarrhea, anaphylaxis/anaphylactoid reactions, ataxia, and convulsions.2,3

Use of maropitant in patients with vestibular dysfunction is extra-label.

MECLIZINE

Correct ResponseSafeMeclizine (anecdotal dosage, ≈4 mg/kg PO every 24 hours; practical dosage, 12.5-50 mg/dog every 24 hours) is an H1-receptor blocker antihistamine with antiemetic and sedative properties frequently used extra-label to treat vestibular dysfunction and motion sickness; no FDA-approved veterinary products are available.4 Common adverse effects are sedation and anticholinergic effects (eg, dry eyes, dry mucous membranes, tachycardia). Paradoxical CNS stimulation has been reported.4 Nighttime administration is usually better accepted by owners.

Although meclizine is frequently recommended for treatment of vestibular dysfunction, there are no peer-reviewed studies that specifically examine use of meclizine in these patients. Meclizine typically has less sedative effect than other antihistamines (eg, diphenhydramine).

CEPHALEXIN

Correct ResponseDo Not UseCephalexin (15-30 mg/kg PO every 12 hours) is a first-generation bactericidal oral cephalosporin FDA-approved for treatment of secondary superficial bacterial pyoderma caused by Staphylococcus pseudintermedius in dogs that can also be used extra-label for treatment of other bacterial infections.5 First-generation cephalosporins generally exhibit bactericidal activity against gram-positive organisms and most anaerobes and have variable activity against gram-negative bacteria. Cephalexin has good penetration into bone and is effective against most bacteria often isolated from patients with otitis media.5-7

No data suggest antibiotics are beneficial for treatment of idiopathic vestibular disease. Antibiotics should not be given indiscriminately and should be prescribed only after infection of the middle ear is confirmed with bacterial culture and susceptibility testing (via myringotomy, if necessary). Empirical treatment may be considered if substantial evidence (ie, clinical signs, otoscopic evidence) of otitis media/interna is present. The recommended duration of antibiotic administration is 6 to 8 weeks.

Cephalexin is the author’s first antibiotic of choice in dogs suspected to have otitis media/interna because the drug is generally inexpensive, is effective for most first-time infections, and has good bone penetration.6 Patients receiving cephalexin should be rechecked at 3 to 4 weeks. If clinical signs have improved or resolved (except for head tilt, which may be permanent), cephalexin can be administered for an additional 3 to 4 weeks, as otitis media/interna can take 6 to 8 weeks to resolve. Advanced imaging (ie, MRI, CT) is recommended in patients in which clinical signs do not resolve (with the exception of head tilt).

ENROFLOXACIN

Correct ResponseDo Not UseEnrofloxacin (dogs, 5-10 mg/kg PO every 24 hours [up to 20 mg/kg PO every 24 hours for up to 30 days, according to some sources]) is a bactericidal fluoroquinolone antibiotic FDA-approved for treatment of dogs with susceptible bacterial infections.8 Enrofloxacin generally has activity against many gram-negative cocci and bacilli (eg, Pasteurella aeruginosa, Escherichia coli, Klebsiella spp, Enterobacter spp, Proteus spp) and is active against Brucella spp, Mycoplasma spp, and some Mycobacterium spp.8 Because of concern for development of bacterial resistance, enrofloxacin should ideally only be used for bacteria in which culture and susceptibility results show susceptibility to enrofloxacin.

No data suggest antibiotics are beneficial for treatment of idiopathic vestibular disease. Antibiotics should not be given indiscriminately but may be considered if clinical signs or otoscopic evidence of otitis media/interna are present. Therapeutic concentrations are attained in bone, making enrofloxacin an acceptable antibiotic for otitis media/interna, but consideration should first be given to a lower tier antibiotic (eg, cephalosporins, amoxicillin/clavulanic acid).8 Adverse effects include GI distress (eg, inappetence, vomiting, diarrhea), which may be offset by concurrent use of probiotics. There have also been rare reports of elevated liver enzymes, lethargy, depression, ataxia, and seizures.8,9

PREDNISONE/PREDNISOLONE

Correct ResponseDo Not UsePrednisone and prednisolone are glucocorticoids with anti-inflammatory activity.

Patients with otitis media/interna and concurrent otitis externa or periauricular inflammation may benefit from short-term corticosteroids or NSAIDs, but routine use of prednisone/prednisolone is not recommended in patients with idiopathic vestibular disease, as there are no data demonstrating efficacy for this condition. In addition, prednisone may mask other underlying diseases, making it difficult to obtain a diagnosis if the patient does not improve or the initial presumptive diagnosis is incorrect.

LEVOTHYROXINE

Correct ResponseDo Not UseLevothyroxine is a synthetic form of thyroxine used to treat hypothyroidism in dogs and, rarely, in cats (most often following thyroidectomy or radioiodine treatment).10 Hypothyroidism has been implicated in both peripheral and central vestibular dysfunction, but causality has not been proven, and concurrent hypothyroidism unrelated to vestibular dysfunction is possible. tT4 can be used as a screening tool but may be artificially low in patients with nonthyroidal illness (ie, euthyroid sick).

Levothyroxine is not indicated in patients with normal tT4, as hypothyroidism is unlikely the cause of vestibular dysfunction when tT4 is in the normal range. In patients with tT4 below the reference range, however, true hypothyroidism should be differentiated from euthyroid sick status via reduced free thyroxine, elevated thyroid-stimulating hormone, and possibly elevated thyroglobulin autoantibody levels prior to initiation of supplementation.

MELOXICAM

Correct ResponseDo Not UseMeloxicam is an NSAID FDA-approved for analgesia, as well as treatment of osteoarthritis and inflammatory conditions in dogs.11 No data suggest meloxicam or other NSAIDs expedite or improve the degree of recovery in patients with idiopathic vestibular disease.12

Although meloxicam has many uses and is generally safe, consideration is needed before administration to patients with potential neurologic concerns (eg, granulomatous meningoencephalomyelitis, necrotizing encephalitis, meningoencephalitis of undetermined etiology) that may need to be switched to corticosteroids because of the prolonged washout period (ie, 5-7 days) required prior to starting corticosteroids. Meloxicam can also cause GI upset and decreased appetite, further complicating recovery.

BUTORPHANOL

Correct ResponseProceed with CautionButorphanol (0.1-0.3 mg/kg IV bolus or 0.2 mg/kg IV loading dose, then 0.1-0.4 mg/kg/hour IV CRI) is an opioid agonist/antagonist used extra-label in dogs as a sedative, a preanesthetic, and an antiemetic.13 Sedation of hospitalized patients with vestibular disease may be necessary to control excessive movement (eg, flailing, rolling, compulsive circling in cage) and patient injury. Injectable (ie, intermittent bolus, CRI) butorphanol may be helpful because of its sedative and antiemetic properties. Caution is warranted when this drug is combined with other sedatives.

DIAZEPAM/MIDAZOLAM

Correct ResponseProceed with CautionDiazepam (0.2-0.5 mg/kg IV as an intermittent bolus) and midazolam (0.3-0.5 mg/kg IV as an intermittent bolus) are benzodiazepines that are schedule IV controlled substances in the United States with anticonvulsive, anxiolytic, sedative, and muscle relaxant properties, as well as possible mild appetite stimulant effects.14,15 These drugs are sometimes used because of their sedative and anxiolytic properties in hospitalized patients with vestibular dysfunction to prevent injury from excessive movement (eg, flailing, rolling, compulsive circling in cage). Benzodiazepines may cause paradoxical excitement.14,15 Caution should be used in patients with liver or kidney disease, aggressive patients, geriatric patients, and debilitated patients (eg, those with moderate to severe respiratory depression, shock, coma).14,15 Benzodiazepines may cause nystagmus in healthy patients.16

ONDANSETRON

Correct ResponseSafeOndansetron is a serotonin type 3 (5-HT3) receptor antagonist that acts on 5-HT3 receptors, peripherally on vagal nerve terminals, and in the CNS in the chemoreceptor trigger zone and is used for the prevention and treatment of vomiting.17 A recent open-label study evaluating use of ondansetron (0.5 mg/kg IV) to control nausea and vomiting in dogs with vestibular dysfunction found a significant reduction in the intensity of nausea, salivation, lip licking, restlessness, and lethargy but not in vocalization.18

CAPROMORELIN

Correct ResponseSafeCapromorelin (3 mg/kg PO every 24 hours; efficacy not tested beyond 4 days) is an FDA-approved appetite stimulant in dogs and a ghrelin-receptor agonist that stimulates growth hormone release and causes the feeling of hunger.19 Patients with vestibular dysfunction frequently have reduced appetite and nausea; capromorelin may therefore be beneficial in patients with reduced appetite not responding to antivertigo medications (eg, meclizine, maropitant). Adverse effects include GI upset (eg, hypersalivation, vomiting, diarrhea) and polydipsia.19 Caution should be used in dogs with hepatic dysfunction or renal insufficiency.19

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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AHS Symposium CB Nov/Dec 2022
Clinician's Forum: Expert Views from a Cross-Specialty Panel on Therapeutic Diets for Adverse Food Reactions

Clinician's Forum: Expert Views from a Cross-Specialty Panel on Therapeutic Diets for Adverse Food Reactions

Nutrition

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Clinician's Forum: Expert Views from a Cross-Specialty Panel on Therapeutic Diets for Adverse Food Reactions
Sponsored by an educational grant from Blue Buffalo

Participants

  • Nolan Frantz,* PhD, Nutrition Technology Group, Blue Buffalo
  • Alice Jeromin, BS (Pharmacy), DVM, DACVD, Consultant, Veterinary Allergy & Dermatology
  • Donna Raditic, DVM, DACVIM (Nutrition), CVA, Nutrition and Integrative Medicine Consultants
  • Adam Rudinsky, DVM, MS, DACVIM, The Ohio State University

Moderator

  • Leighann Daristotle,* DVM, PhD, Professional Services Veterinarian, Blue Buffalo
* Dr. Daristotle and Dr. Frantz are Blue Buffalo employees.

KEY TAKEAWAYS
  • Food-responsive diseases are collectively referred to as adverse food reactions, which include food allergies and food intolerances.1 These diseases often manifest with dermatologic or GI signs.
  • Therapeutic diets can play a key role in both the diagnosis and management of adverse food reactions.
  • Both limited-ingredient diets and hydrolyzed diets are commonly used for the diagnosis and management of adverse food reactions. Neither diet has been shown to be preferred for all situations; the type of diet should be selected based on individual circumstances.
  • Blue Buffalo carries a line of therapeutic diets that are specially formulated and manufactured with rigorous standards to meet the needs of many pets with adverse food reactions.

Dietary Considerations for Food Allergies & Food Intolerances

Therapeutic diets are used across many veterinary specialties to help diagnose, treat, and manage various diseases, including food-responsive diseases, collectively referred to as adverse food reactions. Adverse food reactions include both food allergies and food intolerances. Food allergies differ mechanistically from food intolerances in that food allergies are an immunologic response to dietary antigens,1 whereas food intolerances are nonimmunologic responses caused by metabolic, pharmacologic, and/or idiosyncratic reactions.1 Although GI signs can be exhibited in both conditions, food intolerances do not present with the dermatologic signs commonly seen with true food allergies.1 Understanding how to effectively use therapeutic diets in the diagnosis and management of these conditions is an important tool in the management of clinical signs for this population of pets and their owners.

Dr. Daristotle: What clinical presentations lead you to suspect adverse food reactions in dogs and cats? What proportion of patients have both dermatologic and GI signs?

Dr. Jeromin: I tend to see food allergies most commonly in young dogs. Otitis externa is commonly seen with adverse food reactions, so ear infections are a common sign.2 These dogs are generally pruritic or erythematous, which can result in pyodermas or recurrent yeast infections. The literature says 38% of food-allergic dogs start showing clinical signs before 1 year of age, but food allergies can start at any age.2,3 When I get a patient with GI signs or a history of GI issues with skin signs, the lightbulb kind of goes off for me; we’re going to consider food allergies, especially if clinical signs are nonseasonal. As for cats, they run their own show. Anything can look like food allergies in a cat—miliary dermatitis, eosinophilic granuloma. I’m not going to jump to psychogenic alopecia right away; I’m going to try to investigate the underlying cause. Is it food allergy and we didn’t do a proper elimination diet trial? The literature says the mean age of onset of clinical signs in cats is 4 to 5 years.1,4 Cats always like to do things a little differently.

Dr. Rudinsky: As far as presentations to the internal medicine service, I normally see patients with diarrhea, vomiting, and weight loss, which are classic GI signs. Once they have any sort of concurrent dermatologic sign, that’s going to raise my concern for food allergy immensely and change how I approach them therapeutically, dietarily, and otherwise. I really emphasize that the dermatologic component can vary—from recurrent ear problems to other classic signs of atopic dermatitis.

Dr. Raditic: It’s wonderful to hear from a dermatologist and an internist. I get patients referred to me from both of those services and also often straight from the general practitioner, often presenting with both dermatologic and gastrointestinal signs. I try to explain that the gut is a tube on the inside, and the skin’s the tube on the outside, so both can be involved in food allergy, and food plays a huge role in the health and well-being of the immune system, as well as the lining of the gut and skin.

Dr. Jeromin: Sometimes on initial presentation, you have an owner who has already diagnosed presumed food allergies in their pet. How many times do you hear, “Oh, I took him off all beef!”? I’d rather have a client who hasn’t done any reading about it or spent $300 on an unreliable IgE serum test for food so I don’t have to break all that down, because once they get that in their head and they get that paper that says what that dog or cat’s allergic to, it’s hard to say, “Sorry, I’m the bad guy here, but all that work you did it, it’s not true.”

Dr. Rudinsky: Especially on the GI side of things. Owners will give their dog half a rotisserie chicken as a treat, and at the end of the day, the dog has a relapse in its GI signs and they want to call it a chicken allergy. Then, all of a sudden, they don’t want to feed anything with chicken in it, which may or may not actually be the problem. We need to start from a clean slate and break down all that information they’re finding online, so much of which is misinformation. People are just inundated with this misinformation, and we’re often behind the starting line.

I try to explain that the gut is a tube on the inside, and the skin’s the tube on the outside, so both can be involved in food allergy.—Dr. Raditic

Dr. Jeromin: Mentioning the chicken, do you think there’s a saturation point, Dr. Rudinsky? For example, some protein-allergic dogs can’t handle even a smidge of allergen, but do you think there’s some that can handle so much and then beyond that they react?

Dr. Rudinsky: From a GI standpoint, I would say it’s a very small segment of our chronic GI patients that are actually food-allergic. I think those dogs and cats that have food intolerances, where it’s more chemically based rather than immunologically based, you probably do have this threshold, which is different than with pets that have a true food allergy and may not be able to handle any amount of their given allergen.

Dr. Raditic: We have to think about absolutely everything that goes on them and in their mouth. Anything and everything—all the chews, treats, rawhides, the flea, tick, heartworm preventives. Even if they’re more primary GI chronic enteropathy, I use the word food allergy for them, and I do that because people recognize that term. Pet owners recognize if someone is allergic to peanuts and eats a peanut, that person goes to the hospital. We go ahead and get them on a diet and give them that strict time period during which their clinical signs will hopefully resolve. Once that has happened and they’re in a stable place, we make 1 change at a time. I will usually start with a fruit or vegetable; we’ll try a carrot and give that for a week. As far as commercial treats, if there’s contamination with other ingredients that can occur—which is perfectly legal for over-the-counter diets—I usually explain that treats have even less quality control. So, the contamination factor there is going to be too high, so usually, I am using 1 thing at a time, 1 change at a time, and what we want to do is give that a good week, then we can check it off and just go through that very slow process of trying to build a few treats that they can comfortably give. It’s important to reinforce the message that their dog is special and needs to avoid their allergens at all costs. Every relapse is more damage to the skin surface, more damage to the gut lining, and it’s going to make it more difficult to get them stable again and back on track.

Dr. Rudinsky: I think getting a core list of things owners want to feed can also be helpful. The other thing that I’ve had a lot of success with is having clients bake the canned food to use as treats. For example, if I’m prescribing Blue Buffalo HF Hydrolyzed for Food Intolerance, the owner can buy a case of that canned food to go along with the dry diet. When you turn it into a cookie by slicing it into rounds and baking it, owners feel like it’s a nice activity that can bond them to their dog and allow for that treat reward system they are likely used to.

Dr. Daristotle: Dr. Frantz, regarding formulation and manufacturing, what makes these foods that are used for elimination trials different from over-the-counter diets?

Dr. Frantz: Obviously, there are a couple different kinds of diets—whether that’s hydrolyzed protein or a truly novel protein, but as we design those foods, we want to limit the number of ingredients as much as possible. The end goal is to have a balanced diet, a complete diet that sustains the animal and doesn’t cause any GI issues or other complications. So, finding protein sources that meet that criteria is important, and as we build those diets, a lot of the things go into the process in terms of what carbohydrate sources we’re using and trying to make a diet that avoids the common allergens as much as possible. There are always animals out there that are allergic to something specific or have some unique restriction, so it’s impossible for every diet to work for every animal, but there are 2 categories that pets often have success with: hydrolyzed diets, meaning the proteins have been hydrolyzed down to the point where the body doesn’t necessarily recognize them in the same sense—so you’re tricking the immune system in a way so they’re not reacting to those proteins—or a novel protein diet, where you’re finding a truly new protein that the animal has not been exposed to and not developed an allergy to. Finding truly novel proteins and really good, high-quality, hydrolyzed proteins is a challenge, especially with the diversity of pet foods these days, given that so many protein sources are available over the counter to the consumer and that pets have potentially already been exposed to. In today’s day and age, that’s a lot of what we struggle with in trying to find unique diets that meet our needs to support this type of animal.

Dr. Raditic: What kind of quality control is used for novel and hydrolyzed diets as far as assuring us that these veterinary therapeutic diets are indeed antigen-free?

Dr. Frantz: It’s not just about selecting a hydrolyzed or novel protein. It’s also about avoiding cross-contamination. The term we like to hear is that they’re making it on a “dedicated line,” but even with a dedicated line, you need to take into account all the upstream controls of raw materials—how the ingredients are being batched together and if a common batching system is being used. You can get a lot of cross-contamination that way. So, with Blue Buffalo’s NP alligator diet, one of the ways we went about it was making not only a hydrolyzed protein diet but also using a more novel protein. We also had to be sure that we didn’t have cross-contamination, so we developed a very detailed program, not only to test the finished products but also the raw materials and to validate our extrusion and canning process, including a strict cleaning protocol. So, we make sure we’re testing at different steps during the process to detect any evidence of cross-contamination. We do this through ELISA testing, which tests for the protein, or PCR testing, which can measure any leftover genetic material and is a very sensitive test. In both cases, you can pick up even very small amounts of contamination. It’s not necessarily possible to test for every possible allergen, but we focused on some of the key ones like chicken and beef. Initially, we tested for a larger set of allergens to see how consistently we would see other common allergens like soy or egg. So, we developed a very robust testing plan that screens raw materials for some of the other common animal proteins, then we test the finished product, so the food goes through a rigorous process to ensure the product’s not going to have a contamination issue. We learned a lot while developing our program and routine testing protocols; when you test every single lot of product you make, you’re going to find some contamination, and then you reject that product and keep it from going on the shelves. The last thing we want to do is have a therapeutic diet that doesn’t do what it’s supposed to do. Our goal is to make the owners’ and veterinarians’ lives easier with a product they can count on, and that’s really what we try to deliver through this robust testing process.

The last thing we want to do is have a therapeutic diet that doesn’t do what it’s supposed to do. Our goal is to make the owners’ and veterinarians’ lives easier with a product they can count on, and that’s really what we try to deliver through this robust testing process.—Dr. Frantz

Dr. Raditic: I always tell my clients over-the-counter diets are average diets for average healthy dogs and cats. Once you’ve come to an internist, dermatologist, or nutritionist, you probably don’t have the average healthy dog or cat. When you get into veterinary therapeutic diets, they’re made with research, science, knowledge, and quality control. They’re made more like medicine. Dr. Frantz, are there other benefits to these diets? Other nutrients and functional ingredients to help these patients?

Dr. Frantz: Yes, absolutely. Unique fiber profiles that really help nourish the microbiome, including the right prebiotic fibers to help those good bacteria thrive, are developed. A lot of our formulas have a decent amount of either fish oil or DHA and EPA that come from those products that can help reduce inflammation and help with some skin and coat issues. There’s a lot of technology built into these diets, and we also understand that these diets are often being used in pets that are having an immunologic response to their diet. We will have additional antioxidants and a higher level of vitamin E and C to help support that immune response.

Dr. Raditic: Compared to over-the-counter diets, veterinary therapeutic diets provide so much detailed nutritional information that’s at your fingertips; we can reach out directly to these companies, we have product guides and input from PhD animal nutritionists. So, the quality control—the idea that these diets have added functional ingredients to try to balance that inflammatory response5—really sets them apart from over-the-counter diets.

Dr. Daristotle: How do you decide which type of diet to use in a given patient, whether it’s novel protein or hydrolyzed?

Dr. Rudinsky: We have no comparative studies that really provide guidance on which type of diet to choose. When I’m going to be picking either a hydrolyzed diet or a limited-antigen diet, there are a few things I take into account, and once again, these are presented with GI signs. Hydrolyzed diets tend to be more easily digestible than their parent protein source, as hydrolysis is the basic biochemical breakdown of macronutrients, which I think can benefit a lot of proximal GI cases. A vomiting cat may do really well on Blue Buffalo HF, for example, whereas the novel-ingredient diets tend to be a little bit higher in fiber content, and I like those more for my patients with large-bowel signs. The Comparative Gastroenterology Society did an informal, unpublished poll of who chooses hydrolyzed as their first-line and who chooses novel protein, and it was a 60/40 split, so people have their preferences, and these may vary based on clinical signs, but there’s clearly no single agreed-upon choice for every patient.

Dr. Raditic: A lot of clients come to me for homemade diets, and sometimes, when they realize what it takes to make a homemade diet, as far as time and trying to ensure it’s complete and balanced, we will wind up discussing therapeutic diets. I tend to use hydrolyzed diets because often there are so many proteins that my patients have already been exposed to, which complicates identifying a novel protein for that patient. Finding something truly novel gets more and more difficult for our patients, given the wide range of proteins found in commercial diets these days.

Dr. Jeromin: As far as what diet I would pick for a cat, oftentimes it’s whatever we can get the cat to eat! We send owners home with what we call a “kitty buffet,” with 2 cans of each type of elimination diet and a Ziploc bag of the dry food, and I tell them to call me to tell me which one he likes.

Dr. Daristotle: If the pet’s still growing, how should we approach diet selection for a diet trial or putting them on a therapeutic diet?

Dr. Raditic: It depends on how young the dog is and the breed, because small breeds mature more quickly. Oftentimes, I’ll either look at the AAFCO statement in the product guide and see if the diet is AAFCO-certified for growth. But it’s also easy to just pick up the phone and ask somebody at the company, “Would my 9-month, large-breed dog be okay on this diet?” If there is something missing, they’ll be the first to tell you, and sometimes adding supplemental ingredients to that diet is an option.

Dr. Frantz: That’s one of the unique things we did with our novel-protein diets. They’re actually formulated for all life stages. One of the unique differences between a hydrolyzed protein and a regular protein is those hydrolyzed proteins tend to be more free of ash or bone content, so they’re lower in minerals, and that’s a good thing for digestibility and adult animals, but when it comes to puppies or kittens, they’re going to need a little bit more calcium and phosphorus. So, with novel protein diets, you’re going to get a little bit more of that. And for those who like to be interactive, pet owners—at the guidance of a veterinarian or nutritionist—can always add some supplements with some of the hydrolyzed foods to make it work.

Dr. Jeromin: Dr. Rudinsky, as an internist, are you seeing many patients younger than 1 year that are food-allergic with GI signs?

Dr. Rudinsky: Yes. I think we see both food intolerance and food allergy patients that are pretty young. What’s interesting about our GI cases, as opposed to a lot of medicine ailments, is it’s across age groups—from immature animals up until the 18-year-old cat with chronic diarrhea. That being said, I do think we’re seeing more food allergies in younger pets. I see more of them with those concurrent dermatologic signs, and we’re seeing dogs coming in earlier and earlier.

Dr. Jeromin: When diagnosing these conditions in young patients, I love for all of my atopic patients to be on an elimination diet for life, because there are some studies showing it keeps their atopic flareups down.6,7 I tell that to the owner, and usually by the time they get to the specialist, they’re going to do as they’re told because they’ve been through a lot. I say, “Let food be thy medicine and medicine be thy food.” If I can control many clinical signs with food, I don’t have to use drugs, and they like that, as do I.

When diagnosing these conditions in young patients, I love for all of my atopic patients to be on an elimination diet for life, because there are some studies showing it keeps their atopic flareups down.—Dr. Jeromin

Dr. Raditic: When it comes to keeping a pet on a therapeutic diet long-term, I communicate to the owner that, by the time they get all the diagnostic testing done, as well as various medical therapeutics and everything that goes into symptomatically treating these flareups, versus buying the best food possible and reducing clinical signs, it makes sense to put your money into these diets.

Dr. Rudinsky: As we talk about younger patients’ GI signs from food intolerances, I think stress is another factor to consider. I do think that, in young dogs that are anxious, irritable bowel syndrome-type symptomology is common and definitely skews toward some of those younger patients that maybe weren’t well socialized or have more generalized behavioral disorders. I think it may be more common now because of the COVID pandemic, but I also think there’s increased clinician awareness. In terms of COVID, dogs weren’t going into social settings as often, and I do take that into account when I see patients with these signs. For young dogs with GI signs consistent with IBS, fiber has been shown to potentially be beneficial as well, so this can be something to try before considering other food trials.

Dr. Frantz: That’s what we have to try to get across to pet owners; with therapeutic diets, we’re really trying to make their lives easier. We’ve done the research so they don’t have to worry about trying to find a balanced diet that will work for their pet.

Dr. Rudinsky: When I’m making a diet recommendation to a reluctant client, I have them compare the cost of that diet to any pharmaceutical I use, with maybe the exception of prednisone. Medications like budesonide or cyclosporine are all going to be infinitely more expensive than the cost difference between a commercially available pet food and a veterinary therapeutic diet.

Dr. Daristotle: What are the benefits of fiber for the gut and the immune system?

Dr. Frantz: I think fiber has become much more of a hot topic in the past decade. I think the old theory was to make a diet as highly digestible as possible, which entailed extremely low ash and fiber. That was the old adage, I think, but since then, we’ve learned a lot more about probiotics, prebiotic fibers, and even postbiotics, which we can use to influence the gut. The easiest and most cost-effective way to do that is with the right fiber sources. We know that a lot of our immune system is in the gut; it’s impacted by the health and stability of what we reference as the microbiome now, and you see a lot of research around the microbiome and trying to figure out how to manipulate it. Any diet change will disturb that environment, so knowing what a diet will do and being on something consistent can really help avoid any unwanted shifts in that microbiome. That’s one of the points we’ve emphasized in our products—the importance of fiber. It’s not just about treating a GI disease or whatever. We do that in our puppy foods or kitten foods to try to get that right balance of digestibility and beneficial fibers.

Dr. Raditic: There has been a shift in focus from probiotics to prebiotics. What do we know about fiber, a prebiotic? Let’s play with fiber because we probably statistically have a better chance of creating a healthy GI microbial population and immune response by doing that.

Dr. Rudinsky: We just completed a study on acute diarrhea that will be published later in JAVMA. It showed that psyllium-enhanced, fiber-based diets outperform metronidazole for resolution of clinical signs without any of the deleterious effects of metronidazole. When we looked at the microbiome and metabolome of these dogs, including the dysbiosis index, secondary bile acids, and short-chain fatty acids, these dogs were much closer to being back toward normal values a month out from that diarrhea episode when they were treated with fiber as compared with metronidazole. How many times have we seen someone say, “Add some canned pumpkin”? We should consider instead turning to a therapeutic fiber-enhanced diet, because it’s nearly impossible to add enough canned pumpkin to an existing diet to get a therapeutic benefit. So, it’s nice to see companies like Blue Buffalo investing in fiber because it’s so impactful, and a manufactured diet is probably the best way to deliver it.

It’s nice to see pet food companies like Blue Buffalo investing in fiber because it’s so impactful, and a manufactured diet is probably the best way to deliver it.—Dr. Rudinsky

Dr. Frantz: It’s not just about any one given fiber source, right? It’s a blend of fibers, and that can be beneficial, too. Then, with more novel fibers, some fruits and vegetables, they can bring some antioxidants along with it that have a potential benefit, too, so we find that a nice mix of both soluble and insoluble fiber can really have benefits and perform nicely.

Dr. Daristotle: When we think about diet trials for dermatologic diseases versus for GI diseases, are they the same? How do they differ?

Dr. Jeromin: As a dermatologist, I usually do a full 8 to 10 weeks on a diet trial. We also take a week to wean onto the new diet. We don’t abruptly change their food. I explain that the dog may get diarrhea or soft stool if they switch abruptly. We explain that, once they’re weaned over, they can eat nothing else for the duration of the trial. We check in with them every 2 weeks. I think the studies show that 90% of food-allergic patients will show improvement within an 8-week diet trial.8 With cats, anecdotally, it seems to me you will often know if a food trial is effective in a shorter period of time than dogs, but we still have them go the full 8 weeks.

Dr. Rudinsky: For young dogs with concurrent dermatologic and GI signs, I have the same approach. Where I differ is with pets that have suspected food intolerance, as they can display a robust response after only 2 weeks on a food trial. Depending on the clinical signs we’re treating, pets with food intolerances rather than food allergies will usually respond within 5 to 10 days. Cats often respond really dramatically within just a few days. Vomiting cats have been reported to respond within 24 to 72 hours in a lot of cases,9 so there’s a little bit more immediate gratification in those cases. A lot of my patients are presented with diarrhea, so for those, I usually don’t worry about a tapered food switch.

Dr. Raditic: As a nutritionist, I get a mix of those patients; usually, they have both skin and GI signs. I put them in what I call the “food bubble” and explain that this diet is the only thing they can consume during the food trial. I also make sure we look at the parasite preventives being used. We go through all the medications and supplements to make sure a pet isn’t inadvertently being exposed to an allergen through a flavoring.

Dr. Jeromin: And again, all of these conversations are time-consuming; we spend a lot of time with these clients educating and reeducating.

Dr. Daristotle: Do you have any tips on feeding a multi-pet household and how to make sure the pet being treated is getting the food and that you can monitor how much they’re getting?

Dr. Jeromin: Challenges certainly arise with food trials. For example, you have toddlers who like to drop table scraps and multi-pet households where separating the pets is challenging. For a multi-pet household, if there’s no reason not to, I like them to feed all the pets the same thing. Inevitably, you will have pets licking each other’s bowls or will struggle to feed them separately. I just think it’s easier if they can put them all on the food trial diet. You may get complaints on the cost, but as we discussed, it’s still preferable to other options.

Dr. Rudinsky: As an internist, where I don’t have the ability to intervene is in those early husbandry choices that pet owners are making at home. So, if you think about what we manage dietarily—obesity, gastrointestinal disease, dermatologic disease, cardiac disease, urinary disease—it’s very likely that, at some point, every pet is going to receive a targeted dietary recommendation, so that may be an area where general practitioners can set themselves and their clients up for success and discuss getting into the habit of individualized meal feedings for each pet in the early days of pet ownership.

Dr. Raditic: With mutli-pet households, I really do try to get them on the same diet, and oftentimes, once they see one pet start to reap some of the benefits of a therapeutic diet, they will even ask if they can put their other pet on that diet as well.

Dr. Rudinsky: Another thing to consider in multi-animal household is that, oftentimes, whether due to dermatologic signs where the pet is distracted and itching or chronic GI signs that have led to a decreased appetite, the pet you are targeting is often the animal in the household that is more likely to be a picky or reluctant eater. I think with chronic gastroenteropthies, we’re doing a better job at recognizing when we need to implement dietary therapy, but sometimes, we fail to recognize that we still need to use supportive care measures to help transition to a new diet, to control their signs and get them feeling good enough to accept that new diet. I use mirtazapine a lot in my cats for dietary adherence if I’m worried about the transition to a new diet. Once that animal starts feeling better, you can taper off those initial starter drugs, and once they’re eating robustly, you can then have a distinct mealtime. It’s not me sitting next to my dog for 4 hours in the morning trying to get them to eat that prescribed formula.

Dr. Daristotle: What are some of the most common mistakes you’ve seen with diet trials, especially when a patient comes to you with a diet trial that’s already been done?

Dr. Jeromin: In my experience, recommending over-the-counter, limited- ingredient diets is the number one mistake. The other would be running a blood test for food allergies, which doesn’t actually help determine which foods a pet can or cannot tolerate. It’s also common to see too short of a duration for a food trial.

Dr. Rudinsky: I think looking at the nuanced needs of an individual when selecting a food for a diet trial is often overlooked. When I think of GI disease, the criteria I’m usually looking at in a diet for my patients is digestibility, fat content, fiber content, and hydrolyzed versus novel protein or novel ingredients. As we mentioned, there’s not really a clear definitive answer regarding whether hydrolyzed or novel is the better choice, but in a GI case, it’s helpful to consider the whole nutrient profile when choosing a diet. You can argue that putting a dog on a hydrolyzed diet would be a great option from an allergic standpoint, but if you happen to reach for something like a soy-based vegetarian option, it will be extremely low in fiber. So, regardless of what that does for that dog’s allergies, if the dog requires fiber for its GI health, you’re going to have worse GI signs. So, not considering the global perspective of a GI patient I think can sometimes lead diet trials a little bit astray. Plus, if it’s not set up right, you’re going to waste a lot of time as well as fatigue the client. I think that’s so true about diet trials because owners are fatigued when they’ve bought multiple diets. Now they’re finding out that diet wasn’t the right one or maybe wasn’t the best choice. So, getting the client onboard and maybe taking that extra time upfront to do some diet research will make everyone’s life a little easier down the road, including the person who is in first-opinion practice, because they’re seeing 98% of these animals for their follow-up, not the referral center.

Getting the client onboard and maybe taking that extra time upfront to do some diet research will make everyone’s life a little easier down the road, including the person who is in first-opinion practice, because they’re seeing 98% of these animals for their follow-up, not the referral center.—Dr. Rudinsky

Dr. Raditic: I think general practitioners also need to realize that a lot of the serum testing, saliva testing, hair, etc. for food haven’t been validated. These tests are unreliable and should not be used as a diagnostic test for food allergies.10-12 So, if they’ve been to their GP and did that, we have to break down that misconception and start over with a diet trial. Getting that commitment upfront that this is what it’s going to take is important, and we have to follow up continually to see how they are doing. One thing I do to help with the success of my diet trials is give my clients fecal score charts and itch tracker charts where they can rate their pet’s stool consistency and pruritus level daily. So, I get the owners doing something too during this period so they can start to see some numerical trends. I really would encourage general practitioners to give pet owners something like this to do so they can see the progress. Skin improvements and fecal improvements are like watching grass grow, but if we’re charting these signs, then we can actually show them if it’s getting better or worse. I think that type of approach and getting clients more involved so they can feel like they are part of the process is helpful. You form a team, and that client becomes more committed.

Dr. Rudinsky: I think those clinical scoring systems for chronic enteropathy or PLE can be very useful. Those are really nice because often we’ll see a diet trial that gets us 75% of the way there as far as control of clinical signs. And because the pet isn’t perfectly normal, an owner may have a hard time seeing that diet is still impacting their pet, and those scoring sheets provide a little bit of evidence to say, “Well, look at the improvement your dog has seen; maybe vomiting is the most frustrating symptom to you, but the diarrhea has resolved and your pet is putting on weight and we’ve made these improvements.” From a GI standpoint, the fecal scoring is also really helpful because the nature of stool can serve as clues to what you want to tweak dietary-wise. What does the fecal sample look like? What’s the fecal score? How’s the urgency? Where do we need to target in the gut to manage this? Those are all now forms that we have our clients do while they’re checking in. For any practitioner, those are publicly available (see Suggested Reading). You can include it with your intake forms, have an owner fill it out, and all you have to do is put the total score in the patient record. Another thing to keep in mind is that, if a practitioner can’t initially convince the pet owner to start a diet trial and instead we start a corticosteroid or something else, there’s often a tendency to say, “Well, a diet change wasn’t an option,” and if initially the dog’s not eating, then maybe you do need steroids to get it started, but we still need to circle back on diet because that’s still the ultimate goal for long-term maintenance therapy for that animal.

Dr. Jeromin: I agree. I tell them we’re going to try to control their allergic pet completely with food and use meds for flareups, because there will be flareups. Allergies are dynamic, not static. And like Dr. Rudinsky said about achieving 100%, we may not get to 100%, but we’re going to get that pet much more comfortable and then have the ability to treat with medication during those flareups, but we don’t want to keep them on those meds long-term if we don’t have to. We’d rather control the pet’s clinical signs with the food.

References & Suggested Reading

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