August 2018   |   Volume 16   |   Issue 8

Vitamin A Deficiency in Insectivorous Lizards

in this issue

in this issue

Vitamin A Deficiency in Insectivorous Lizards

Thoracic Limb Lameness in a Dog

Differential Diagnosis: Epistaxis

Top 5 Mechanisms of Adverse Drug Events in the Intensive Care Unit

Pregnancy in Dogs

Cheyletiellosis

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Vitamin A Deficiency in Insectivorous Lizards

Thomas H. Boyer, DVM, DABVP (Reptile & Amphibian), Pet Hospital of Penasquitos, San Diego, California

Exotic Animal Medicine

|Peer Reviewed

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Vitamin A Deficiency in Insectivorous Lizards

Vitamin A is an essential hormone that activates genes for maturation of immature epidermal cells (ie, keratinocytes). Without vitamin A, cells undergo hyperkeratosis (ie, an abnormal thickening of the stratum corneum, associated with excess keratin) and squamous metaplasia (ie, transformation of cuboidal, columnar, or ciliated glandular or mucosal epithelium into keratinizing stratified squamous epithelium), particularly in the respiratory, ocular, endocrine, GI, and genitourinary systems.1

Background & Pathophysiology

Vitamin A deficiency is common in all captive insectivorous reptiles, including leopard geckos (Eublepharis macularius), chameleons (most commonly panther [Furcifer pardalis], veiled [Chamaeleo calyptratus], and Jackson’s [Trioceros jacksonii]), and anoles. It occurs less often in wild reptiles, likely because of their varied diet, which typically includes other reptiles, mammals, birds, and invertebrates.

Vitamin A deficiency is thought to result from dietary deficiency; it is unknown if insectivorous lizards can synthesize vitamin A from carotenoids in their diet. Dietary history and multivitamin review may disclose a lack of vitamin A in the patient’s diet2; for example, the patient may not be fed multivitamins that contain vitamin A or may be fed insects that do not receive gut-loading diets or other foods containing vitamin A. Feeder insects are generally deficient in vitamin A and often receive diets deficient in vitamin A. In addition, many food manufacturers omit vitamin A and substitute β-carotene in reptile multivitamins because of misinformation that vitamin A is toxic to insectivores.1

Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.
Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.

Figure 1 Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.

Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.
Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.

Figure 1 Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.

Figure 1 Healthy panther chameleon (Furcifer pardalis; A) with clear rounded eyelids as compared with a panther chameleon with vitamin A deficiency (B). Dull coloration, cheilitis, blepharedema, squinting, mucoid ocular buildup, and dysecdysis are visible over the head and eyelid openings.

Many patients with vitamin A deficiency have long-term ocular disease that is not responsive to multiple antibiotics.2 Both lacrimal and salivary glands are commonly affected, and patients may have blepharitis, blepharospasm (Figure 1), and cheilitis. These patients typically are anorexic and have difficulty shedding (ie, dysecdysis). Leopard geckos may be presented with mucoid-to-solid cellular debris under the eyelids (Figures 2 and 3), ulcerative keratitis, and/or abscessation of periocular glands. Chameleons may have mucoid buildup in the eye, thickened conjunctiva, difficulty capturing prey with the tongue (possibly from dysfunction of sticky mucus glands in the tongue tip), and dull coloration (Figure 4, page 18), which can be difficult to identify on examination. Chronic cases may result in blindness.

Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.
Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.

Figure 2 Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.

Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.
Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.

Figure 2 Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.

Figure 2 Vitamin A deficiency in a leopard gecko (Eublepharis macularius). Solid cellular debris in the right (A) and left (B) eyes, cheilitis, and dysecdysis can be seen.

Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)
Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)

Figure 3 Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)

Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)
Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)

Figure 3 Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)

Figure 3 Leopard gecko from Figure 2 with solid cellular debris in both eyes due to vitamin A deficiency shortly after debris removal (A), with enhanced view of removed cellular debris (B)

Herbivores (eg, tortoises, green iguanas [Iguana iguana]) and omnivores (eg, bearded dragons [Pogona vitticeps]), along with carnivorous lizards and snakes that eat the entire body of an animal, generally are not affected by vitamin A deficiency. Omnivorous Emydidae turtles (eg, box turtles [Terrapene spp]) and red-eared sliders (Trachemys scripta elegans) can develop vitamin A deficiency.

Diagnosis

Diagnosis of vitamin A deficiency is based on dietary history and clinical signs. Because most vitamin A is stored in the liver and circulating levels do not fall until liver reserves are exhausted, circulating levels may not be an accurate indicator of overall vitamin A status. Normal values for liver or circulating levels of vitamin A or retinol are often unknown. Required blood and liver biopsy sample sizes may be greater than can be obtained safely in small patients, and incorrect sample handling and assay techniques can alter values.

Differential diagnoses for ocular and gingival disease may have numerous causes, including infectious (eg, bacterial, fungal, parasitic, viral), neoplastic, metabolic (eg, calcium deficiency [exposure gingivitis], uric acid deposits [conjunctivitis, retinal detachment, blepharospasm]), traumatic, and environmental (eg, from substrate, ultraviolet light, inappropriate humidity). 

Fluorescein staining may reveal corneal ulcers. Corneal cytology may disclose secondary bacterial, fungal, parasitic, or neoplastic disease.

Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.
Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.

Figure 4 Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.

Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.
Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.

Figure 4 Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.

Figure 4 Panther chameleon with vitamin A deficiency and blepharospasm on presentation (A) and 2 weeks after a single injection of vitamin A palmitate (B). The eye is markedly improved, but some blepharedema remains.

Treatment

A vitamin A supplement should be added to the patient’s diet. All vitamin A doses are empiric and range from 5000-66 666 IU vitamin A palmitate per kg IM, SC, or PO every 1 to 2 weeks for 2 treatments.1,3 Injectable vitamin A has been associated with hypervitaminosis A; oral supplementation is preferred. Fat-soluble vitamin A is much less toxic than water-soluble vitamin A.

Broad-spectrum ophthalmic antibiotic ointments or antibiotic drops should be administered to lubricate and prevent secondary bacterial infection of the cornea, if compromised. In leopard geckos, solid cellular debris should be moisturized under the eyelids with saline and removed with blunt probes, hemostats, or fine forceps. The patient should be checked for ulcers using fluorescein staining, and eyes should be flushed copiously with saline. Similarly, eyes of chameleons should be flushed with sterile saline to remove thickened mucus and accumulated cellular debris secondary to xerophthalmia. Retained sheds around the eyes and feet and retained hemipenal casts should be removed with the patient under anesthesia.

If the patient has not eaten recently, nutritional support should be provided via fluid therapy and oral caloric supplementation. If the patient is eating, the quality of its diet should be improved. Owners should be instructed to gut load feeder insects with a diet containing vitamin A, at least 8% calcium, multivitamins, trace minerals, proteins, carbohydrates, and fat; to dust all insects with calcium before each patient feeding; and to feed multivitamins containing vitamin A—rather than calcium—twice a month. 

Wild insectivorous reptiles eat hundreds of invertebrates (eg, insects, arachnids, mollusks, crustaceans), other lizards, mammals, and birds, so pet lizards should be fed as wide a variety of insects as possible; diet should not be restricted to crickets, mealworms, super or king mealworms, waxworms, and/or Dubia roaches. Reptile specialty stores and online vendors sell a wide variety of insects, including other cricket species (eg, black, field, banded), silkworms, black soldier fly larvae (sold as Phoenix worms), tobacco or tomato horn worms (sphinx or hawk moth larvae [sold as goliath worms or green giants]), butterworms, bean beetles, fruit flies, springtails, and wood lice, as well as wild-caught seasonally available insects (eg, moths, cicadas, flies, grasshoppers, katydids, bees [with stingers removed], cockroaches, crustaceans [eg, pill bugs, roly-poly bugs], mollusks [eg, snails, slugs]). Fireflies contain highly toxic lucibufagins and should never be fed to pet lizards.4 Some insectivorous reptiles will also eat neonatal mice, which are rich in vitamin A.

Patients should be re-evaluated every 1 to 2 weeks until they are eating readily and appear healthy. Body weight should be monitored to determine if nutritional supplementation is indicated, and dietary recommendations should be reviewed with the owners at each appointment to ensure they understand and have implemented the changes.

Precautions

In one study of cricket gut-loading diets, 3 of 4 diets did not improve the crickets’ calcium content because they were not calcium enriched.5 Feeder insects should be fed a gut-loading diet high in calcium. Calcium- fortified, high-moisture cricket wafers or high-moisture foods (eg, gel water cubes) are ineffective at increasing calcium or vitamin A content and are not recommended, even as a water source.6 Studies have shown that cubes decrease the effectiveness of gut-loading diets. Larvae will take water from damp paper towels, and other insects will drink from water-filled cotton balls in a bottle or syringe cap. Multivitamins should be discarded if no vitamin A is present, the supplement has expired, or the supplement is more than a year old.

Prognosis

Prognosis is poorer when clinical signs are more advanced or have been present for 6 months or longer. Patients with concurrent disease (eg, hepatic lipidosis, nutritional secondary hyperparathyroidism) also have a poor prognosis. If vitamin A deficiency is diagnosed early and treated appropriately, most patients will make a full recovery. 

Patients with long-term vitamin A deficiency may be blind, and patients with severe cases may have corneal fibrosis similar to chronic canine keratoconjunctivitis (Figure 5). Patients with a history of anorexia lasting several months may have hepatic lipidosis and may be susceptible to refeeding syndrome.

Corneal scarring in a leopard gecko as a sequela to chronic untreated vitamin A deficiency
Corneal scarring in a leopard gecko as a sequela to chronic untreated vitamin A deficiency

Figure 5 Corneal scarring in a leopard gecko as a sequela to chronic untreated vitamin A deficiency

Figure 5 Corneal scarring in a leopard gecko as a sequela to chronic untreated vitamin A deficiency

Conclusion

Vitamin A deficiency in insectivorous reptiles is common and can result in severe epithelial disease, especially involving the eyes. Close attention to diet can prevent and diagnose this deficiency. Insectivores must be fed a varied diet, insects should be dusted with multivitamins containing vitamin A twice monthly, and, most importantly, feeder insects must be fed a balanced diet that contains vitamin A and 8% calcium. Clinicians should discuss these requirements in detail with all owners of insectivorous reptiles and amphibians.

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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Top 5 Mechanisms of Adverse Drug Events in the Intensive Care Unit

Andrew Linklater, DVM, DACVECC, Lakeshore Veterinary Specialists, Glendale, Wisconsin

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Top 5 Mechanisms of Adverse Drug Events in the Intensive Care Unit

FIGURE 1 Cloudy precipitate in a syringe after combining butorphanol and furosemide

Drug interactions can occur in the veterinary setting and may result in negative consequences to the patient. A drug interaction refers to a reaction between one or more drugs that alters the effect of or affects the properties of one or both drugs.

Drug interactions can occur during or after administration and may be synergistic, antagonistic, or additive. Interactions between incompatible drugs are always antagonistic. Antagonistic interactions result in decreased drug effectiveness when one drug alters the absorption, distribution, metabolism, or excretion of another or when the interaction causes a direct pharmacodynamic effect 1 that harms the patient. An adverse drug event (ADE) refers to patient injury related to a medical intervention involving a drug.

Critically ill patients are at increased risk for ADEs because they often receive multiple medications concurrently and have serious diseases that may be exacerbated by administration of these medications. The frequency and severity of drug interactions in veterinary intensive care units (ICUs) are unknown, as no standard reporting mechanisms have been established. Reports in human medicine vary substantially: 8.5% to 15% (per 100 admissions) of patients admitted to an ICU may have an ADE,2-4 with up to 54% of patients having a potential drug–drug interaction.5 Adverse events have been associated with a more costly and longer ICU stay.2,4 Most reported ADEs in humans were considered significant or serious, with a smaller percentage being potentially life-threatening or fatal.3,6 Extra-label use of medications, a common practice in veterinary medicine, has been reported to increase ADEs in ICUs.7 Veterinary staff must be diligent in reviewing all medications prescribed to a patient, including reviewing each drug’s dosage, potential adverse effects, and known and potential interactions with other medications.1,8

Drug interactions come in many forms, including:

  • Incompatibilities of drugs administered at the same time to the same patient 
  • Ineffectiveness of a single drug when a certain carrier or environment (eg, gastric acidity) is present 
  • Dosing errors that move outside the therapeutic dose (likely the most frequent)9-11 
  • Drugs or certain disease processes that alter a drug’s absorption, distribution, metabolism, or excretion
  • Direct pharmacodynamic interactions 
  • Adverse effects1 

This article presents the author’s top 5 potential mechanisms of ADEs in the ICU.

1

Incompatibility

Many drugs are chemically incompatible, often due to the pH or carrier molecules in the drug formulation. For example, diazepam is not compatible with many drugs because of the propylene glycol carrier, enrofloxacin may have decreased availability when administered with divalent cation (calcium or magnesium)-containing solutions, and the injectable forms of butorphanol and furosemide—both often administered to patients presented with respiratory distress from congestive heart failure—may form a precipitate if administered together.

Butorphanol (for sedation) and furosemide (a potent loop diuretic) are common initial treatment choices for patients presented with acute congestive heart failure. Both injectable medications can be given intravenously or intramuscularly, but they cannot be combined. Furosemide is a mildly alkaline, buffered product and should not be mixed with solutions that have a pH less than 5.5; the pH of butorphanol varies between manufacturers but may be between 3.0 and 5.5.8,12,13 When these drugs are allowed to interact through combination in a syringe or an IV line, a cloudy precipitate may form (Figure 1, above). This precipitate can damage tissue or occlude a vessel—particularly in the cerebral and pulmonary vasculature, which can be life-threatening—and one or both drugs may be ineffective. To prevent this interaction, drug compatibility should always be determined prior to combination (in a syringe) or coadministration of drugs in any fluid lines; in addition, the fluid line should be thoroughly flushed with a compatible solution between administration of each drug.

2

Related Mechanisms of Action & Additive Effect

Critically ill patients are susceptible to GI ulceration (Figure 2) because of many factors, including primary or secondary GI disease, surgery, hypoperfusion, and mechanical ventilation. These patients also often require corticosteroids or NSAIDs because of inflammation, pain, and adrenal or immune-mediated disease. Ulceration can result in GI dysfunction, hemorrhage, and/or perforation.

Endoscopic image of duodenal ulcers in a critically ill patient
Endoscopic image of duodenal ulcers in a critically ill patient

FIGURE 2 Endoscopic image of duodenal ulcers in a critically ill patient

FIGURE 2 Endoscopic image of duodenal ulcers in a critically ill patient

Corticosteroids and NSAIDs typically should not be used together, as their combined actions are likely to cause severe GI ulceration. Corticosteroids exert their anti-inflammatory effect in part through inhibition of several enzymes in the arachidonic acid cascade (eg, phospholipase A2, cyclooxygenase); NSAIDs also inhibit cyclooxygenases.14 The arachidonic acid cascade is important for maintaining normal GI mucosa and renal perfusion. Inhibition of prostaglandin production results in poor GI blood flow and poor mucosal barrier function, exposing the mucosa to the low pH of gastric acid and causing development (and poor healing) of gastric and intestinal ulcers.15,16

When a patient requires a change in anti-inflammatory medication, a “washout” period between medications should be observed. The ideal washout period has not been established for all drugs, but a period of 4 to 5 half-lives of the individual drug (resulting in a time frame of 3-5 days for many drugs) has been suggested anecdotally.17-19 When a washout period is not possible, a patient has inadvertently been administered more than one anti-inflammatory drug, an overdose is suspected, or a patient is known or suspected to have GI ulceration, gastroprotective medications should be started, and the anti-inflammatory drug should be discontinued, if possible. Medications that may treat or prevent gastric ulcer formation include H2-receptor antagonists, proton pump inhibitors, sucralfate, or prostaglandin analogues.20 Although proton pump inhibitors are more effective as acid reducers than are H2-receptor antagonists, their onset of action may be prolonged.

3

Inhibition of Absorption

GI ulceration is common in critically ill patients and can cause protein and blood loss, poor appetite, pain, poor nutrition, vomiting, and sepsis. Sucralfate is a sucrose–sulfate–aluminum complex that in the acidic environment of the stomach is converted into a paste to provide a physical barrier over an ulcer. It adsorbs pepsin and bile acids, prevents diffusion of hydrogen ions into the gastric mucosa, and may stimulate the production of prostaglandin E,21 all of which promote an environment for GI ulcers to heal.

Sucralfate interferes with the absorption of many drugs, such as antibiotics and antifungal drugs.22-24 Because it has the potential to decrease absorption and the effectiveness of other orally administered medications,21,25-27 sucralfate should be administered at least 2 hours before or after other oral medications. This separation has resulted in improved absorption of some drugs; however, ideal time frames for all drugs have not been determined.

4

Neurologic Side Effects

Many ICU patients may have either an existing primary neurologic disease or have a condition that secondarily affects the neurologic system (eg, hypoglycemia, hypokalemia, hypernatremia). In addition, ICU patients are commonly exposed to a variety of medications that can affect the neurologic system, such as analgesics (eg, opioids, tramadol), prokinetic medications (eg, metoclopramide), antibiotics (eg, metronidazole), and sedatives (eg, acepromazine, trazodone, benzodiazepines, α2 agonists). 

Trazodone and tramadol are commonly used drugs for which use has increased substantially in the last several years. Trazodone is a serotonin antagonist and reuptake inhibitor and has several reported mechanisms of action.28 When combined, these drugs can cause serotonin syndrome (Figure 3), a condition characterized by GI signs (eg, vomiting, diarrhea), cardiorespiratory signs (eg, dyspnea, arrhythmias), and neurologic signs (eg, seizures, hyperthermia, hyperesthesia, depression, vocalization, ataxia, coma). Although serotonin syndrome has not been reported with coadministration of trazodone and tramadol in animals, it has been observed in humans when both trazodone and tramadol are used in combination with opioids and other serotonin and norepinephrine reuptake inhibitors—occasionally with lethal consequences.29-31

Patient with serotonin syndrome with tachypnea, tachycardia, mydriasis, and agitation
Patient with serotonin syndrome with tachypnea, tachycardia, mydriasis, and agitation

FIGURE 3 Patient with serotonin syndrome with tachypnea, tachycardia, mydriasis, and agitation

FIGURE 3 Patient with serotonin syndrome with tachypnea, tachycardia, mydriasis, and agitation

Any medications with a similar mechanism of action should be prescribed together cautiously; if adverse effects are noted, both drugs should be discontinued and appropriate supportive care initiated.

5

Effects on Potassium

ICU patients often require treatment for conditions that affect serum potassium concentration, including urinary tract disease, toxicities, diabetes, adrenal gland disease, abdominal effusions, and nutritional deficiencies. Potassium concentration should be monitored closely in these patients, as severe hyperkalemia can lead to altered cardiac function and death (Figure 4), and severe hypokalemia can cause muscle weakness, poor GI function, hypoventilation, and death.

ECG from a cat with hyperkalemia caused by urethral obstruction. Atrial standstill (absent P waves) can be seen with supraventricular escape beats at 140 bpm.
ECG from a cat with hyperkalemia caused by urethral obstruction. Atrial standstill (absent P waves) can be seen with supraventricular escape beats at 140 bpm.

FIGURE 4 ECG from a cat with hyperkalemia caused by urethral obstruction. Atrial standstill (absent P waves) can be seen with supraventricular escape beats at 140 bpm.

FIGURE 4 ECG from a cat with hyperkalemia caused by urethral obstruction. Atrial standstill (absent P waves) can be seen with supraventricular escape beats at 140 bpm.

Many drugs can alter potassium levels and exacerbate many of these conditions. Hyperkalemia can occur after administration of potassium-containing fluids, potassium supplementation (eg, potassium chloride, potassium phosphate, potassium acetate), NSAIDs, ACE inhibitors, and spironolactone. Hypokalemia may occur following administration of IV fluids, insulin, sodium bicarbonate, dextrose, diuretics, and β agonists (eg, epinephrine, terbutaline). Any patient that is hospitalized and receiving any of these medications, particularly if any of the conditions noted in this article are present, should have serum potassium concentration monitored closely and corrected if necessary.

ADE = adverse drug event, ICU = intensive care unit

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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Transitioning Cats from Lente Insulin to Protamine Zinc Insulin

Andrew Bugbee, DVM, DACVIM, University of Georgia

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Transitioning Cats from Lente Insulin to Protamine Zinc Insulin

In the Literature

Gostelow R, Hazuchova K, Scudder C, Forcada Y, Church D, Niessen SJM. Prospective evaluation of a protocol for transitioning porcine lente insulin-treated diabetic cats to human recombinant protamine zinc insulin. J Feline Med Surg. 2018;20(2):114-121.


FROM THE PAGE …

This study* assessed a protocol for transitioning cats from a porcine-source lente insulin (LI) to a human-recombinant protamine zinc insulin (PZI). Although both insulin formulations have been shown to be efficacious in the management of feline diabetes mellitus, PZI has been reported to exhibit a longer duration of action in a model of healthy cats.1-3

Inclusion criteria included diagnosis of diabetes mellitus within the previous 5 months, twice-daily LI injections for at least 6 weeks, and eating a low-carbohydrate, high-protein diet for at least 10 days. Cats (n = 22) were screened for concurrent conditions and underwent a 24-hour glucose curve to assess response to LI (median dose, 0.5 U/kg). A validated clinical scoring system (Diabetic Clinical Score) and patient and owner quality-of-life (QOL) assessments were serially evaluated at set time points over the study period. Following determination of glycemic responses to LI, patients were transitioned to twice-daily PZI at manufacturer-recommended starting doses (median dose, 0.5 U/kg). Glucose curves were serially assessed over a 12-week period, with PZI doses adjusted using a preinsulin and nadir glucose concentration-based protocol.      After the 12-week PZI period, diabetic cats had statistically significant reductions in serum fructosamine, lower clinical scores, and lower administered insulin doses; QOL scores were indicative of improved QOL. Although true duration of action is difficult to define when insulin is administered twice daily, 6 LI-treated cats were documented to have short durations of action (<9 hours); only 2 PZI cats were found to have an action duration <9 hours. All cats noted to have durations of insulin action <9 hours were found to experience improved durations when treated with the opposite formulation.  

Periods of subclinical and clinical hypoglycemia were uncommon (15.8%) but were noted with both insulin formulations. Although the study was not designed to prove superiority of one insulin formulation, 22.7% of cats entered remission within 12 weeks of being transitioned to PZI, which suggests that PZI is a viable treatment option for diabetic cats.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

PZI may result in improved diabetic outcomes in cats as compared with LI, which is likely attributable to a consistently more appropriate duration of insulin action.

 

2

In cases of poor duration of insulin action, cats may exhibit more favorable responses when transitioned to a different insulin type.

 

3

Transition to PZI can be safely accomplished using manufacturer-recommended starting doses, with subsequent dose titrations directed by serial glycemic monitoring of the patient’s insulin response.

*This study was supported by Boehringer Ingelheim.

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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Immune-Mediated Neutropenia

Shawn Kearns, DVM, DACVIM (SAIM), Angell Animal Medical Center, Boston, Massachusetts

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Immune-Mediated Neutropenia

In the Literature

Devine L, Armstrong PJ, Whittemore JC, et al. Presumed primary immune-mediated neutropenia in 35 dogs: a retrospective study. J Small Anim Pract. 2017;58(6):307-313.


FROM THE PAGE ...

This retrospective study examined records of a cohort of dogs with presumed primary immune-mediated neutropenia. Included in the study were 35 dogs with neutrophil concentrations <1.5 × 109 cells/L (based on a minimum of 2 CBCs) and for which other causes of neutropenia or secondary immune-mediated neutropenia were excluded. The authors sought to describe presenting clinical characteristics, CBC results, bone marrow characteristics, therapies used, clinical response to treatment, and outcomes at 6 months and one year.

The most common presenting clinical complaints included lethargy and anorexia (63%); 46% of dogs had increased body temperature. Neutropenia was <0.5 × 109 cells/L in 60% of dogs; 8 had thrombocytopenia, which was severe in 3 dogs. Twenty-three dogs had myeloid hyperplasia, 10 had myeloid hypoplasia, and 2 had normal myelopoiesis. Serum chemistry results included elevated liver values and various electrolyte abnormalities. Abdominal ultrasonographic images and thoracic and abdominal radiographs were unremarkable in most cases; splenomegaly was the most common finding. Dogs were started on a corticosteroid initially; 43% required adjunctive treatment using either azathioprine or cyclosporine. Neutropenia resolved in 32 of 33 dogs within 2 weeks of beginning treatment and in all dogs within 1 month. 

Although response rates for resolution of neutropenia were rapid in this report, other cytopenias may take longer to resolve or may require additional treatment. In addition, relapse was common in this study (34.3%), emphasizing the need for consistent patient follow-up and the need for further studies to determine optimal therapy—in particular, steroid doses, treatment duration, and secondary immunosuppressive drugs.

A diagnosis of immune-mediated neutropenia remains a diagnosis of exclusion. Because it is considered an uncommon cause of neutropenia,1-3 testing to exclude other causes should include urine culture, abdominal ultrasonography, thoracic radiography, and vector-borne disease testing. Other infectious disease (eg, fungal, parvovirus) testing may be warranted depending on the patient’s geographic location, age, and vaccination status. In one retrospective evaluation of neutropenia, nonbacterial infectious diseases were found most commonly.4


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Because immune-mediated neutropenia remains primarily a diagnosis of exclusion, ancillary testing is important to exclude other causes of neutropenia.

 

2

Although the initial response to treatment appears favorable and fast, owners should be educated about the need for follow-up due to potential relapse during drug tapering or treatment cessation.

 

3

Although the ideal secondary immunosuppressive drug remains unknown, additional therapies beyond glucocorticoids can be considered to maintain remission.

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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Adequan CB August 2018

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NY Vet CB August 2018

Short-Term Anxiolysis for Feline Visits

Glenn A. Olah, DVM, PhD, DABVP (Feline), Winn Feline Foundation, Albuquerque Cat Clinic, Albuquerque, New Mexico

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Short-Term Anxiolysis for Feline Visits

In the Literature

van Haaften KA, Forsythe LR, Stelow EA, Bain MJ. Effects of a single preappointment dose of gabapentin on signs of stress in cats during transportation and veterinary examination. J Am Vet Med Assoc. 2017;251(10):1175-1181.


FROM THE PAGE …

Stress associated with transportation, examination, and diagnostic procedures often deters owners from bringing their cats to the clinic to receive regular veterinary care. Multiple strategies have been explored to reduce stress and increase cat cooperation during veterinary visits.

Gabapentin has traditionally been prescribed as an adjuvant for seizure control and chronic or neuropathic pain.1-4 Its exact mechanism is not entirely clear. Studies on gabapentin’s efficacy as an anxiolytic agent and its safety in cats are scant, limited to only one recent study.5

A random, blinded crossover study was conducted to determine whether a single 100-mg oral dose of gabapentin would be effective in reducing signs of stress and aggression during travel and improving cooperation during physical examination. Twenty clinically healthy cats with a history of fractious behavior or signs of stress during veterinary examination were included. Cats were randomly assigned to receive 100-mg gabapentin (13-29.4 mg/kg PO) or placebo prior to a veterinary visit; the opposite treatment was given prior to a second visit one week later. The assigned capsule was orally administered by owners 90 minutes prior to placing the cat in a carrier and transporting it to the veterinary clinic.

Owner-assessed cat stress scores during transportation and veterinary examination, as well as veterinarian-assessed cooperation (compliance) scores, were significantly lower in cats that received gabapentin as compared with cats that received placebo. Owner-perceived peak effect of gabapentin occured approximately 2 to 3 hours postadministration. Adverse effects occurred in 6 cats and included vomiting (n = 2), hypersalivation (n = 1), muscle fasciculation (n = 2), and anisocoria (n = 1). Follow-up with owners regarding their continued observations upon returning home was available for 15 cats; sedation was reported in 12 (80%) and ataxia (concurrent with sedation) in 6 (40%). All effects resolved within 8 hours of gabapentin administration.

The authors concluded that oral administration of 100-mg gabapentin to cats 90 minutes before travel led to a significant reduction in stress-related behaviors during transportation and examination and in attenuated aggression, thereby increasing cooperation during examination. The study authors further recommended that gabapentin at 20 mg/kg PO (vs 100 mg/cat) be given approximately 2 to 3 hours before transportation to the clinic for short-term anxiolysis. Owners should be warned about the potential for ataxia, and cats should be confined indoors until the effects resolve.

This study did not include additional diagnostics to assess each cat’s health (eg, urinalysis, FeLV/FIV status); thus, stable systemic disease may have been missed. In mice, rats, monkeys, and humans, gabapentin is not metabolized or protein-bound and is cleared via renal excretion; thus, it is reasonable to consider a dose reduction in cats with kidney disease.6,7


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Administering gabapentin at 20 mg/kg PO approximately 2 to 3 hours before placing cats in a travel carrier may reduce stress. A dose reduction in cats with kidney disease (or possibly liver disease) should be considered until further gabapentin metabolism data in cats are available.

2

Fear Free methods and minimum, low-stress, gentle handling are recommended (see Suggested Reading).

 

3

Common side effects include ataxia, so cats should be kept indoors for at least 6 to 8 hours postadministration.

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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Osurnia CB August 2018

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Merck CB August 2018

Craniocervical Junction Abnormalities in Chihuahuas

Erin Y. Akin, DVM, DACVIM (Neurology), Bush Veterinary Neurology Service, Woodstock, Georgia

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Craniocervical Junction Abnormalities in Chihuahuas

In the Literature

Kiviranta AM, Rusbridge C, Laitinen-Vapaavuori O, et al. Syringomyelia and craniocervical junction abnormalities in Chihuahuas. J Vet Intern Med. 2017;31(6):1771-1781.


FROM THE PAGE …

Chiari-like malformation (CM) is a multifactoral craniocervical junction (CCJ) abnormality in dogs in which a portion of the cerebellum is herniated through the foramen magnum secondary to congenital hypoplasia of the supraoccipital bone. Syringomyelia (SM) is the development of fluid-filled cavities in the spinal cord parenchyma.1 These malformations have been widely reported in Cavalier King Charles spaniels, Brussels Griffons, and other small-breed dogs.2 This prospective study investigated the presence of SM and CCJ abnormalities and their associated clinical signs and neurologic deficits in 53 Chihuahuas.

The study found CM, SM, and other CCJ abnormalities to be prevalent in Chihuahuas. CM/SM-related clinical signs such as facial rubbing, spinal pain, vocalization, incoordination, weakness, and persistent scratching of the ears, shoulders, or cranial thoracic spinal area were observed in dogs with SM and other CCJ abnormalities such as atlanto-occipital overlapping. Neurologic deficits, most commonly decreased postural reactions and ataxia, were noted in >50% of study subjects. The presence of postural reaction deficits was predictive of the presence of syringomyelia grade 2.

CM was observed in all 53 Chihuahuas. The presence of SM is thought to predispose animals to neuropathic pain, as pain correlates to syrinx width on MRI3; however, the CM/SM-related clinical signs, most commonly scratching and facial rubbing, were detected in dogs with and without SM. The large number of dogs that did not have SM but did have CM/SM-related clinical signs suggestive of neuropathic pain (ie, scratching, facial rubbing) may indicate that other CCJ abnormalities play an important role in the development of neuropathic pain. Seventy percent of study dogs had presence of atlanto-occipital overlapping, but this was not associated with CM/SM-related clinical signs, presence of SM, or severity of CM. Other CCJ abnormalities included medullary kinking and dorsal spinal cord compression.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

CM and SM have been reported in many breeds, most notably Cavalier King Charles spaniels, Brussels Griffons, and Chihuahuas.

 

2

SM, CM, and other CCJ abnormalities appear to be prevalent in Chihuahuas. These conditions should be considered in Chihuahuas with scratching of the ears, shoulders, or cranial thoracic area; facial rubbing; vocalization; spinal cord pain; ataxia; and/or postural reaction deficits.

3

Advanced imaging (eg, MRI, CT) is necessary to achieve diagnosis; thus, referral may be necessary.

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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Mirataz CB August 2018

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Arthrex CB August 2018

Potential Biomarkers of Systemic Inflammatory Response

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

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Potential Biomarkers of Systemic Inflammatory Response

In the Literature

Rejec A, Butinar J, Gawor J. Evaluation of complete blood count indices (NLR, PLR, MPV/PLT, and PLCRi) in healthy dogs, dogs with periodontitis, and dogs with oropharyngeal tumors as potential biomarkers of systemic inflammatory response. J Vet Dent. 2017;34(4):231-240.


FROM THE PAGE …

Periodontal disease and oral neoplastic conditions can exhibit both local and systemic effects. A systemic inflammatory response can be elicited by dissemination of bacterial metabolic products in the case of periodontal disease or by secretion of proinflammatory and anti-inflammatory cytokines/chemokines by tumors, thus attracting leukocytes.

This retrospective study aimed to identify potential systemic inflammatory markers within the parameters of the different cell types measured on a CBC. In humans, the neutrophil:lymphocyte ratio (NLR), platelet:lymphocyte ratio (PLR), mean platelet volume:platelet ratio (MPV/PLT), and platelet large cell ratio index (PLCRi) have been identified as biomarkers of systemic inflammatory response and potentially as prognostic/diagnostic biomarkers in both inflammatory and neoplastic conditions, including those of the head and neck region.

Neutrophils are the first leukocytes to circulate in response to systemic inflammation, and lymphopenia has been accepted as a negative prognostic indicator in humans with some types of cancer. A high NLR, another negative biomarker in human cancer patients, demonstrates an enhanced neutrophil response and relative lymphopenia. Platelets play a role in biologic progression and metastatic spread of tumors; PLR, MPV/PLT, and PLCRi are all biomarkers of platelet activation. The potential value of these indices in companion animals has yet to be determined.

Three populations of dogs were evaluated in this study: healthy dogs, dogs with periodontal disease, and dogs with oral tumors. The results ultimately were not supportive of systemic inflammatory response assessment by CBC indices in dogs with periodontal disease. However, 2 indices (ie, NLR and PLCRi) were associated with oral neoplastic conditions and could potentially be used as biomarkers of systemic inflammatory response if given further investigation.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Periodontal disease and oral tumors can elicit both local and systemic inflammatory responses.

 

2

Understanding how CBC parameters in conjunction with other diagnostics may indicate systemic inflammation can be useful in developing a list of differential diagnoses.

 

3

The conclusions of this study are limited by the retrospective design. Prospective studies are needed before these results can be clinically applied. Further studies could support the use of CBC evaluation as a cost-effective tool for therapeutic decision-making and identification of prognostic biomarkers.

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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Mission Rabies CB August 2018

Feline External Fixators

Jonathan Miller, DVM, MS, DACVS (Small Animal), Oradell Animal Hospital, Paramus, New Jersey

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Feline External Fixators

In the Literature

Beever L, Giles K, Meeson R. Postoperative complications associated with external skeletal fixators in cats. J Feline Med Surg. 2017;19(7):727-736.


FROM THE PAGE …

External skeletal fixators (ESFs) are commonly used by surgeons to correct bone fractures in cats. Common complications of ESFs include infection, pin loosening, and pin breakage. The incidence of complications in dogs is relatively high, but few studies have examined this in cats.

This retrospective study of 140 cats treated with ESF had an overall complication rate of 19% at a median time to diagnosis of 43 days postoperation. All fixators had a mean of 6 pins placed to secure the bone. Superficial pin tract infections (n = 13) were most often observed in humeral and femoral fractures; implant failure (n = 12) occurred more often in tibial and tarsal fractures. Together, these complications accounted for 86% of all reported problems. Serious complications of bone fracture (n = 2) or osteomyelitis/bone sequestrum (n = 2) were uncommon, accounting for 14.8% of all reported complications. The only significant association between complications and ESF frame feature was the use of intramedullary pins.

Higher rates of infection in the femur and humerus were suspected to occur due to discomfort, joint stiffness, and decreased use of the limb caused by interference of regional tendons and musculature. Pin failures in the tarsus were attributed to the ESF crossing a joint and use of smaller pins for these smaller distal bones.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

ESF appears to be a safe method for correcting feline fractures, as 81% percent of fractures corrected via ESF in this study healed without complication.

 

2

Superficial infections and pin loosening or breakage may occur with ESF.

 

3

Infection may occur more commonly with fractures of the femur and humerus, whereas pin failure may occur more often with fractures of the tarsus and femur.

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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Claro CB August 2018

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Jorvet half CB August 2018

Topical Antimicrobial Therapy with Fusidic Acid

Alison Diesel, DVM, DACVD, Texas A&M University

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Topical Antimicrobial Therapy with Fusidic Acid

In the Literature

Frosini SM, Bond R, Loeffler A, Larner J. Opportunities for topical antimicrobial therapy: permeation of canine skin by fusidic acid. BMC Vet Res. 2017;13(1):345.


FROM THE PAGE …

Increased isolation of resistant organisms from skin infections—particularly methicillin-resistant Staphylococcus pseudintermedius and other staphylococci—in veterinary patients is resulting in intensified concern due to the potential impact of these organisms in both veterinary and human medicine.1 This concern has led to several studies evaluating topical therapeutic options for superficial infections in companion animals with the goal of decreasing the chance for development of resistance.

This in vitro study aimed to determine the depth of penetration of fusidic acid (FA) in canine skin. FA is a lipophilic antibiotic with activity against coagulase-positive staphylococci, including methicillin-resistant S pseudintermedius. Skin biopsy samples were obtained from the dorsum and groin of canine cadavers to evaluate body regions with different hair follicle density. The samples were either left untreated or repeatedly tape-stripped to mimic skin damage often seen with inflammatory skin disease. Skin samples were assembled into Franz diffusion cells, and a 10-mg/g FA suspension was applied to the surface. After 24 hours, receptor fluid and cryosectioned skin samples from various depths were evaluated for FA concentration. FA was detected only in samples in which the follicular infundibulum and more superficial structures (eg, surface epidermis, hairs) were present. The antibiotic did not penetrate past the isthmus of the hair follicle, thus supporting the potential use of FA for the treatment of both surface and superficial bacterial infections in dogs.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Although FA appears to be a viable treatment option for surface and superficial bacterial skin infections in dogs, this antibiotic is not currently available in any formulations in the United States for either human or veterinary use.

2

Due to the concern about increased isolation of resistant organisms from bacterial skin infections in veterinary patients, clinicians are encouraged to employ appropriate antimicrobial stewardship when recommending specific therapy.2

3

Increased use of topical antimicrobial therapy in veterinary patients may help decrease the chance for development of resistance. Bacteria are less likely to develop resistance to an antiseptic (eg, chlorhexidine, sodium hypochlorite) than to an antibiotic. Continued evaluation of novel antimicrobial agents will likely remain a focus in veterinary dermatology in the coming years.

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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Norbrook CB August 2018

Xylazine & Induction of Emesis in Cats

Edward Cooper, VMD, MS, DACVECC, The Ohio State University

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Xylazine & Induction of Emesis in Cats

In the Literature

Thies M, Bracker K, Sinnott V. Retrospective evaluation of the effectiveness of xylazine for inducing emesis in cats: 48 cats (2011-2015). J Vet Emerg Crit Care. 2017;27(6):658-661.


FROM THE PAGE …

There are important differences between dogs and cats with regard to inducing emesis for suspected toxin or foreign body ingestion. Although apomorphine or hydrogen peroxide are often used in dogs, these are generally ineffective in cats and may be harmful. Based on relative receptor density in the chemoreceptor trigger zone, α2-adrenergic agonists (eg, xylazine, dexmedetomidine) have been recommended instead, although there is relatively little clinical evidence supporting their use. This retrospective study sought to assess the efficacy of xylazine for inducing emesis in cats and determine the rate of complications associated with administration.

Medical records from a referral center from 2006 to 2015 reviewed clinical characteristics of cats receiving xylazine for emesis induction after known or suspected toxin or foreign body ingestion. Forty-eight cats were included in the study, with an even split between known/suspected toxin exposure (n = 24) versus foreign body ingestion (n = 24). Xylazine was administered at a median dose of 0.49 mg/kg IM. Emesis was achieved in 60% (29/48) of patients; the aim of emesis (ie, recovery of foreign body or decontamination) was successful in 72% of these patients. Adverse effects were noted in 33% (16/48) of cats, with sedation being the most common (15/16); one of these cats also experienced pytalism. Another cat experienced bradycardia alone. Almost all (46/48) of the cats received a reversal agent; most (37/46) received yohimbine, whereas the remainder (9/46) received atipamezole. No differences were found with regard to age, sex, breed, reason for induction of emesis, or the occurrence of adverse effects between those that successfully vomited and those that did not.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Xylazine at 0.5 mg/kg may be effective in inducing emesis in approximately 50% of feline foreign body or intoxication cases, with approximately three-fourths of those patients successfully expelling the ingested toxin or foreign body. Dexmedetomidine has also been shown to be effective in this regard and, in one study, was found to be superior to xylazine.1

2

The most common adverse effect to be expected is sedation, which can be reversed using an α2-adrenergic antagonist (eg, yohimbine, atipamezole).

 

3

Age, breed, sex, or reason for emesis induction did not appear to impact whether xylazine is effective in inducing vomiting in cats.

Reference

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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PVD CB August 2018

Surveillance of Surgical Site Infections

Kristyn D. Broaddus, DVM, MS, DACVS, Veterinary Services of Hanover, Mechanicsville, Virginia

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Surveillance of Surgical Site Infections

In the Literature

Garcia Stickney DN, Thieman Mankin KM. The impact of post-discharge surveillance on surgical site infection diagnosis. Vet Surg. 2018;47(1):66-73.


FROM THE PAGE …

Surgical site infections (SSIs) are infections present at a surgical site within 30 days of surgery or within a year of surgery if the patient has implants. SSIs can result in increased owner costs and patient morbidity and, although rare, may even result in patient death. The incidence of SSIs may be underestimated by surgeons due to lack of appropriate surveillance and documentation. In human medicine, active surveillance occurs routinely, improving patient outcomes.

This study sought to document the incidence of SSIs that occurred postoperatively at a veterinary teaching hospital via prospective and retrospective means. SSIs from soft tissue, orthopedic, and neurologic surgeries were documented through repeat presentation to the surgeon, pet owner questionnaires, review of medical records, and/or communication with primary veterinarians. The study found that, if the medical record had been the sole source of surveillance, 27.8% (10/36) of infections would have gone unidentified. Active postdischarge surveillance increased known incidence of infection that would have otherwise been missed. Culture testing was not performed in approximately two-thirds of suspected SSIs to confirm infection versus inflammation.

The most effective means of surgical follow-up is direct observation through recheck examination, including culture and susceptibility testing if SSI is suspected. This direct observation occurs frequently with the patient’s primary veterinarian. If an infection is noted by the primary veterinarian, this information should be reported to the surgeon to improve awareness of SSI incidence. With this proactive team approach, infections may be minimized and patient health improved.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Communication between primary veterinarians and referral centers is critical for optimal patient care.

 

2

Culture and susceptibility testing of surgical sites suggestive of infection before administration of antibiotics is warranted to document and treat SSIs. If cost is a limiting factor, compromised patients and patients with implants must be prioritized.

3

Culture testing allows for identification of the offending bacteria and helps define its prevalence. Through identification of the offending bacteria, SSIs can be accurately classified and managed as nosocomial infections versus infections caused by incisional disruption from patients or lack of owner compliance.

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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Nestle CB August 2018

Differential Diagnosis: Epistaxis

Shanna Hillsman, LVMT, University of Tennessee

M. Katherine Tolbert, DVM, PhD, DACVIM (SAIM), Texas A&M University

Internal Medicine

|Peer Reviewed

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Differential Diagnosis: Epistaxis

Following are differential diagnoses, listed in order of likeliness, for patients presented with epistaxis.

Localized

  • Nasal tumor
  • Trauma
  • Idiopathic rhinitis
  • Periapical abscess
  • Fungal rhinitis
  • Nasal foreign body
  • Oronasal fistula
  • Leishmaniasis 

Systemic

  • Thrombocytopenia
  • Thrombocytopathia
  • Coagulopathy
  • Vasculitis
  • Hypertension
  • Less commonly:
    • Leishmaniasis
    • Angiostrongylus vasorum
    • Scott syndrome

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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Aratana CB August 2018

Pregnancy in Dogs

Bruce W. Christensen, DVM, MS, DACT, Kokopelli Assisted Reproductive Services, Woodland, California

Reproduction

|Peer Reviewed

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Pregnancy in Dogs
Clinician's Brief
Clinician's Brief

PURPOSEFUL BREEDING OPTIONS

Breeding should be timed and managed using vaginal cytology, vaginoscopy, and progesterone to determine luteinizing hormone surge, ovulation date, fertile period, and estimated whelping date. Insemination options include:

  • Fresh semen (natural mating, vaginal AI, TCI)
  • Chilled/shipped semen (vaginal AI, TCI)
  • Frozen semen (TCI, surgical AI)
*Although negative predictive value of vaginal cytology within the first 24 hours of mating has been reported to be as great as the positive predictive value,1 the possibility of a false negative still warrants confirming pregnancy later. Therefore, the value of performing vaginal cytology is questionable. **Must administer within 1 to 2 days of mating. Use caution with timing and dose. Adverse effects include aplastic anemia and pyometra.

AI = artificial insemination, TCI = transcervical insemination

Reference

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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WMPB CB August 2018

Cheyletiellosis

Darren Berger, DVM, DACVD, Iowa State University

Dermatology

|Peer Reviewed

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Cheyletiellosis

Figure 1 A 10-year-old spayed Scottish terrier with cheyletiellosis demonstrating excessive, large scale formation. Photo courtesy of J.O. Noxon, DVM, DACVIM, Iowa State University

Cheyletiellosis, also known as walking dandruff, is an uncommon, contagious dermatosis caused by an infestation of the surface-dwelling Cheyletiella spp mite.

Cheyletiellosis may occur in dogs (caused by C yasguri), cats (caused by C blakei), or rabbits (caused by C parasitivorax) and can also cause a transient infestation in humans that come in contact with pets carrying the mites. An increased incidence of mites may be observed in immunocompromised patients, in geographic regions where routine flea prevention is not practiced, or following exposure to high-volume housing situations (eg, catteries, breeding facilities).

Cheyletiella spp mites have a standard life cycle of egg, larva, nymph, and adult that can be completed in roughly 21 days. Mite life stages can be identified via direct examination of collected debris using a powerful magnifying lens or via microscopic examination of superficial skin scrapings, acetate tape impressions, and fecal flotation specimens. Cheyletiella spp mites are obligate parasites, as larvae, nymph, and adult male mites die soon after leaving the host; however, adult female mites are more robust and may survive up to 10 days off the host.1

Clinical Signs

Clinical signs are highly variable, and subclinical carriers may be encountered. The most common clinical findings include mild-to-intense pruritus, excessive scaling (particularly over the dorsum), and erythema (Figures 1 and 2). In addition, cats may be presented with barbering alopecia or miliary dermatitis.1

Diagnosis

Diagnosis is confirmed via visualization of the mite or ova, which may be difficult to recover from some patients with low-grade infestations. Adult mites can be easily identified by the presence of prominent hooks on their accessory mouthparts (Figures 3 and 4). Cheyletiella spp ova appear similar to louse eggs but are nonoperculated, smaller, and loosely attached to hairs (Figures 5 and 6).

Cheyletiellosis should be considered a differential diagnosis in patients with pruritus and excessive scaling; other ectoparasites, poor nutrition, intestinal parasitism, and primary seborrhea would also be considered differential diagnoses. In addition, Cheyletiella spp infestation should be eliminated as a potential cause in any patient presented for evaluation of a suspected allergic hypersensitivity (eg, atopy, food allergy).

Treatment

No licensed products are indicated specifically for the treatment of cheyletiellosis. Therapeutic protocol and medication selection primarily depend on the species of the animal affected and clinician preference. Most acaricidal flea preventive products and lime sulfur are effective, provided all in-contact animals are treated, the patient is treated for 6 weeks to disrupt the parasite’s life cycle, and conventional environmental treatment—similar to what is recommended for flea infestation—is performed to prevent reinfestation.

Reference

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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Aesculight CB August 2018

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Tonopen CB August 2018

Thoracic Limb Lameness in a Dog

Nicole S. Amato, DVM, DACVS (Small Animal), Massachusetts Veterinary Referral Hospital, Woburn, Massachusetts

Orthopedics

|Peer Reviewed

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Thoracic Limb Lameness in a Dog

Maggie, a 5-year-old, 79.4-lb (36-kg), spayed golden retriever crossbreed, was presented to a specialty practice with chronic right-sided thoracic limb lameness of one month’s duration that began acutely soon after a rigorous hike in the mountains. She had no prior medical history and had not limped on the limb previously. She was active and athletic and exercised with her owner on a regular basis. The limping was initially subtle and intermittent but progressed to an obvious and persistent lameness that worsened with activity.

Maggie was initially examined by her primary veterinarian, who localized discomfort to her elbow, recommended 4 weeks of exercise restriction, and initiated subcutaneous polysulfated glycosaminoglycan injections and carprofen for pain. Despite these efforts, the limping continued for 3 weeks and worsened. Maggie was then referred to the specialty practice for further evaluation and a diagnostic investigation.

Physical Examination Findings

On presentation, Maggie was bright and alert. Subjective gait evaluation revealed moderate right-sided thoracic limb lameness. Objective gait analysis was not performed due to the obvious lameness observed on initial presentation. Maggie was observed circumducting her right thoracic limb and abducting her elbow during the swing phase of her stride. Orthopedic examination revealed palpable elbow effusion, pain on direct palpation of the medial compartment of the right elbow, and significant discomfort when this elbow was hyperflexed, extended, and supinated. There was no evidence of chronic thickening or reduced range of motion affecting either elbow joint. Goniometry of both elbows revealed flexion and extension angles of 37° and 167°, respectively. Although differences in range-of-motion values likely exist between breeds, Maggie’s range of motion was consistent with that found in a study of healthy Labrador retrievers.1 The remainder of the orthopedic examination, including that of the left thoracic limb, was unremarkable.

Diagnosis

Following examination, Maggie was sedated with dexmedetomidine (3 μg/kg IM) and butorphanol (0.1 mg/kg IM), and orthogonal radiographs of both elbows were obtained. The left elbow appeared radiographically normal on the lateral view, whereas the right elbow had mild subtrochlear sclerosis subjacent to the trochlear notch and apparent loss of detail of the coronoid process (Figure 1). No abnormalities were detected on the craniocaudal view (Figure 2).

Because Maggie’s injury was acute and she had no historic, radiographic, or physical signs of chronicity, a traumatic fragmented medial coronoid process (TFMCP) was suspected as the cause of elbow effusion and pain. Because CT imaging provides excellent visualization of medial coronoid pathology and correlates well with arthroscopic findings,2 a CT scan of both elbows was offered before surgery for further diagnostic evaluation but was declined by the owner due to financial constraints. Thus, arthroscopy was elected as a single diagnostic and potentially therapeutic approach to reduce the overall cost of the treatment plan.

DIAGNOSIS:

TRAUMATIC FRAGMENTED MEDIAL CORONOID PROCESS

Discussion

TFMCP, also referred to as jump down syndrome, is a condition in the elbow joint of dogs that has only recently been described, with limited literature available on the topic.3-7 Whereas the classic condition of fragmented medial coronoid process (FMCP) is thought to be a component of developmental elbow dysplasia, TFMCP appears to be potentially traumatic in nature and is not thought to be caused by developmental or genetic abnormalities.3-7 The true etiology of TFMCP is unknown, and it is unclear if it is related to elbow dysplasia or a separate entity.

Although unproven, it has been suggested that medial coronoid disease or fragmentation, whether traumatic in nature or not, may occur as the result of repetitive or acute loading of the joint during activity, causing microfractures or microcracks in the subchondral bone that result in eventual fatigue fracture and fragmentation.8 TFMCP is different from FMCP due to elbow dysplasia in that TFMCP is thought to occur in dogs with previously normal elbows; however, it has been proposed that dogs with elbow dysplasia may also be prone to TFMCP due to elbow incongruity.7

Treatment at A Glance

  • Arthroscopy with fragment removal is considered the gold standard treatment for surgical management of TFMCP and FMCP.3-7,10,11
  • Adjunctive pain management with oral analgesics (eg, NSAIDs, gabapentin, amantadine) can be beneficial to the patient postoperatively.
  • Rehabilitation therapy to promote and maintain elbow range of motion and limb strength and function may optimize outcome in all patients with conditions localized to the medial compartment of the elbow caused by TFMCP or elbow dysplasia.7,11 
  • If evidence of osteoarthritis is observed on arthroscopy, long-term management with joint injections (eg, hyaluronic acid, cortisone), platelet-rich plasma or stem cell injections, chondroprotective agents, and long-term NSAIDs may be beneficial.7,11

Treatment

Short-term management of TFMCP typically involves arthroscopy to remove the abnormal bone fragment, followed by pain medication, joint supplements, and physical rehabilitation during postoperative recovery (see Treatment at a Glance).3-7,9

Both elbows were prepared for surgery. Maggie was premedicated with hydromorphone (0.1 mg/kg IM) and dexmedetomidine (3 μg/kg IM), and anesthesia was induced with propofol (4 mg/kg IV) and ketamine (1 mg/kg IV). A traditional brachial plexus block was performed on both thoracic limbs using a nerve locator and 0.5% bupivacaine (2 mg/kg). Bilateral elbow arthroscopy was performed to remove the suspected TFMCP in the right elbow and examine the left elbow for subclinical disease. The right elbow was found to have minimal signs of osteoarthritis. Fibrillation, which is characterized by splitting of the superficial layers of cartilage (modified Outerbridge system, grade 2), was the only observed cartilage abnormality and was localized to the region of the medial coronoid process. A large osteochondral fragment arising from the medial coronoid process was identified in the right elbow and removed (Figure 3), and an abrasion arthroplasty of underlying subchondral bone was performed using a mechanical shaver. Elbow incongruity was not appreciated on full arthroscopic examination. The left elbow appeared arthroscopically normal, with no cartilage abnormalities or signs of osteoarthritis. No additional abnormalities were observed.

Arthroscopic image of the right elbow. A large osteochondral fragment is arising from the medial coronoid process (arrow), and cartilage fibrillation is present.
Arthroscopic image of the right elbow. A large osteochondral fragment is arising from the medial coronoid process (arrow), and cartilage fibrillation is present.

Figure 3 Arthroscopic image of the right elbow. A large osteochondral fragment is arising from the medial coronoid process (arrow), and cartilage fibrillation is present.

Figure 3 Arthroscopic image of the right elbow. A large osteochondral fragment is arising from the medial coronoid process (arrow), and cartilage fibrillation is present.

Maggie was discharged the following day with instructions for strict rest for 8 weeks, which included no running, jumping, playing, or leash walks longer than 5 to 10 minutes, to allow her joint surface to heal. She was prescribed gabapentin (5 mg/kg PO q8h) and carprofen (2.2 mg/kg PO q12h) for 2 weeks to control discomfort. It was recommended that Maggie also receive an oral chondroprotective supplement and continue the weekly polysulfated glycosaminoglycan injections for 4 weeks postsurgery. Rehabilitation therapy was instituted several days postoperatively and involved cryotherapy, manual therapies (eg, soft tissue massage, mobilization exercises, passive range-of-motion exercises, stretching), laser treatments, and strength-building exercises.

Take-Home Messages

  • TFMCP should be suspected in adult (ie, older than 2 years) dogs with acute unilateral elbow pain if no signs of chronicity of the condition are present (ie, joint thickening, reduced range of motion, evidence of osteoarthritis on imaging).3-7
  • Elbow dysplasia should be suspected as the inciting cause of FMCP if the patient is younger than 2 years, has a history of chronic lameness affecting the leg, has evidence of significant developmental abnormalities (eg, elbow incongruity, humeral osteochondritis dissecans, ununited anconeal process), or has evidence of chronicity on physical examination or imaging of the joint.7,8,11
  • Radiographs of dogs with acute-stage TFMCP are often unremarkable, making a thorough physical examination and advanced imaging via CT scan or arthroscopy vital to proper diagnosis.3-7,9 
  • Prognosis is thought to be good to excellent if the injury is noted early before the onset of osteoarthrosis.3-7

Prognosis & Outcome

Maggie was evaluated at the end of the 8-week rehabilitation period. Lameness had completely resolved. No effusion was appreciated, and she did not appear painful. The owner was instructed to slowly return her to normal activity over an additional 6 weeks and reported that Maggie was able to return back to athletic activities after 4 months. She did not require any long-term treatment. 

Although limited reports are available, the prognosis for dogs with TFMCP treated prior to the development of osteoarthritis appears to be good to excellent.3-7 However, further research is needed to further clarify the causes, treatment strategies, and prognosis for dogs with TFMCP.

FMCP = fragmented medial coronoid process, TFMCP = traumatic fragmented medial coronoid process

References

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