September 2020   |   Volume 18   |   Issue 9
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Anesthetic Management Differences in Dogs & Cats

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Top 5 Anesthetic Management Differences Between Dogs & Cats

Hyperglycemia: A Complete Guide for Dogs & Cats

Hypoglycemia

Separation Anxiety in a Dog with Fear-Based Behavior

Chronic & Persistent Coughing in a Dog

Differential Diagnosis: Lymphocytosis

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Top 5 Anesthetic Management Differences Between Dogs & Cats

Khursheed Mama, DVM, DACVAA, Colorado State University

Anesthesiology & Pain Management

|Peer Reviewed

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Top 5 Anesthetic Management Differences Between Dogs & Cats

When planning for and managing anesthesia in cats and dogs, there are differences beyond size that should be considered.

Following are 5 of the most common key differences in anesthetic management for cats and dogs according to the author.

1

Restraint & Instrumentation

Minimal restraint is frequently most effective in achieving efficiency, which is key when working with cats. Previsit oral medications (eg, gabapentin and trazodone) given at home have been shown to minimize anxiety and stress and increase compliance.1-3 Alfaxalone and dexmedetomidine can also help alleviate agitation; these drugs are typically administered IM after the overall health of the cat has been evaluated.

Because of the small size of cats, IV catheterization can be more challenging in cats than in dogs. Although the cephalic vein can be catheterized in both cats and dogs, the medial saphenous vein is more commonly catheterized in cats, and the lateral saphenous vein is more commonly catheterized in dogs. Intubation can also be more challenging in cats because of the size and reactivity of the upper airway. If care is not used, a greater incidence of tracheal tears following intubation is possible4,5; however, use of topical lidocaine on the arytenoids and an appropriate tube without a stiff stylet can greatly minimize these problems. Diligent cuff inflation and disconnection of the tube from the breathing circuit are also important when turning the patient.

Postanesthesia, cortical blindness also has been reported in cats (but not in dogs) and associated with the influence of spring-loaded mouth gags on maxillary artery blood flow6,7; therefore, it is important that use of these devices be minimized or avoided when anesthetizing cats for bronchoscopy, endoscopy, or dentistry.

2

Anesthetic Equipment

A nonrebreathing circuit (eg, Bain) is commonly used to anesthetize cats weighing <11 lb (5 kg). These circuits must be appropriately assembled and used in order to minimize complications, including excessive pressure in the system. A nonrebreathing system also requires higher flow rates on a per-kilogram basis to minimize rebreathing of carbon dioxide, which can dry the respiratory tract and increase patient cooling. Although not routinely used during anesthetic management, there are tools that can help alleviate these concerns by heating and humidifying the breathing system. Pediatric circle systems can be used in cats, but inspiratory and expiratory valves and carbon dioxide absorbent increases the work required for breathing in spontaneously ventilating animals, possibly resulting in fatigue and hypoventilation.

Similar considerations relative to breathing circuits exist for small dogs. Larger dogs can typically be maintained on circle breathing systems with appropriately sized hoses and rebreathing bags.

3

Medications & Patient Response

Cats differ in their requirements for and responses to numerous medications commonly used in the perianesthetic period. Acepromazine is considered an effective tranquilizer in dogs, particularly when used in combination with other drugs, but equivalent acepromazine-associated tranquilization in cats may not result, despite signs suggesting efficacy (eg, a raised third eyelid). Conversely, dexmedetomidine provides good sedation in both dogs and cats. The anesthetic induction dose needed to facilitate intubation is lower following dexmedetomidine premedication than with acepromazine.8

Opioids are reported to cause a higher degree of signs of euphoria or dysphoria in cats than in dogs, especially with IV administration.9 The analgesic- and inhalant-sparing effects in cats also differ from those in dogs, and a ceiling effect (ie, increased dose does not result in additional clinical benefits) may occur at a lower dose.10 Unlike in dogs, large or repeated doses of opioids may result in hyperthermia in cats.11 The cause of hyperthermia is unknown. Elevations in body temperature are not typically reported in dogs, even when panting is observed following administration. Opioid-associated sedation may contribute to lack of hyperthermia in dogs.

Lidocaine given IV with a bolus or constant-rate infusion has been increasingly used in dogs for its anesthesia-sparing effects and possible analgesic benefits. However, IV lidocaine is not routinely recommended in cats because the associated cardiovascular depression is worse than an equivalent dose of inhalant, and drug-related toxicity is possible.12 When comparing isoflurane requirements, the minimum alveolar concentration is higher in cats than in dogs.13

4

Monitoring

Cardiovascular and respiratory monitoring can be challenging in cats because of their size and limitations with monitoring equipment not specifically developed for use in cats. For example, many oscillometric noninvasive blood pressure monitors provide only intermittent readings in cats, and obtaining a reliable signal from a Doppler crystal can be difficult. These obstacles can be further complicated by the use of certain drugs (eg, dexmedetomidine) that cause vasoconstriction, bradycardia, and decreased cardiac output. Similar challenges can occur with the use of a pulse oximeter to monitor oxygen saturation. Amplitude of the electrocardiogram may also hinder accurate heart rate measurement and assessment of rhythm changes in cats as compared with dogs. Typically, cats have higher heart rates than dogs, but their blood pressure during anesthesia tends to be more labile or stimulus-responsive. It is therefore important to evaluate physiologic monitors to be used during anesthesia in the clinic to ensure functionality. In addition, using an appropriately sized Doppler crystal or an alternate site (eg, tail vs distal limb) may help improve performance. Similarly, for pulse oximeter probes, placement of a moist gauze sponge over the tongue prior to probe placement can be beneficial.

When a nonrebreathing system is used, side-stream capnography can result in significant underestimation of the end-tidal carbon dioxide tension because of the constant flow of oxygen diluting exhaled gas at the sampling site. A mainstream capnometer can alleviate this issue, but weight on the endotracheal tube can cause kinking or dislodging.

Pain assessment in cats is also more difficult and requires close observation of specific behaviors and interaction with the patient as needed.14 There are an increasing number of pain scales and assessment tools available.

5

Support

Fluid therapy during anesthesia is critical for maintaining blood pressure and vital organ perfusion during anesthesia in cats and dogs. Because older cats are frequently diagnosed with varying stages of renal disease, fluid support is essential in the perianesthetic period.15 To account for blood volume differences (ie, ≈60-70 mL/kg in cats vs ≈80-90 mL/kg in dogs), the volume of both fluids and blood products should be lowered for cats, especially when administered via bolus. Because universal feline donors do not exist, all cats, including naive cats, should be typed and cross-matched to donors in cases in which use of blood products is anticipated.

Conclusion

Although anesthesia in cats is often thought to be more challenging than in dogs, knowledge of species-specific requirements and responses can help improve patient management during the perianesthetic period.

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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Hyperglycemia: A Complete Guide for Dogs & Cats

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

Internal Medicine

|Peer Reviewed

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Hyperglycemia: A Complete Guide for Dogs & Cats

Hyperglycemia is defined as an increase in blood glucose levels above the physiologic range for a given species. Hyperglycemia may be physiologic or pathologic and is always secondary to a disorder that disrupts one or more of the homeostatic mechanisms that maintain euglycemia.

Background & Pathophysiology

Glucose is a principal fuel metabolized to produce adenosine triphosphate for use in cellular-energy–requiring processes and is vital for normal cell function. Homeostatic mechanisms maintain blood glucose levels within narrow physiologic limits (ie, euglycemia).1 Glucose ranges in dogs and cats vary slightly but generally measure ≈90 mg/dL.2

Glucose homeostasis is a balance between glucose appearing in and disappearing from the blood (Figure). Normoglycemia is maintained by the complex interactions of a group of hormones that exert hyperglycemic or hypoglycemic actions by altering the metabolic pathways that produce or consume glucose.3 Insulin, produced by β cells in the pancreatic islets, is the most important hormone for maintaining glucose homeostasis. Insulin secretion is precisely regulated by glucose. In circulation, it exerts potent hypoglycemic actions by promoting cellular uptake of glucose, stimulating hepatic glycogenesis, and suppressing hepatic gluconeogenesis.4 Several hormones that promote hyperglycemia oppose insulin’s hypoglycemic actions. Glucagon, also of pancreatic islet origin, activates hepatic glycogenolysis and gluconeogenesis pathways that increase net glucose production by the liver.3 Thyroid hormones exert a hyperglycemic action, especially when secreted in excess, as in hyperthyroidism.3 Adrenal catecholamines (eg, epinephrine, norepinephrine),5 cortisol,6 and growth hormone7 also antagonize insulin action. Glucagon, growth hormone, catecholamines, and cortisol are collectively called “counterregulatory hormones” to reflect their functions as insulin antagonists. These hormones are the physiologic foundation of hyperglycemia that develops as part of the “fight-or-flight” response, but individual hormones play roles in various disorders that have insulin resistance as a common pathology.8

The relative rates of glucose appearance into and disappearance from the blood affects glycemic status. Normoglycemia (solid line) is maintained when the rates of appearance and disappearance are balanced. Hyperglycemia (dotted line) results when the rate of appearance exceeds the rate of disappearance, and hypoglycemia (dashed line) occurs when disappearance exceeds appearance.
The relative rates of glucose appearance into and disappearance from the blood affects glycemic status. Normoglycemia (solid line) is maintained when the rates of appearance and disappearance are balanced. Hyperglycemia (dotted line) results when the rate of appearance exceeds the rate of disappearance, and hypoglycemia (dashed line) occurs when disappearance exceeds appearance.

FIGURE The relative rates of glucose appearance into and disappearance from the blood affects glycemic status. Normoglycemia (solid line) is maintained when the rates of appearance and disappearance are balanced. Hyperglycemia (dotted line) results when the rate of appearance exceeds the rate of disappearance, and hypoglycemia (dashed line) occurs when disappearance exceeds appearance.

FIGURE The relative rates of glucose appearance into and disappearance from the blood affects glycemic status. Normoglycemia (solid line) is maintained when the rates of appearance and disappearance are balanced. Hyperglycemia (dotted line) results when the rate of appearance exceeds the rate of disappearance, and hypoglycemia (dashed line) occurs when disappearance exceeds appearance.

Mechanisms of Action

Homeostatic mechanisms responsible for normoglycemia maintenance are robust and persistent. Hyperglycemia does not occur when physiologic pathways are intact; instead, it appears when glucose enters the blood faster than it can be removed (Figure). Pathologic hyperglycemia develops when physiologic mechanisms that suppress glucose are lacking (as in hypoinsulinemic states) or attenuated (as in insulin-resistant states).9 Once hyperglycemia is established, chronic elevation of blood glucose levels exacerbates the existing defects in pathways for β-cell secretion and insulin action in target tissue, a phenomenon termed glucose toxicity.

Hypoinsulinemia

Hypoinsulinemia is an absolute or a relative decrease in blood insulin levels. Absolute hypoinsulinemia is caused by β cell loss, whereas relative hypoinsulinemia occurs when insulin is unable to mount an appropriate response to increased blood glucose levels. Hypoinsulinemia is a hallmark of advanced diabetes mellitus in dogs and cats, regardless of the underlying pathology.10

Insulin Resistance

Insulin resistance is a metabolic state in which target tissues resist the hypoglycemic actions of insulin (ie, decreased insulin sensitivity). Insulin resistance interferes with insulin-mediated cell signaling and reduces glucose uptake in peripheral tissues, especially skeletal muscles and adipose tissue.4 With reduced insulin effects at the cellular level, the pancreas must produce more insulin. This insulin resistance results in hyperinsulinemia, an early feature of hyperglycemia (ie, hyperinsulinemic hyperglycemia). However, patients that are chronically insulin-resistant may develop β-cell failure and hypoinsulinemia (ie, hypoinsulinemic hyperglycemia).4

Hyperglycemia produces pathology by inducing hyperosmolality (which underlies the commonly observed clinical signs) and producing advanced glycation end products (AGEs), a process that is associated with end-organ damage in vascular and neuronal cells.11

 

Pathology

Glucose is a serum osmole but contributes little (3-5 mOsm/L) to the total serum osmolality in normoglycemic dogs and cats.12,13 The osmolar contribution of glucose parallels the magnitude of hyperglycemia and can be substantial in cases of severe hyperglycemia (eg, >50 mOsm/L when glucose exceeds 1000 mg/dL).12 Complications of hyperosmolality observed with severe hyperglycemia include vomiting, neurologic impairment, seizures, and coma.13 The onset of hyperosmolality initially triggers corrective physiologic responses, including thirst and reduced renal excretion of free water.14 Chronic hyperosmolality induces additional adaptations, including expanded blood volume and altered water metabolism.

Hyperglycemia also permanently alters cellular and serum proteins through a nonenzymatic glycation reaction that produces a series of AGEs.11 Some glycated proteins (eg, hemoglobin A1c and fructosamine) serve as clinical biomarkers that reflect average blood glucose levels over time.15 Other AGE proteins interact with specialized receptors of AGEs that are expressed by vascular and neuronal tissues, a reaction that is implicated in long-term diabetes complications, such as microangiopathy and neuropathy.11

Common Conditions Associated with Hyperglycemia

Numerous causes of hyperglycemia have been identified in dogs and cats (see Causes of Hyperglycemia). Several frequently encountered endocrine causes illustrate how pathologic disorders disrupt normal homeostatic mechanisms to cause this disorder.

Causes of Hyperglycemia2

Common Causes2*

  • Physiologic (ie, stress hyperglycemia) hyperglycemia (cats, dogs)
  • Diabetes mellitus (cats, dogs)
  • Hyperadrenocorticism (dogs)
  • Acromegaly (cats)
  • Acute pancreatitis (cats, dogs)
  • Drug- and toxin-induced hyperglycemia (cats, dogs)
    • Glucocorticoids
    • Progestogens
    • α2-receptor agonists
    • β blockers
    • Glucose-containing crystalloid fluid
    • Parenteral feeding solution
    • Ethylene glycol ingestion

Uncommon & Miscellaneous Causes

  • Postprandial hyperglycemia
  • Pancreatic neoplasia
  • Diestrus (dogs)
  • Critical illness or sepsis
  • Pheochromocytoma
  • Hyperthyroidism (cats)
  • Head injury/trauma
*Although these etiologies are diverse, common mechanisms underlie the development of hyperglycemia. Hyperglycemia in these conditions is caused by either a pathophysiologic disturbance in the ability to produce/secrete normal amounts of insulin or, more commonly, induction of insulin resistance. For some disorders (eg, pancreatitis), both mechanisms may contribute to hyperglycemia.
Diabetes Mellitus

Diabetes mellitus (DM) is the most frequently encountered and clinically significant hyperglycemic disorder in small animals. Hyperglycemia in DM arises from the combined influences of hypoinsulinemia and insulin resistance. However, the proportional contribution of each mechanism may vary, depending on underlying diabetes pathology or even the stage of disease. Hyperglycemia in humans with type 1 diabetes is caused by severe hypoinsulinemia that develops as a result of autoimmune-mediated destruction of β cells.16 Likewise, marked hypoinsulinemia is a typical finding in canine DM, which shares certain pathogenic features with human type 1 diabetes. In humans, an islet defect causes disordered glucose sensing and an abnormal insulin secretion pattern in response to a glucose challenge.16 Affected humans retain the ability to make and secrete insulin, but the quantity and timing of insulin release is insufficient to maintain euglycemia, and hyperglycemia develops.16 Islet defects are not well described in canine DM and, if present, occur early in the development of DM and are not recognized clinically. In cats with overt DM due to insulinopenia, the early role of abnormal insulin secretion (the consequence of an islet defect) is not appreciated due to profound islet loss. However, the presence of an islet defect is suggested when islet mass is adequate but there is evidence for impaired glucose tolerance. For example, an islet defect is suggested by the abnormal glycemic response to a glucose challenge in obese cats at risk for DM and the abnormal glucose tolerance documented in cats that have entered diabetic remission.17 These cats are normoglycemic and have no requirement for exogenous insulin.17 Insulin resistance is a major pathologic feature of type 2 diabetes in humans, which may contribute to islet exhaustion and, eventually, hypoinsulinemia.16 Insulin resistance is not a major feature of uncomplicated canine DM but seems to play a role in pathogenesis and progression of feline DM.18 

Catecholamine & Cortisol Excess

Conditions associated with elevated concentrations of catecholamines and/or cortisol produce hyperglycemia by inducing insulin resistance. Catecholamines contribute to the phenomenon of stress hyperglycemia, which serves a physiologic function and is frequently encountered in veterinary patients.5,19 The stress response is transient and typically results in mild to moderate hyperglycemia; severe hyperglycemia can occur but is uncommon. Excessive production and secretion of norepinephrine by neuroendocrine paraganglioma, as is seen in adrenal medullary tumors (pheochromocytoma), can produce hyperglycemia in ≈25% of affected dogs.20

Hypercortisolemia caused by canine hyperadrenocorticism can cause persistent hyperglycemia of varying severity via several mechanisms, including inhibition of insulin secretion and exacerbation of peripheral insulin resistance.21 Hyperglycemia due to insulin resistance can resolve when hypercortisolemia is addressed, but persistent severe insulin resistance can lead to β cell exhaustion and hypoinsulinemia that results in permanent DM.21

Growth Hormone Excess

Growth hormone (GH), or somatotropin, antagonizes insulin action and, in excess, induces severe insulin resistance. The best example in companion animals is feline acromegaly, which is caused by a functional GH-secreting pituitary adenoma. Cats with acromegaly are usually initially presented for signs related to GH excess, including glucose intolerance, insulin resistance, or, frequently, overt DM.22 In addition to commonly reported anatomic changes that accompany acromegaly, large pituitary tumors may produce neurologic signs through compression and damage to local brain structures.22

History

Patient history will vary depending on the underlying cause of hyperglycemia. DM is the most frequently encountered disorder associated with clinically significant hyperglycemia. Patients may have a subtle history that includes weight loss, often despite maintaining a normal appetite, along with increased water consumption and changes in urination habits. Patients with complicated diabetes may appear to be ill and exhibit lethargy, diminished appetite, reduced water consumption, or vomiting.2

Dogs with hyperadrenocorticism typically demonstrate profound polydipsia and polyuria secondary to hypercortisolemia, so any additive effects of hyperglycemia may go unnoticed in this setting. In some cases, the development of polydipsia or polyuria in a dog with well-controlled hyperadrenocorticism signals the onset of diabetes.21

Cats with acromegaly are often presented with uncontrolled DM. They show typical signs of DM but uniquely display persistent hyperglycemia despite provision of high doses of insulin (>2.2 U/kg/dose). It is only after other signs are recognized (eg, increased body mass, organomegaly, changes in facial structure) that acromegaly is suspected.22

Clinical Signs

The primary clinical signs of hyperglycemia are polyuria and polydipsia.2,9 These signs are most obvious with the onset of moderate to severe hyperglycemia, specifically when blood glucose levels begin to exceed the ability of the proximal tubules to reclaim filtered glucose. Glucose is freely filtered at the glomerulus, but avid reabsorption in the proximal tubules ensures that normal urine does not contain glucose. Glucosuria occurs when the amount of filtered glucose exceeds the capacity of the proximal tubules to reclaim glucose from filtrate. The renal threshold for glucose is exceeded when serum glucose levels range from >180 to 200 mg/dL in dogs and >250 to 280 mg/dL in cats.2 Polyuria and polydipsia are interrelated and develop as a result of glucose-mediated plasma hyperosmolality (which stimulates thirst and drinking behavior) and glucose-mediated osmotic diuresis (which increases the volume of urine and frequency of urination).23

Diagnosis

Hyperglycemia is diagnosed using any of several widely available laboratory methods. In most clinical situations, glucose is measured as part of most routine serum chemistry profiles but can also be measured using other methods, such as a portable glucometer or interstitial glucose monitor. Mild hyperglycemia in the absence of clinical suspicion of a hyperglycemic disorder may be transient physiologic hyperglycemia and should be re-evaluated; persistent hyperglycemia, even if relatively mild, warrants a diagnostic investigation. DM is a likely diagnosis when hyperglycemia is the sole or primary finding and clinical signs are present. However, careful evaluation is necessary to avoid DM misdiagnosis in patients presented under circumstances that might induce stress hyperglycemia (eg, severe illness, fear, anxiety), which is frequent in cats and can be marked in some patients. In rare circumstances, it may be challenging to confirm a DM diagnosis in a patient with hyperglycemia due to illness or stress. Fasting hyperglycemia or hyperglycemia that persists over multiple sampling periods or marked glucose elevation (>250 mg/dL) is suggestive of DM rather than a stress response. Although glucosuria is not essential for a diagnosis of DM, most dogs and cats have glucosuria at the time of diagnosis. Glucosuria may occur secondary to marked stress hyperglycemia in some cases and is present without concurrent hyperglycemia with conditions associated with renal tubule dysfunction (eg, primary renal glucosuria, Fanconi’s syndrome, acute renal tubular injury).24

Treatment & Management

Principal management of hyperglycemia aims to address the underlying cause. Hyperglycemia caused by insulin resistance may be ameliorated as the associated condition resolves, endocrine pancreatic function (eg, glucose-sensing, insulin secretion) normalizes, and an appropriate insulin response can be mounted. For example, hyperglycemic humans with obesity-associated insulin resistance may return to normoglycemia after weight loss. Hyperglycemia associated with glucocorticoid excess resolves when hyperadrenocorticism is addressed if β cell function is normal. Likewise, although hyperglycemia is an infrequent finding with functional canine pheochromocytoma, normoglycemia is expected to be restored after successful adrenalectomy. The insulin resistance that accompanies feline acromegaly is severe and often only fully resolves with appropriate therapy that effectively addresses excessive growth hormone.

Hyperglycemia caused by hypoinsulinemia is treated with insulin replacement. Most patients requiring insulin replacement have permanent DM, although the diabetic state can resolve under some circumstances. For example, severe pancreatitis may be accompanied by hyperglycemia, which, if severe enough, warrants use of insulin to restore euglycemia. Hyperglycemia in this setting is due to the combined effects of insulin resistance (secondary to marked inflammation) and hypoinsulinemia (secondary to islet cell injury or loss). In some cases of pancreatitis-associated DM, the need for exogenous insulin decreases and eventually resolves with resolution of pancreatitis.

Prognosis & Clinical Follow-Up

The pathologic consequences of untreated chronic hyperglycemia are similar regardless of the underlying cause. Risk for complications increases with the duration and magnitude of hyperglycemia. Microvascular injury caused by chronic hyperglycemia causes the common diabetic complications in humans (eg, retinopathy, nephropathy). Hyperglycemia also has a role in cataract formation in dogs and diabetic neuropathy in dogs and cats, as well as in humans.

Hyperglycemia is a common clinical problem in dogs and cats. The prognosis is difficult to determine because it depends on whether the underlying cause can be effectively controlled. DM in dogs and cats carries a guarded prognosis, depending on the establishment of an effective control protocol. Canine hyperadrenocorticism has a variable prognosis, depending on the initiating pathology (ie, pituitary, adrenal), but prognosis for return to euglycemia is good if hypercortisolemia is effectively controlled. Hyperglycemia associated with feline acromegaly carries a poor prognosis, primarily because diabetes control is difficult, options for treatment of growth hormone excess and pituitary adenoma are limited, and cats are often presented with advanced disease.

References

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

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

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

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Hypoglycemia

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

Internal Medicine

|Peer Reviewed

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Hypoglycemia

Hypoglycemia is a manifestation of a pathologic process—not a diagnosis. It is always secondary to a disorder that disrupts or overwhelms one or more of the homeostatic mechanisms responsible for maintenance of normoglycemia.

Background & Pathophysiology

Glucose is a dietary carbohydrate used as a substrate for adenosine triphosphate production via anaerobic and aerobic pathways. Its use as a cellular source of fuel requires regulation at multiple points during metabolism. As a result, glucose homeostatic pathways are highly integrated to maintain blood glucose levels within precise physiologic limits.1

Hypoglycemia is defined as a decrease in blood glucose below the physiologic range and is considered clinically relevant when levels decrease below 60 mg/dL.2

Blood Glucose Regulation

Normoglycemia is maintained by the actions of multiple hormones that regulate the metabolic pathways responsible for glucose addition and removal from blood (Figure). Insulin and glucagon are the most important hormones involved in glucose homeostasis. The major pathways through which glucose is added to blood are intestinal absorption of dietary glucose and hepatic glucose production via glycogenolysis and gluconeogenesis.3 Insulin and glucagon play opposite roles in blood glucose regulation. Insulin exerts hypoglycemic effects through actions that stimulate glucose uptake by target tissues and reduce hepatic glucose output.3 Glucagon has no effect on cellular glucose uptake but potently increases the rate of glucose appearance in blood through stimulation of glycogenolysis and gluconeogenesis.4 It is the balance of these hormones—the insulin:glucagon ratio—that determines whether there is a net gain or loss of glucose from blood.

When glucose decreases below its physiologic set point, insulin secretion is typically inhibited and glucagon secretion is stimulated; when the decrease in glucose levels is rapid, a marked counterregulatory response serves to rescue the organism from severe hypoglycemia.5 The counterregulatory response is mediated through the actions of hormones such as cortisol and other glucocorticoids, catecholamines, and growth hormone, which induce a degree of insulin resistance that helps increase blood glucose. Hypoglycemia occurs when the rate of glucose removal exceeds the rate of its addition to blood.1 Endogenous or exogenous substances that mimic or potentiate insulin action or enhance or accelerate glucose metabolism increase glucose removal, whereas failure of endogenous glucose production decreases the rate of glucose addition to blood. Disruptions of the pathways responsible for glucose addition or removal may overwhelm homeostatic mechanisms and produce clinical hypoglycemia.

Normoglycemia represents balance between glucose addition and removal from the blood. Hypoglycemia results when the rate of glucose addition falls below the removal rate (ie, hypoinsulinemic hypoglycemia) or when the rate of removal exceeds the addition rate (ie, hyperinsulinemic hypoglycemia).
Normoglycemia represents balance between glucose addition and removal from the blood. Hypoglycemia results when the rate of glucose addition falls below the removal rate (ie, hypoinsulinemic hypoglycemia) or when the rate of removal exceeds the addition rate (ie, hyperinsulinemic hypoglycemia).

FIGURE Normoglycemia represents balance between glucose addition and removal from the blood. Hypoglycemia results when the rate of glucose addition falls below the removal rate (ie, hypoinsulinemic hypoglycemia) or when the rate of removal exceeds the addition rate (ie, hyperinsulinemic hypoglycemia).

FIGURE Normoglycemia represents balance between glucose addition and removal from the blood. Hypoglycemia results when the rate of glucose addition falls below the removal rate (ie, hypoinsulinemic hypoglycemia) or when the rate of removal exceeds the addition rate (ie, hyperinsulinemic hypoglycemia).

Mechanisms of Action

Hypoglycemia has been associated with a variety of clinical conditions but is a consistent feature of relatively few disorders. Because artifactual and factitious causes for hypoglycemia are fairly common, it is important to rule out the possibility of preanalytic (eg, improper sample collection, handling or storage) or analytic (eg, inaccurate glucometer) errors before accepting the validity of a test result consistent with hypoglycemia, especially when clinical signs are lacking or the finding is unexpected. Confidence in the result can be improved by repeating the analysis or using a different technique to measure glucose. Clinical disorders produce hypoglycemia through one or more pathophysiologic mechanisms. Clinical hypoglycemia can be broadly divided into several categories: hyperinsulinemic hypoglycemia, hypoinsulinemic hypoglycemia, and miscellaneous disorders (Table 1).6

Hyperinsulinemic hypoglycemia is the most common mechanism of hypoglycemia in dogs and cats, with relative or absolute insulin excess being a common feature (Table 1). Exogenous insulin administered to diabetic patients is responsible for most cases of hyperinsulinemic hypoglycemia in veterinary medicine; typically, the cause is insulin overdose, although pharmacologic doses of insulin given to diabetic cats may result in onset of diabetes remission with subsequent hypoglycemia.7,8 Accidental or nefarious injection of insulin has been described in nondiabetic humans but is an unlikely cause of hyperinsulinemic hypoglycemia in animals.9

Table 1

Pathophysiologic Mechanisms & Major Causes of Hypoglycemia

  Mechanism of Action Clinical Notes
Hypoinsulinemic hypoglycemia    
Congenital portosystemic shunt Reduced hepatic glycogen storage and gluconeogenesis Signs observed at young age. Breed conveys risk in dogs. Signs are similar for intra- and extrahepatic shunt locations.
Liver failure (acute or chronic) of any cause, including feline hepatic lipidosis Impaired or reduced hepatic glucose production due to hepatocellular dysfunction, injury, or loss Frequently accompanied by elevated levels of hepatic transaminases and bilirubin; however, blood levels of other hepatic function markers (eg, urea, albumin, cholesterol) will be low.
Hypoglycemia of fasting Limited hepatic glycogen stores are exhausted after a short fast. Hepatic glucose production is less efficient in young puppies and kittens than in adults due to reduced glycogen stores and limited gluconeogenic substrates. Fasting does not cause hypoglycemia in healthy adult animals. Most common cause for hypoglycemia in neonatal and young puppies and kittens
Glycogen storage disorders Genetic condition that causes impaired glycogen metabolism Type 1 (von Gierke’s disease) and type 3 (Cori’s disease) are rare conditions that have been described in dogs.
Counterregulatory hormone deficiency Deficiency results in decreased antagonism of insulin action, which favors development of hypoglycemia. Clinical disorders include cortisol deficiency (hypoadrenocorticism) and growth hormone deficiency (eg, pituitary dwarfism).
Polycythemias Increased cellular glucose use Infrequent complication of hematologic cancers and other disorders associated with marked erythrocytosis (eg, polycythemia vera) or leukocytosis (eg, leukemias)
Hyperinsulinemic hypoglycemia    
Insulin overdose Accidental or intentional administration of excess dose of exogenous insulin Affected patients have a history of diabetes mellitus; many are considered poorly regulated diabetics. Inadvertent overdose of prescribed insulin is the most common error. Using insulin to cause intentional harm is reported in humans but appears rare in veterinary medicine.
Insulinoma Neuroendocrine tumor of islet cells secretes endogenous insulin in excess Vague, nonspecific signs may precede onset of hypoglycemia. Recent weight gain is reported before diagnosis in some patients.
Paraneoplastic hypoglycemia Tumor produces an insulin-like substance. Some nonpancreatic tumors release a humoral factor that causes hypoglycemia; tumor may produce other signs along with hypoglycemia. Increased glucose consumption by very large tumors may also contribute to hypoglycemia.
Xylitol toxicity Stimulation of insulin release in dogs Hypoglycemia is secondary to increased insulin secretion but may be exacerbated in dogs with xylitol-associated liver failure.
Miscellaneous    
Sepsis Cause is not fully understood; multiple mechanisms have a role. Hypoglycemia is related to more severe cases of sepsis and may signify a worse prognosis.
Infections, toxins, and drugs Various mechanisms Infections infrequently associated with hypoglycemia include bartonellosis and babesiosis.2 Hypoglycemia can result from ethylene glycol toxicity or ethanol intoxication (rare in dogs and cats) and has been observed in a dog after oleander ingestion.2 Hypoglycemia due to drugs (other than insulin), including oral hypoglycemic drugs, is rare in dogs and cats.
Idiopathic or episodic hypoglycemia Unknown cause; multiple factors (eg, prandial state, level of anxiety/excitement, level of exertion, diet) are likely to be involved. Episodes of hypoglycemia occur in an otherwise healthy animal. Triggering events or circumstances may be identified; clinical examples include small-breed hypoglycemia and hunting dog hypoglycemia. Hypoglycemia may rarely develop during pregnancy in dogs.

Insulinoma, a neuroendocrine tumor of the pancreas, is the most common disorder associated with hyperinsulinemic hypoglycemia due to excess production of endogenous insulin.10 Insulin excess due to islet cell hyperplasia has been suspected in some dogs.11,12 In humans, oral hypoglycemic drugs (eg, sulfonylureas) that stimulate release of endogenous insulin can cause hyperinsulinemic hypoglycemia. However, these drugs are infrequently used in veterinary medicine, so this effect is unlikely to be encountered clinically.13

Ingestion of xylitol, an artificial sweetener used in many products intended for human use, causes profound hypoglycemia in dogs.14 Uniquely in dogs, xylitol is a potent stimulator of insulin release, and toxicity occurs after ingestion of more than 0.1 g/kg.15,16 Hypoglycemia results from insulin excess with or without concurrent failure of hepatic glucose output, which is caused by xylitol-induced liver damage.

Hypoinsulinemic hypoglycemia describes hypoglycemia that develops independent of insulin; in associated conditions, blood insulin is appropriately low with hypoglycemia. Non-insulin–mediated hypoglycemia may develop via one of several mechanisms (Table 1). Several tumor types (eg, hepatomas, hepatocellular carcinomas, leiomyomas, leiomyosarcomas) produce humoral insulin-like substances (eg, insulin-like growth factor-1) that promote hypoglycemia.2,6,17 Hypoinsulinemic hypoglycemia can also occur with disorders that increase use of glucose by body tissues or those associated with failure of hepatic glucose production.18

History & Clinical Signs

Hypoglycemia is a manifestation of disease rather than a specific diagnosis. Patient age and breed, previous diagnoses (eg, diabetes), and information about the conditions that elicit signs (eg, fasting, exercise) provide clues about possible causes. Patients may not share a consistent history except when the only signs displayed are those of hypoglycemia. Signs of hypoglycemia can be divided into signs related to impaired tissue energetics (neuroglycopenic) and those related to sympathetic activation (neurogenic; see Signs of Hypoglycemia).19 Acute hypoglycemia can produce a variety of nonspecific signs, including muscle tremors or weakness, ataxia, nausea, vomiting, behavior changes, confusion, collapse, seizures, and coma.2 Chronic or intermittent hypoglycemia is often associated with vague signs of decreased activity or reduced energy, which may be accompanied by signs that are usually associated with acute exacerbations.19

Signs of Hypoglycemia19

  • Signs may be triggered under such circumstances as fasting, stress, or exercise.
  • Severity of signs depends on hypoglycemia duration and severity.
  • Marked hypoglycemia may be tolerated in dogs and cats with chronic or episodic hypoglycemia.

Neurogenic Signs

  • Restlessness
  • Hunger/food seeking
  • Nausea/vomiting
  • Tachycardia
  • Tremors
  • Signs reported in humans include feeling shaky, sweating, and anxiety, but equivalent signs are difficult to define in dogs and cats.

Neuroglycopenic Signs*

  • Weakness
  • Unusual behaviors, confusion, apparent vision abnormalities
  • Ataxia
  • Lethargy
  • Seizure
  • Coma
*Severe or prolonged neuroglycopenia may be fatal.

Diagnosis

Hypoglycemia is diagnosed when the measured blood glucose level is below the reference range, which is generally centered around 90 to 100 mg/dL and ranges from 70 to 120 mg/dL. Clinically, signs are most likely to appear when the glucose level is ≤60 mg/dL.2,19 Hypoglycemia may be documented using a variety of clinical testing methods, including serum chemistry profile, whole blood testing using a portable glucometer, or interstitial fluid analysis using a continuous glucose monitor. Artifactual hypoglycemia is a preanalytic error that occurs when glucose in the sample is consumed by blood cells during processing. Some examples include consumption by RBCs when clot removal is delayed during serum processing or by WBCs when severe leukocytosis is present.20 If laboratory error is eliminated as a cause, persistent or recurrent hypoglycemia should be investigated. Because recognition of hypoglycemia per se is not sufficient to make a diagnosis, patient history, physical examination, and other diagnostic findings must be carefully evaluated to identify the underlying cause. A diagnosis of clinically relevant hypoglycemia is confirmed by satisfying the criteria of Whipple’s triad: 1) clinical signs of hypoglycemia, 2) concurrent biochemical hypoglycemia, and 3) resolution of clinical signs with correction of hypoglycemia. In many cases, a series of diagnostic tests and imaging studies are needed to identify an underlying cause for hypoglycemia.

Treatment & Management

Treatment aims to eliminate the clinical signs of hypoglycemia and address any underlying pathology (Table 2). Mild hypoglycemia may be alleviated by feeding, especially in young animals or small-breed dogs in which hypoglycemia may develop due to rapid depletion of glycogen. Blood glucose can be increased rapidly via oral or IV glucose supplementation. Oral glucose is usually provided as corn syrup or honey, both of which contain large amounts of glucose in the form of simple sugars.19 IV glucose is usually supplied via bolus injection or CRI of a glucose solution prepared from a sterile 50% dextrose solution. Infusion of glucagon, a hormone that antagonizes insulin-mediated inhibition of gluconeogenesis and promotes hepatic glucose production, has been used to treat hypoglycemia associated with insulin overdose and insulinoma in dogs.21,22

Some medications are useful for addressing chronic hypoglycemia associated with specific disorders. Glucocorticoids (eg, prednisone, dexamethasone) are used as replacement therapy for cortisol deficiency that accompanies hypoadrenocorticism.23 Given at doses sufficient to induce insulin resistance, these drugs are also used as adjunctive treatment for insulinoma-associated hypoglycemia.10 Anecdotally, L-carnitine supplementation may help ameliorate hypoglycemic events in susceptible small-breed puppies, including those with hypoglycemia caused by portosystemic shunting.

Table 2

Treatment of Hypoglycemia

Treatment Formulations & Dosing Guidelines Clinical Notes
Food A small snack or meal portion of a commercial balanced diet is a source of carbohydrates as well as substrates that support gluconeogenesis.
  • Only indicated for treatment of mild hypoglycemia
  • Requires patient to be alert and have the ability to swallow normally
  • Not suitable for emergency treatment of hypoglycemia
  • Small meals fed frequently may be part of an effective strategy for hypoglycemic management in some patients.
Glucose-containing syrup
  • Corn syrup or honey contains a high percentage of glucose as the simple sugar.
  • 50% dextrose for injection (0.5 g glucose/mL); can be given PO if IV access is not available
  • Apply liberally along gingiva and buccal mucosa; allow ingestion if patient is able to swallow.
  • Owners should be advised to start therapy as soon as hypoglycemia is recognized.
  • Caregivers should be warned to take care not to be bitten during administration and to withhold treatment if patient is nonresponsive or unable to swallow.
Glucose solution

50% dextrose for injection (50-mL vial); each vial contains 25 g dextrose

Glucose bolus

  • IV injection is administered at 0.5-1.0 g/kg (1-2 mL/kg) over 10-15 minutes; the dose is diluted 1:4 with 0.9% sodium chloride before administration.

Glucose CRI

  • A 5% glucose infusion solution is prepared by adding 25 g dextrose/500 mL isotonic fluid (eg, lactated Ringer’s solution).
  • A glucose bolus may be given at the start of CRI.
  • The infusion rate is started at 2-3 mL/kg/hour and titrated to achieve normoglycemia.
  • An indwelling catheter is recommended to avoid complications (eg, phlebitis, pain) associated with injection of hypertonic glucose solutions.
  • Bolus injection will rapidly correct hypoglycemia but may stimulate insulin release in nondiabetic patients. In such cases, the effect of the bolus may wane rapidly, necessitating administration of multiple boluses; beginning a glucose CRI should be considered.
  • In a study of insulin overdose in dogs and cats, glucose supplementation was continued for a median of 18 hours and 8.5 hours, respectively, until euglycemia was restored.7 The same study found that the total amount of glucose needed to restore normoglycemia was >1 g/kg, with some patients requiring much greater quantities.
Glucagon

Available in 1-mg vials for rescue treatment of hypoglycemia in diabetic humans; drug is administered via CRI for veterinary applications

CRI preparation and dosing

  1. Glucagon is reconstituted using supplied diluent.
  2. The infusion solution (1 µg glucagon/mL) is prepared by adding the entire reconstituted volume (containing 1 mg glucagon) to 1 L bag of 0.9% sodium chloride solution.
  3. A bolus injection of glucagon (0.05 µg/kg) IV can be given before starting CRI.
  4. The initial CRI dose is 0.005-0.01 µg/kg/min IV and is titrated to achieve normoglycemia.
  5. Blood glucose should be monitored hourly until normoglycemia is achieved.
  6. CRI can be maintained until blood glucose is stable and the rate tapered with monitoring to ensure normoglycemia is sustained.
  • Glucagon infusion is reported in dogs and has been used to treat hypoglycemia due to insulinoma9,24 and insulin overdose.9,25
  • Glucagon infusion is effective and well-tolerated in dogs24 and should be considered when glucose infusion fails to maintain blood glucose. 
Adjunctive treatment    
Glucocorticoids

Prednisone

  • Dose for hormone replacement is 0.1-0.2 mg/kg daily.
  • Dose to induce insulin resistance is 1-2 mg/kg daily. (higher dose is also immunosuppressive)

Dexamethasone

  • More potent than prednisone and requires appropriate dose reductions
  • Replacement dose is 0.01-0.02 mg/kg/day.
  • Dose sufficient to induce insulin resistance is 0.1-0.2 mg/kg/day.
  • Use of low-dose glucocorticoids as hormone replacement is only indicated for treatment of hypoglycemia caused by cortisol deficiency associated with hypoadrenocorticism. The dose is insufficient to induce insulin resistance.
  • Adverse effects (eg, polydipsia, polyuria, weight gain) occur when doses exceed the replacement dose.
  • Glucocorticoid induction of insulin resistance is a helpful adjunctive treatment for insulinoma when definitive therapy is not pursued. Improvement or resolution of insulinoma-induced hypoglycemia is usually temporary, although some dogs will remain subclinical for several months.
L-carnitine

A recommended empiric dose is 50 mg/kg twice daily.

The use of L-carnitine for this purpose is based on anecdotal reports and the author’s clinical experience.
  • L-carnitine is believed to increase the metabolic efficiency of mitochondria and to improve cellular energy production.26
  • L-carnitine is commercially available as a nutritional supplement. The powder form is easily given mixed with food.
  • L-carnitine supplementation may be useful for decreasing the frequency and severity of hypoglycemia in young animals. Supplementation can usually be discontinued after the animal matures.
  • Anecdotally, L-carnitine may provide similar benefits for animals with liver impairment secondary to portosystemic shunting and animals with some forms of idiopathic hypoglycemia.

Prognosis

Correction of hypoglycemia is readily accomplished with glucose supplementation. However, initial improvement will wane if the underlying pathology of hypoglycemia is not addressed or resolved. Frequent or continuous glucose supplementation may be needed to support patients with hypoglycemia caused by insulin overdose until the exogenous insulin is fully metabolized. Insulin excess due to insulinoma causes a similar problem, but release of endogenous insulin from insulinoma is ongoing and may be unpredictable. Some of these tumors may retain the ability to secrete insulin in response to hyperglycemia, which may develop during bolus glucose administration. The severity of hypoglycemic episodes experienced by juvenile animals or small-breed dogs may decrease with treatment and time as the animal matures and grows.

Idiopathic hypoglycemia carries a good prognosis if triggering factors can be identified and avoided. Prognosis for paraneoplastic hypoglycemia depends on whether effective treatment of the underlying neoplasm is possible. Hypoglycemia secondary to liver failure subsequent to cirrhosis or other disorders carries a poor prognosis, whereas hypoglycemia in patients with portovascular anomaly is expected to resolve after shunt closure.

References

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

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Selarid CB Sept 2020
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Differential Diagnosis: Lymphocytosis

Julie Allen, BVMS, MS, MRCVS, DACVIM (SAIM), DACVP (Clinical), Durham, North Carolina

Internal Medicine

|Peer Reviewed

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Differential Diagnosis: Lymphocytosis

Following are differential diagnoses for patients presented with lymphocytosis.

  • Age-related cause (eg, dogs and cats <6 months of age often have mild lymphocytosis due to vaccination or exposure to novel antigens)
  • Antigenic stimulation
    • Immune-mediated disease (rare; eg, immune-mediated hemolytic anemia in cats) 
    • Infection (most commonly, Ehrlichia canis; rarely, protozoal [eg, Leishmania infantum], Spirocerca lupi, FIV)
  • Endocrine disease
    • Hyperthyroidism (cats; usually mild; can be seen prior to diagnosis [possibly epinephrine-related] or secondary to methimazole treatment)
    • Hypoadrenocorticism (primarily dogs; lack of a stress leukogram in a sick patient can indicate disease)
  • Lymphoid neoplasia
    • Acute lymphoblastic leukemia
    • Chronic lymphocytic leukemia (± small cell lymphoma)
  • Nonlymphoid neoplasia (eg, thymoma)
  • Physiologic (eg, epinephrine-induced) response (primarily cats)

References

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

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PVD CB Sept 2020

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Bravecto CB Sept 2020
Bravecto CB Sept 2020

Environmental Decontamination for Ringworm

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

Dermatology

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Environmental Decontamination for Ringworm

In the literature

Moriello KA. Decontamination of 70 foster family homes exposed to Microsporum canis infected cats: a retrospective study. Vet Dermatol. 2019;30(2):178-e55.

FROM THE PAGE …

As part of successful treatment of dermatophytosis, environmental decontamination is recommended to eliminate infective material in the home environment. Although environmental contamination is considered an unlikely source of dermatophyte transmission, many pet owners may be fearful of persistent organisms in the environment and/or frustrated at the perception of difficult successful home decontamination.

This retrospective study evaluated the success of decontamination of homes in which Microsporum canis-infected cats lived as part of a foster program. Seventy homes were evaluated over a 10-year period as part of establishing a dermatophyte treatment program for shelters. Foster families were instructed to confine cats to a single room. Once the cat left the home, the environment was cleaned and sampled for residual contamination. The cleaning process involved removal of all visible debris, followed by wiping of surfaces with an over-the-counter household detergent. Once excess water was removed, all surfaces were disinfected with either 1:100 household bleach or 1:16 accelerated hydrogen peroxide.

Culture results were negative after a single cleaning in 38 of the 70 homes. In the other homes, complete decontamination was achieved after an additional 1 to 3 cleanings. Cultures were taken from furnace filters and room vents in 9 homes and were all negative. There were no reports of dermatophyte transmission to animals or humans during the study period.

Positive Wood’s lamp fluorescence result in a kitten with Microsporum canis dermatophytosis
Positive Wood’s lamp fluorescence result in a kitten with Microsporum canis dermatophytosis

FIGURE Positive Wood’s lamp fluorescence result in a kitten with Microsporum canis dermatophytosis

FIGURE Positive Wood’s lamp fluorescence result in a kitten with Microsporum canis dermatophytosis

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Dermatophytosis affects adoptable populations of animals, primarily puppies and kittens. The infectious nature of this condition is troublesome for shelters; some elect to “recognize and euthanize” to keep disease transmission to a minimum. There have, however, been several successful dermatophyte treatment programs developed in animal shelters, many of which use foster care families to aid in treatment delivery. By incorporating multimodal therapy (ie, combination of oral and topical antifungal therapy) with routine cleaning and disinfection, it is possible to eliminate environmental contamination and thereby reduce risk for reinfection and contagion.

2

Dermatophytosis is considered to be a generalized infection in cats due to the increased amount of infective material (ie, infective spores) present and distributed over the body as part of normal grooming behavior. This is different than in dogs, in which infection may be resolved with localized topical therapy. For cats, a combination of topical (eg, lime sulfur dips, miconazole/chlorhexidine combination shampoos) and systemic (eg, itraconazole, terbinafine) therapy is typically recommended.1

3

For most cats with alopecia, dermatophytosis should be considered a possible differential diagnosis. Positive Wood’s lamp fluorescence results will only be seen with Microsporum canis infections; a negative result does not rule out infection. Fungal culture remains the preferred diagnostic method to confirm disease, although dermatophyte PCR can also provide a rapid result to help confirm clinical suspicion.

References

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Research Note: Potential Use of Activity Monitor to Evaluate Osteoarthritis in Cats

Orthopedics

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This study evaluated data signatures from an activity monitor of jumps performed by 13 healthy cats that had no evidence of osteoarthritis or degenerative joint disease. Each cat was encouraged to jump up, jump down, or jump horizontally during a 5- to 8-hour observation period. Mean misclassification error rate per cat was 5.4%, which indicates this model is reliable in correctly identifying jumping events in healthy cats. Further studies are expected to show similar results in cats with signs of pain and may be useful in early detection of osteoarthritis and joint pain and in identifying objective end points to assess treatment efficacy.

Source

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Research Note: Cleaning Procedures & Bacterial Contamination of Feline Inhalation Chambers

Respiratory Medicine

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Inhalation chambers are commonly used to deliver aerosol drugs to cats with lower airway disease. Manufacturers recommend different cleaning procedures to minimize bacteria buildup in these spacer devices, but no studies have been performed to evaluate their effectiveness. The investigators in this study placed standardized inoculations of Pseudomonas aeruginosa into spacer devices from 2 different manufacturers. Devices were then cleaned according to manufacturer recommendations. Chambers were air dried for 24 hours, and samples were obtained from 3 sites and submitted for bacterial culture testing. No bacterial contamination was detected in any of the devices tested. The authors concluded that successful bacterial decontamination occurs when inhalation chambers are cleaned following manufacturer instructions.

Source

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Allergies & CCDs: What You Need to Know

Dermatology

|Sponsored

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Allergies & CCDs: What You Need to Know
Sponsored by Spectrum Veterinary

Canine atopic dermatitis is a complex, multifactorial disease. Allergen immunotherapy (AIT; ie, hyposensitization) is considered to be the only treatment that can impact the course of disease. The gold standard for identifying allergens for immunotherapy has traditionally been intradermal testing (IDT); however, there is no clear evidence that AIT based on IDT results is more effective than AIT based on immunoglobulin E (IgE) serum allergy testing, and not all pet owners have access to IDT.1,2,6

Serum Allergy Testing Benefits

Serum allergy testing has some practical advantages over IDT. IDT can be traumatic for some patients and requires the withdrawal of comfort medications (eg, antihistamines [7 days], short-acting glucocorticoids [14 days]), which can potentially impact patient quality of life.3-5 Similar withdrawals are not required for serum allergy testing.4 Unlike IDT, serum allergy testing generally does not require referral,6 allowing testing to be performed by the primary veterinarian. This can be helpful for owners who may prefer to work with a team they already know and trust or for those with whom cost may be a factor. In addition, serum allergy testing does not require sedation or the shaving of fur and typically takes less time.3

Challenges in Allergy Testing

There is increasing concern regarding inconsistencies between and within both allergy testing methodologies. This has led to speculation regarding whether standardization could further improve AIT outcomes.

With IDT, the allergens tested, test concentrations, and volumes injected vary, even with tests conducted in a specific geographic area and allergens purchased from the same source.7 There are also inconsistencies in the interpretation of results8 and only fair to moderate consistency between interevaluator wheal scoring.9  Multiple studies have found variability in and among different serum allergy testing laboratories,10-13 with one study indicating that interlaboratory agreement is only slightly higher than chance.10 Differences may stem from variability in cut-off values, laboratory methodology, batches of allergen extract, and nonspecific binding interactions, among others.10 

IDT and serum allergy testing of the same patient may also have discordant results, with the most common cause being positive IgE results when IDT is negative.6,14,15 Cross-reactive carbohydrate determinants (CCDs) may be a cause of this discrepancy.

CCDs

CCDs are antigens with carbohydrate epitopes that stimulate the formation of IgE antibodies and have broad crossreactivity but no apparent clinical significance.16 CCDs appear to occur in 22% to 35% of atopic humans17 and 17% to 73% of atopic dogs.18 When present, CCDs usually result in multiple falsepositive or clinically irrelevant serum allergy testing results that correlate poorly with IDT results, particularly with regard to pollens.16,19 CCD blockers can improve the specificity of serum allergy testing.16,17,19 Their efficacy may be impacted by test protocol.17,19-21

When testing was performed against 94 potential allergens in US patients, the use of Spectrum’s proprietary CCD blocker reduced the average number of allergens testing positive by 19.21 The environmental allergens most impacted were the pollens of weeds and trees. This new methodology has also been shown to increase the assay sensitivity and intra-assay reproducibility.

Eliminating false-positive results decreases unnecessary allergens included in a patient’s individualized AIT plan. Fewer treatment vials decrease costs and improve long-term compliance.

Conclusion

Allergies impact the lives of animals and their owners5 and are a top source of pet insurance claims.22 AIT based on serum allergy testing appears to result in similar success rates as compared with IDT but has additional key advantages. Choosing a test that has quality control features, including those available through Spectrum Veterinary’s SPOT Platinum+ panel, may help ensure more reproducible results and improve AIT recommendations. Further research should be conducted to assess the additional potential benefits in safety and efficacy of AIT when CCD blocking is utilized in conjunction with serum allergy testing.

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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Spectrum CB Sept 2020

Animal Toxicosis to Human Topical Dermatologic Products

Sarah Gray, DVM, DACVECC, Horizon Veterinary Specialists, Ventura, California

Toxicology

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Animal Toxicosis to Human Topical Dermatologic Products

In the literature

Tater KC, Gwaltney-Brant S, Wismer T. Dermatological topical products used in the US population and their toxicity to dogs and cats. Vet Dermatol. 2019;30(6):474-e140.

FROM THE PAGE …

This study aimed to describe the range of topical dermatologic medications used in human medicine in the United States and their potential toxicity to dogs and cats. Prescription data from 2011 to 2014 were collected from the National Health and Nutrition Examination Survey (NHANES) database, which provided a dataset of 10,170 individuals representative of 311,065,381 US residents. Results revealed that 1.33% (±0.21%) of the US population used prescription topical dermatologic medications; 50 different products were identified. This information was paired with a description of the epidemiology of dog and cat exposures to dermatologic products (both human and veterinary). 

A data search from the ASPCA Animal Poison Control Center from 2001 to 2018 revealed 61,169 exposures (dogs, 46,289; cats, 14,880) to 177 veterinary and human topical dermatologic products. These exposures resulted in clinical signs in 37.5% (22,910) of cases. Human-labeled products were involved in 15.1% (3,463) of cases, 73.5% (2,545) of which involved a prescription topical dermatologic drug. Clinical outcomes were categorized as mild (ie, non-life–threatening, transient signs, minimal veterinary intervention), moderate (ie, more intense or longer duration of clinical signs, some veterinary intervention), major (ie, potentially life-threatening, intensive intervention, and/or long-term or permanent sequelae), and death (ie, found dead, died, or were euthanized as a result of toxicosis). Of the identified human-labeled products, 56% (28/50) showed medium to high risk for toxicity. Exposure to human-labeled products was primarily via oral exposure (94.2% of cases); dermal (ie, dermal only or dermal + oral) exposures accounted for 5.3% of cases. Clinical outcomes were mild in 68.2% of cases and moderate, major, or death in 31.2% of cases; of the latter cases, 44 active ingredients were involved in the toxicosis.

The data presented in this study are broad and extrapolated from 2 databases. One database allowed collection of representative human topical dermatologic agents used and potentially accessible to pets. In the NHANES database, humans were selected through complex, multistage, highly stratified cluster samples of households; these data allowed collection of the topical products used but may not be comprehensive or all-inclusive. Pet information was collected from the ASPCA Animal Poison Control Center, which limits the reports of pet cases, as these calls and data may alternatively be documented by company adverse-effect reporting call centers or other animal poison centers in the United States. 

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Most of the literature on toxicoses from human-labeled topical dermatologic products involves individual case reports. Thus, this study is a useful reference to evaluate possible adverse effects caused by topical dermatologic agents in dogs and cats, as the study attempts to aggregate a plethora of information, although broad, into a single source.

2

Clinicians should be aware of the risk for topical dermatologic human (and veterinary) products to result in moderate or major clinical patient outcomes.

3

Increased public awareness of the risks these products pose to pets may help decrease toxic exposures, particularly in regard to home storage practices.

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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Epicur CB Sept 2020

Effect of Expiratory Phase in Detecting Left Heart Enlargement

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

Cardiology

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Effect of Expiratory Phase in Detecting Left Heart Enlargement

In the literature

Chhoey S, Lee SK, Je H, Jung JW, Jang Y, Choi J. Effect of expiratory phase for radiographic detection of left heart enlargement in dogs with mitral regurgitation. Vet Radiol Ultrasound. 2020;61(3):291-301.

FROM THE PAGE …

Myxomatous mitral valve disease (MMVD) is the most common acquired heart disease diagnosed in dogs.1 Echocardiography is the gold standard for diagnosing MMVD but is not always readily available. Left atrial (LA) size correlates with the severity of mitral regurgitation; thus, echocardiographic assessment of LA size is most commonly performed using the left atrial:aortic root ratio (LA:Ao). A variety of methods have been described for radiographically assessing LA and overall heart size, and phase of respiration has been shown to influence some radiographic findings (eg, pulmonary opacity, relative cardiac size).

This study investigated whether the phase of respiration on thoracic radiographs would influence detection of left heart enlargement in normal dogs and dogs with MMVD. The study group included 100 dogs with echocardiographic documentation of mitral regurgitation (MR) secondary to MMVD. To be included in the study, patients had to have inspiratory and expiratory thoracic radiography performed the same day as the echocardiogram and could not have any concurrent diseases affecting the cardiovascular system or evidence of congestive heart failure. The healthy group consisted of 20 purpose-bred beagles. LA:Ao was measured on standard right parasternal short axis view, and a LA:Ao >1.5 was used to define LA enlargement. Quantitative measurements of LA size on thoracic radiographs consisted of vertebral heart size (VHS) and vertebral LA size, a recently described radiographic measurement.2 Qualitative radiographic assessment of the left heart was also performed; on the lateral view, presence or absence of dorsally deviated carina was noted, and bulging of the caudal cardiac waist in the region of the left atrium was graded 0 to 3, with 0 representing no bulging and 3 representing severe bulging. Similarly, on the ventrodorsal view, the severity of bulges associated with the left auricular appendage and left ventricle were also graded on a scale of 0 to 3.

For the normal group, respiratory phase did not affect radiographic measurements or heart assessments. For dogs with MMVD, with the exception of qualitative assessment of left ventricular bulge on expiration, all radiographic measurements on both inspiration and expiration had moderate positive correlation with echocardiographic-derived LA:Ao. Vertebral LA size measured larger on inspiration, whereas qualitative assessments of bulges associated with the LA, left auricular appendage, and left ventricle were greater on expiration. Moreover, there was a higher chance of false-positive assessment of LA enlargement on expiratory views. There was no difference in VHS on inspiratory and expiratory views. 

Overall, use of both inspiratory and expiratory thoracic radiography can be helpful in assessing left heart enlargement in dogs with mitral regurgitation due to MMVD. Caution should be used when interpreting expiratory radiographs, as LA enlargement can be overestimated, but, ultimately, several radiographic assessments described in this study showed good correlation with echocardiographic measurement of LA:Ao.

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Expiratory thoracic radiography can be helpful in detecting left heart enlargement, but caution should be used, as LA enlargement can be overestimated.

2

VHS assessment remains stable regardless of the phase of respiration.

 

3

When echocardiography is not readily available, thoracic radiography can be used to assess LA size as a surrogate for severity of MMVD. In this study, all assessments of LA size and VHS had moderate positive correlation with echocardiographic-derived LA:Ao.

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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JorVet CB Sept 2020

Ultra-Low–Fat Diets in Dogs with Protein-Losing Enteropathy

Jan S. Suchodolski, MedVet, DrVetMed, PhD, AGAF, DACVM (Immunology), Gastrointestinal Laboratory at Texas A&M University

Internal Medicine

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Ultra-Low–Fat Diets in Dogs with Protein-Losing Enteropathy

In the literature

Nagata N, Ohta H, Yokoyama N, et al. Clinical characteristics of dogs with food-responsive protein-losing enteropathy. J Vet Intern Med. 2020;34(2):659-668.

FROM THE PAGE…

Protein-losing enteropathy (PLE) is characterized by intestinal protein loss, often as a consequence of various intestinal disorders (eg, intestinal lymphangiectasia, chronic enteropathy). Therapies involve immunosuppressive agents and dietary modifications (ie, novel or hydrolyzed protein, fat restriction). Dogs with PLE carry a poor prognosis, with many becoming refractory to standard therapy. Recent studies have suggested that ultra-low–fat diets may be of benefit to dogs with PLE, especially those with intestinal lymphangiectasia.1-4

This retrospective study describes clinical characteristics of dogs with PLE (n = 33). Diagnosis of PLE was based on presence of hypoalbuminemia (albumin <2.6 g/dL) after exclusion of other causes of hypoalbuminemia. Dogs with concurrent disorders (eg, intestinal lymphoma, pancreatitis, hepatic dysfunction), with other causes of hypoalbuminemia (eg, renal protein loss), and/or that were lost to follow-up were excluded.

Of the 33 dogs, 27 received a homemade, boiled, ultra-low–fat diet as initial management. The diet consisted of 1 part skinless chicken breast and 2 parts rice or white potato without skin.4 Fat content was 0.35 g/100 kcal.

Response was defined as a decrease in clinical activity (see Suggested Reading), and responders were subclassified as complete (ie, normal serum albumin [≥2.6 g/dL], no requirement for additional prednisolone treatment) or partial (ie, only partial improvement in serum albumin and/or required additional prednisolone). Of the 27 dogs receiving the ultra-low–fat diet, 23 (85%) responded; of those, 12 were classified as complete and 11 as partial. Median duration to response was 15 days (range, 6-32 days). Responders had significantly lower clinical activity scores as compared with nonresponders. Survival times were longer in responders as compared with nonresponders.

After initial improvement, dogs were gradually transitioned (median, 47 days) to either a commercial dry low-fat (fat content, 2.03 g/100 kcal or 2.3 g/100 kcal) or hydrolyzed diet (fat content, 4.25 g/100 kcal) to prevent secondary nutritional deficiencies.

… TO YOUR PATIENTS

Key pearls to put into practice:

1

Dietary modifications are crucial in the management of dogs with chronic enteropathy, with several studies showing that most dogs respond to dietary intervention alone. However, because of the complexity of PLE, there is no one-size-fits-all approach, and clinicians should experiment with different diet types. This study confirms that a homemade ultra-low–fat diet can be beneficial in dogs with PLE. After initial response, some dogs can be transitioned to a commercial low-fat or hydrolyzed protein diet.

2

Ultra-low–fat diets have a considerably lower fat content than commercial low-fat diets. It is important for clinicians to correctly assess the macronutrient content (ie, fat, protein, fiber) of different diets. When comparing diets, it is best to assess these nutrients per caloric concentration (eg, grams of fat per 100 or 1000 kcal).

3

Incorporating clinical activity scores (see Suggested Reading) when assessing the patient can add valuable information about the prognosis and clinical response to therapy. Although both the canine inflammatory bowel disease activity index (CIBDAI) and canine chronic enteropathy clinical activity index (CCECAI) are used, the CCECAI may be more useful for dogs with PLE, as it incorporates serum albumin concentrations, which are important when monitoring response to treatment in dogs with PLE.

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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Advantage Multi CB Sept 2020
Advantage Multi CB Sept 2020
Feline Osteoarthritis Pain: Tools for Clinicians & Pet Owners

Feline Osteoarthritis Pain: Tools for Clinicians & Pet Owners

Tamara Grubb, DVM, PhD, DACVAA, Washington State University

Anesthesiology & Pain Management

|Sponsored

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Feline Osteoarthritis Pain: Tools for Clinicians & Pet Owners
Sponsored by Zoetis

Osteoarthritis (OA), a form of degenerative joint disease (DJD), is the most common cause of chronic pain in mammals, including cats. More than 90% of adult cats may have radiographic evidence of OA, with the presence/severity of disease expected to increase by >10% each year.1

Pain can be classified as either adaptive (physiologic) or maladaptive (pathologic). Adaptive pain facilitates tissue protection and healing, whereas maladaptive pain negatively impacts health, quality of life (QOL), and behavior, which can impact the human–animal bond, potentially leading to surrender or euthanasia of the pet.2 OA is a nonhealing disease, with OA-associated pain having no protective benefit; thus, OA causes maladaptive pain that, without treatment, progressively worsens as peripheral and central sensitization and neuropathic pain develop.1

Although OA is not curable, if identified and treated early, the progression of the intensity of OA pain can be slowed, providing a prolonged period of controllable pain and good QOL (likely a normal lifespan). Because OA is more common in geriatric cats,1,3 OA screening should begin when cats reach 7 to 10 years of age.

Key Points

  • Owners should be educated that cats experience pain from OA, which impacts health, QOL, and behavior. Behavioral and QOL scores and mobility animations such as those available through Zoetis can be useful tools on educating owners how to recognize OA-associated pain (see Education & Diagnostic Tools).
  • Using pain-specific questionnaires and performing feline-friendly, OA pain-specific examinations can help expedite a diagnosis of pain (see Education & Diagnostic Tools). 
  • Feline OA patients should be treated with the drugs and techniques currently available, but clinicians should stay abreast of future data and new treatment options as they emerge.

Recognizing OA-Associated Pain

OA-associated pain may not be obvious—to owners and to veterinary teams.4 Because cats are evolutionarily both predators and prey, their natural instinct is to hide any vulnerability that could increase predation, including pain. Tools such as checklists, animations, and videos can help owners and veterinary teams accurately recognize and assess pain associated with OA in cats.

Tools for Owners

Although the expected prevalence of OA is similar between dogs and cats, cat owners may be less likely than dog owners to identify pain in their pet.4 However, educating owners on the prevalence of OA-associated pain and available treatment options may make owners more likely to bring their cat to the clinic.5

Owner education starts with an understanding of feline behavior and mobility. Owners should understand that the clinical signs of OA-associated pain are rarely what is expected but the impact of pain (ie, pain-mediated changes in behavior, activity, and mobility) can still be identified. Behavior and activity changes related to urination/defecation, grooming, and social interactions (with humans and/or other pets) are often indicators of pain and, if not due to pain, could be due to other conditions that may require medical attention. Cats are largely sedentary, making pain-related mobility changes challenging to observe. Cats are also often seminocturnal, so owners may be sleeping when cats exhibit mobility changes. Feline OA is often idiopathic and bilateral as compared with canine OA, which is primarily secondary and unilateral.6-8 Thus, classic limping as exhibited by dogs is unlikely to be exhibited by cats. In addition, cats also spend more time moving vertically (eg, jumping, climbing) as compared with dogs. Vertical mobility changes, which most owners do not know how to identify, are important indicators of OA-associated pain.

Checklists can be useful in a variety of settings, including medical diagnostics. Using checklists with specific painrelated behavior/activity questions can educate the owner on the potential presence of pain and expedite diagnosis by alerting the clinician to pain-related concerns (see Education & Diagnostic Tools). Questions on a checklist should focus on the cat’s behavior and activity. Mobility discussions should center on the cat’s ability to jump and climb.

Videos and animations may help owners understand mobility in patients with OA, as the owner may more readily identify with observing the cat in motion. Detailed animations are available and can be effective diagnostic tools, comparing the movement of a cat with healthy, nonpainful joints with a cat with painful osteoarthritic joints as the cats climb up and down stairs, jump up and down, and jump to/from elevated surfaces, among others (see Education & Diagnostic Tools). Providing mobility animations on the clinic website and/or social media can also be beneficial; they can also be displayed on TV or computer screens in the lobby or examination rooms.

Infographics describing changes in behavior-related pain are also available (see Education & Diagnostic Tools). Clinicians should strive to be a preeminent resource for animal health information. Thus, infographics and questionnaires should be shared on the clinic website and/or social media and hard-copies made available in the clinic. Information regarding this material can also be included by audio in the clinic’s on-hold phone recording.

Tools for Clinicians

In a study of 90 geriatric cats with radiographic changes of DJD, only 4 had DJD or arthritis mentioned in their medical records.3 Although radiographic changes do not consistently predict the presence of pain, there is some correlation,9  and it could therefore be assumed that >4 of these 90 cats were painful. 

Identifying feline pain can be difficult for the clinician if not specifically investigated. Clinicians rarely observe a cat walking at the clinic as commonly occurs with dogs; thus, gait analysis is not typically a normal part of a non-pain–related examination. Having the owner explore checklists and mobility animations prior to the visit can increase the likelihood of pain being identified, as the owner’s input will provide a template for pointed pain-related, cat-specific questions. 

A feline-friendly musculoskeletal examination focused on joint-specific pain and mobility using gentle palpation and range of motion should be a part of any examination for patients in which pain is a potential problem and for every examination for cats >7 to 10 years of age. Detailed videos on feline-friendly, painfocused musculoskeletal examinations in cats are available (see Education & Diagnostic Tools) and include thorough evaluative descriptions of the patient and several joints, including the hip, stifle, tarsus, and elbow—common locations for feline OA. Asking the owner to video their cat at home can also help facilitate diagnosis, as mobility and behavior can be more accurately assessed when the cat is in an environment it is familiar with. Radiography can provide valuable information and is recommended; however, some patients will have radiographic lesions with no pain, and some patients may have pain that is worse than the radiographic evidence.7,10 Regardless, pain should be the focus of treatment, not the radiographic changes.

Education & Diagnostic Tools

Treatment of Feline OA

There are no research-backed, FDA-approved, easy-to-administer, long-lasting analgesic treatments for chronic pain in cats. NSAIDs are currently the most effective treatment option but are not approved in the United States for chronic use in cats and can cause adverse effects, including renal dysfunction, which is a common concern in cats.11 NSAIDs are typically a first-line treatment option in all species but often do not control pain—especially moderate to severe pain—when used alone. Other pharmaceuticals can be used to treat OA pain in cats, but most have little to no demonstrated efficacy in cats and typically require oral administration. For advantages and disadvantages of drugs commonly used to treat chronic pain in cats, see Table. 

Nonpharmacologic treatment (eg, acupuncture, laser and physical therapy) should be considered, although these techniques are largely unproven by research and require frequent treatment visits. Nutraceuticals and specific joint diets may be effective and could be added to the protocol as multimodal therapy but also have little to no demonstrated efficacy in cats. Most of these compounds are likely most effective at slowing disease progression, which may potentially delay the onset of worsening pain, than they are at providing analgesia directly.

Table

Common Medications Used to Treat Chronic Pain in Cats: Advantages, Disadvantages and Dosages

Drug & Class Dose, Frequency, & Route Advantages Disadvantages Notes
Robenacoxib (NSAID) 1-2.4 mg/kg PO every 24 hours* Class is effective against OA-associated pain

Oral administration, which may be difficult for owners

Adverse effects are possible with NSAIDs, which can frequently be an owner concern

Approved outside the United States for treatment of chronic pain in cats

No limit on duration of therapy
Meloxicam (NSAID) 0.1 mg/kg PO first day, then 0.05 mg/kg every 24 hours thereafter* Class is effective against OA-associated pain

Oral administration, which may be difficult for owners

Adverse effects are possible with NSAIDs, which can frequently be an owner concern

Approved outside the United States for treatment of chronic pain in cats

No limit on duration of therapy

Doses as low as 0.01-0.03 mg/kg every 24 hours may be effective17
Gabapentin 3-20 mg/kg PO every 8-12 hours

Minimal adverse effects

One study has indicated efficacy for treatment of OA-associated pain in cats18

Oral twice- to three-times-daily administration

Can cause sedation 

Often a controlled drug

 Proven effective for calming prior to transport to the clinic, which may decrease pain, as pain causes anxiety and anxiety exacerbates pain
Amantadine (NMDA-receptor antagonist) 3-5 mg/kg PO every 12 hours

Minimal adverse effects

Potential for significant pain relief due to monoamine oxidase inhibition

Oral twice-daily administration

Efficacy can be difficult to determine

Dosing is based on one canine study and may be inadequate

Neither pharmacokinetics nor pharmacodynamics have been studied in cats
Ketamine (NMDA-receptor antagonist) 4-10 µg/kg/min IV following a loading dose of 0.5 mg/kg

Minimal adverse effects

Potential for significant pain relief due to monoamine oxidase inhibition

Patient must be hospitalized for infusion

Repeat infusions may be necessary

Proven effective in other species, particularly in patients with pain of central sensitization

Most effective dose and infusion duration are unknown and are likely highly individual
Amitriptyline (tricyclic antidepressant) 3-4 mg/kg PO every 12 hours Minimal adverse effects

Oral twice-daily administration

Cats typically do not like the taste

 Serotonin-reuptake inhibition may provide analgesia through the descending inhibitory limb of the pain pathway 
Tramadol (opioid) 1-2 mg/kg PO every 12 hours  Two studies indicate efficacy for treatment of OA-associated pain in cats19,20

Cats typically do not like the taste 

Oral twice- to three-times-daily administration

Can cause sedation or dysphoria

Controlled drug

 Adverse effects like dysphoria, sedation, and diarrhea are common at the effective dose19
Buprenorphine (opioid) 0.02-0.05 mg/kg oral transmucosal every 8-12 hours Opioid-level pain relief

Potential adverse effects

Oral twice- to three-times-daily administration

Controlled drug

Opioids are not ideal for treatment of chronic pain

 Oral transmucosal absorption is fairly low, potentially leading to the need for higher doses
*Dosage used outside the United States to treat chronic pain

The Future of Treating OA-Associated Pain

Nerve growth factor (NGF) is a cytokine that has recently been recognized as a major factor in the generation, propagation, and sensation of pain.12-14 Once released from damaged tissue, including tissue in an osteoarthritic joint, NGF rapidly escalates pain due to its impact on multiple pain pathway components, resulting in maladaptive pain.12-14 NGF binds to tropomyosin receptor kinase A (trkA receptors) and causes nociceptor sensitization, which can lead to hyperalgesia and/or allodynia; this is augmented by the release of other inflammatory mediators (eg, histamine, bradykinin) and additional NGF following NGF binding to trkA receptors on proinflammatory cells (eg, mast cells). In addition, the NGF/trkA receptor complex is internalized and transported to the neuronal cell body in the dorsal root ganglion, where it promotes the expression and/or upregulation of a variety of other pronociception ion channels and receptors, including transient receptor potential vanilloid receptor 1, which is integral for development of central sensitization.12-14 Because of profound pronociceptive involvement and the ability to rapidly produce both peripheral and central sensitization, NGF is an obvious target for the control of OA pain. Monoclonal antibodies could potentially be an option for anti-NGF therapeutics; they can bind to specific target molecules, including cytokines, and block the activity of the target. Specified (felinized and caninized) anti-NGF monoclonal antibodies for dogs and cats are in development but not yet available.15,16 In proof-of-concept studies, anti-NGF monoclonal antibodies have shown promise for relief of OA-associated pain for ≈1 month following SC injection. 

Conclusion

OA can cause maladaptive, potentially excruciating, pain in cats. Although owners may struggle to identify pain in their cat, educating owners on the prevalence of OA-associated pain and available treatment options may make owners more likely to bring their cat to the clinic. Education can be provided through numerous resources, such as posters, questionnaires, and mobility animations. Providing education to owners through these means can also help expedite a diagnosis of OA, as pointed questions regarding changes in behavior and vertical movement can help more quickly identify pain. Incorporating these tools for both the owner and the clinician can help to more readily identify and treat feline OA-associated pain, improving patient quality of life. 

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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Hills Home CB Sept 2020

Chronic & Persistent Coughing in a Dog

Douglas Palma, DVM, DACVIM (SAIM), The Animal Medical Center, New York, New York

Respiratory Medicine

|Peer Reviewed

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Chronic & Persistent Coughing in a Dog

Clinical History & Signalment

Louie, an 11-year-old, 53-lb (24-kg) neutered male Labrador retriever–poodle crossbreed, was presented for intense, productive coughing, gagging, and retching of 8 days’ duration. He had no known travel history or recent exposure to other dogs, and he was current on vaccinations and heartworm preventive. His owners reported no chronic respiratory signs, including voice change and/or coughing or gagging while eating or drinking.

Physical Examination

On physical examination, Louie was bright, alert, and responsive. Vital signs were within normal limits. His temperature was 101.3°F (38.5°C), heart rate was 80 bpm, respiratory rate was 30 bpm with normal effort, and capillary refill time was <2 seconds. Cardiac, pulmonary, laryngeal, and tracheal auscultation were all normal. No ocular or nasal discharge was present. Mild tracheal sensitivity was noted on direct palpation; abdominal palpation was normal. Several freely movable, homogeneous, subcutaneous masses were appreciated.

Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)
Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)

FIGURE 1 Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)

Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)
Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)

FIGURE 1 Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)

FIGURE 1 Thoracic radiographs showing a characteristic diffuse, patchy bronchointerstitial pattern (arrows)

Diagnosis

Differential diagnoses for acute onset cough should include canine infectious respiratory disease complex, pulmonary edema (cardiogenic or noncardiogenic), tracheal collapse, aspiration tracheitis/pneumonia, eosinophilic bronchopneumopathy (EBP), inhaled foreign bodies, and infectious disease (eg, fungal, protozoal, parasitic). Additional considerations include acute presentations of chronic processes, including bronchitis (eg, eosinophilic, chronic) or neoplasia.

Canine infectious respiratory disease complex was considered less likely based on lack of exposure to other dogs. Tracheal collapse and lung lobe torsion were of lower likelihood due to signalment, and fungal disease was considered less likely due to age and lack of exposure to enzootic areas. Heartworm disease was considered less likely based on chronic heartworm preventive administration, annual heartworm testing, and low geographic prevalence. Pulmonary edema was considered unlikely based on normal pulmonary auscultation, lack of heart murmur, and normal respiratory effort.

Thoracic radiographs revealed a moderate, diffuse, bronchointerstitial pattern (Figure 1). The cardiac silhouette, pulmonary vasculature, and extrathoracic structures were normal. Airway sampling via bronchoscopy was recommended based on radiographic findings. CBC and serum chemistry profile were performed prior to sedation. Serum chemistry results were within normal limits. CBC revealed leukocytosis (24.3 x 103/µL; normal range, 4.9-17.6 x 103/µL) characterized by marked eosinophilia (10.4 x 103/µL; normal range, 0.07-1.49 x 103/µL), monocytosis (1.4 x 103/µL; normal range, 0.13-1.15 x 103/µL), and band neutrophilia (729/µL; normal range, 0-170/µL). Heartworm antigen test was negative.

Bronchoscopic visualization revealed a moderate amount of thick, adherent, greenish-yellow mucus in the trachea and secondary and tertiary bronchi; mucosa was moderately irregular and erythematous (Figure 2). There was no evidence of airway collapse. Samples were collected via bronchoalveolar lavage for cytology, aerobic culture, and Mycoplasma spp culture.

Clinician's Brief
Clinician's Brief
Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate
Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate

FIGURE 2 Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate

Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate
Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate

FIGURE 2 Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate

FIGURE 2 Bronchoscopy results demonstrating mucosal irregularity, hyperemia, and characteristic greenish-yellow airway exudate

Cytologic evaluation revealed a marked eosinophilic inflammatory response with no evidence of bacteria or sepsis; eosinophils made up 96% of total nucleated cells. The remaining cells were consistent with nondegenerate neutrophils (2%) and alveolar macrophages (2%) (Figure 3).

Mycoplasma spp culture was negative. Aerobic culture demonstrated small growth of Citrobacter freundii, Klebsiella pneumoniae, and Stenotrophomonas maltophilia, all of which were suspected to be contaminants in the absence of septic cytology.

A Baermann test and fecal centrifugation via zinc sulfate were performed because of the peripheral eosinophilia and eosinophilic cytology; results of both were negative. Repeat Baermann testing was not pursued due to the low clinical concern; however, repeat testing may increase sensitivity in populations with higher prevalence (ie, young dogs, immunosuppressed dogs, research dogs).

Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).
Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).

FIGURE 3 Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).

Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).
Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).

FIGURE 3 Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).

FIGURE 3 Characteristic cytologic eosinophilic inflammation. Pink granules typical of eosinophils can be seen (arrows).

DIAGNOSIS:

EOSINOPHILIC BRONCHOPNEUMOPATHY

Treatment & Long-Term Management

Treatment for EBP requires anti-inflammatory medications (see Treatment at a Glance). Louie was discharged on fenbendazole (1500 mg [50 mg/kg] once daily for 14 days) and prednisone (30 mg every 12 hours [2 mg/kg/day] for 5 days tapered to 20 mg every 12 hours [1.5 mg/kg/day] for 5 days; 15 mg every 12 hours [1 mg/kg/day] for 2 weeks; 10 mg every 12 hours for 2 weeks [0.67 mg/kg/day]; 10 mg every 24 hours for 2 weeks [0.33 mg/kg/day]; and finally 10 mg every 48 hours [0.33 mg/kg every other day]. Based on Louie’s clinical response, eventual discontinuation of steroids could have been considered.

Louie’s owner was asked to report any clinical signs (eg, coughing, gagging, retching) and corticosteroid adverse effects before each taper. Recheck examination and repeat radiography were recommended 1 month after discharge.

Treatment of inflammation should include corticosteroids, with or without immunomodulating medications, which should be gradually and slowly tapered. In endemic regions, concurrent treatment for parasitic disease (fenbendazole, 50 mg/kg for 10-14 days) should be considered to address migrating nematodes and/or primary pulmonary or tracheal parasites (eg, Paragonimus kellicotti, Filaroides spp, Crenosoma vulpis, Oslerus osleri), as false-negative results from traditional fecal testing are possible.

TREATMENT AT A GLANCE

  • Treatment should be provided for parasitic disease if necessary (ie, fenbendazole 50 mg/kg every 24 hours for 10 to 14 days.
  • Prednisone should be initiated at 1 to 2 mg/kg/day.
  • Prednisone should be tapered gradually, ideally every 1 to 2 weeks to the lowest effective dose.
  • Clinical signs should be monitored, and regular communication with the pet owner is recommended.
  • Radiography should be repeated to assess the patient’s response to treatment.
  • Relapse is common, and long-term therapy may be necessary.
  • Steroid adverse effects should be minimized; if these are excessive, alternative medications may include other immunosuppressants (eg, cyclosporine, azathioprine) and/or inhaled corticosteroids (eg, fluticasone, beclomethasone).

Prognosis & Outcome

At 1 week after discharge, Louie’s owner reported he had marked improvement in coughing (ie, ≈80% reduction) and increased energy; however, his owner also noted Louie had excessive thirst, urination, and appetite. At 2 weeks, his owner reported intermittent coughing and persistent signs of corticosteroid excess.

At 1 month after discharge, thoracic radiography was repeated and revealed marked improvement in diffusion of the bronchointerstitial pattern (Figure 4). Prednisone was tapered over the next 6 weeks to 10 mg every other day. Intermittent coughing returned, and the dosage was increased to 10 mg once daily (0.33 mg/kg/day), which maintained clinical control. Because this regimen did not result in significant adverse effects and maintained clinical control, adjunctive or alternative anti-inflammatory medications were not prescribed.

Louie was managed on a low dose of prednisone (10 mg once daily) for 5 years with no complications. The primary care clinician attempted to taper prednisone but was unsuccessful—coughing returned as the frequency of medication was reduced.

Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern
Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern

FIGURE 4 Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern

Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern
Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern

FIGURE 4 Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern

FIGURE 4 Radiograph 1 month after therapeutic initiation showing an improved bronchointerstitial pattern

Discussion

EBP (historically known as pulmonary infiltrates with eosinophils) is a disease characterized by eosinophilic infiltration of lung and bronchial mucosa and an important differential diagnosis for patients presented with chronic cough, acute onset of respiratory distress, and/or exercise intolerance.1,2 Cough is typically harsh and may be associated with gagging and retching.

This disease can be seen at any age; however, dogs 4 to 6 years of age are most commonly represented.1-3 Although Siberian huskies and Alaskan malamutes may be overrepresented,2 the disease can occur in any dog breed.

Physical examination findings may reveal abnormal lung sounds, but auscultation can be normal.1,2 In addition, ≤24% of patients may have concurrent nasal discharge.1,2,4

Diagnosis requires strong clinical suspicion, as EBP is an uncommon cause of the primary clinical signs (ie, coughing, gagging, exercise intolerance). CBC may reveal an inflammatory leukogram (eg, eosinophilia, neutrophilia) in ≤60% of cases.4 Eosinophilia may raise clinical suspicion, but its absence does not rule out disease, as it is only present in 50% to 60% of cases.1,2,5

Thoracic radiographs are generally characterized by a diffuse bronchointerstitial pattern with peribronchial cuffing and thickening of the bronchial walls. In some cases, bronchiectasis or alveolar infiltration may be observed.2,6-8 Occasionally, patchy pulmonary opacities create a nodular appearance.4 Radiography is critical for ruling out other common causes of cough and/or acute respiratory distress. Concurrent disease processes (eg, cardiomegaly, tracheal collapse) can complicate diagnosis.

EBP on thoracic computed tomography has been characterized by parenchymal abnormalities (93%) and bronchial wall thickening (87%) in most dogs. Many dogs also had mucus and/or debris that occluded the bronchial lumen (73%), lymphadenopathy (67%), or bronchiectasis (60%).9 Approximately 33% of dogs had pulmonary nodules, as has been identified on radiographs.4,9

Cytologic evaluation of the airways confirms eosinophilic inflammation, which is the hallmark of diagnosis. The percentage of eosinophils (mean, 61% of the total nucleated cell population4) exceeds that of healthy dogs (5%-24%).2,5,10 Samples can be obtained via tracheal wash or bronchoscopy. Bronchoscopy allows for visualization of more characteristic airway associated changes (eg, greenish-yellow secretions, irregular mucosa, hyperemia).2,5,11 Occasionally, intraluminal granulomas may be present,4 allowing for mucosal brush samples or biopsies that can further support a diagnosis. Tracheal washes provide appropriate cytologic samples in most cases. Bronchoscopy is generally reserved for patients with more focal radiographic disease, concerns for neoplasia, or suspicion for concurrent structural disorders (eg, bronchial collapse, tracheal collapse). 

Cytologic evaluation is critical to help rule out parasitic disease that can also result in eosinophilic inflammatory response. Fecal testing (ie, Baermann test, fecal centrifugation) for parasitic disease is recommended; however, because negative results do not rule out parasitic disease, repeat testing and/or empirical therapy is advisable, particularly in at-risk patients.12 Heartworm testing is also indicated because heartworm disease may be associated with pneumonitis and eosinophilic inflammation (Table).13

Table

COMMON FINDINGS IN EOSINOPHILIC BRONCHOPNEUMOPATHY

Clinical signs

Coughing

Acute respiratory distress
Radiographic evaluation

Bronchointerstitial pattern

Peribronchial cuffing

Alveolar disease

Bronchiectasis

Nodular pattern
CBC Leukocytosis ± eosinophilia
Airway cytology Eosinophilic ± neutrophilic airway cytology
Airway culture Generally negative
Bronchoscopy

Greenish-yellow secretions

Irregular, hyperemic mucosa

± nodular changes

 

Eosinophilic bronchitis (EB), eosinophilic granuloma (EG), and EBP have been retrospectively evaluated and may provide information regarding therapeutic response, indications for chronic therapy, and overall prognosis.4 EB is associated with less severe airway remodeling, reduced eosinophilic inflammation (ie, percent of nucleated cells in airway samples), reduced total inflammation (bronchoalveolar lavage total nucleated cell count/µL), and lower incidence of peripheral eosinophilia. Patients with EG demonstrate intraluminal granulomas/masses not present in EBP. Overlap still exists among these disorders, and the impact on therapeutic outcome is not yet known; however, EB may be more responsive and EG less responsive to therapy.4 Eosinophilic pulmonary granulomatosis may also be associated with eosinophilic inflammation, but it is least common and may represent a spectrum of disease characterized by masses that involve the pulmonary parenchyma (not exclusively luminal). EPG may also have systemic organ involvement and be the least responsive to therapy.14,15

Corticosteroids are the mainstay of therapy. Prednisone is typically initiated at 1 to 2 mg/kg/day and gradually tapered to the lowest effective dose.1,2,4 It is important to note that clinical relapse is common and can reach ≈30% after corticosteroids are tapered.5 In some cases, medications can be discontinued after months with no evidence of relapse. Some clinicians may taper the drug faster, but the author believes that tapering faster than 1 to 2 weeks may increase the rate of relapse.

Patients with severe signs (eg, hypoxemia, oxygen dependency, alveolar disease) may also benefit from higher doses initially.

Alternative options for management include inhaled corticosteroids or additional immunosuppressive medications. Fluticasone has been evaluated and may be successful in some cases but is not always adequate for maintaining clinical remission.16 The author has successfully used cyclosporine in some cases in which corticosteroid adverse effects were intolerable. However, cyclosporine and other immunosuppressive drugs (eg, azathioprine, mycophenolate) have not been evaluated in randomized, controlled studies despite sporadic clinical use. Cyclosporine has been used for the treatment of other eosinophilic disorders in dogs.17,18

TAKE-HOME MESSAGES

  • EBP should be considered in patients with chronic cough and in patients with acute respiratory distress.
  • Radiographs may reveal nodules, mimicking neoplasia.
  • Absence of eosinophilia does not rule out the disease.
  • Diagnosis requires cytologic evaluation. 
  • Parasitic disease can mimic EBP and cannot be definitively ruled out with negative testing. 
  • Corticosteroids (ie, prednisone) are the hallmark of therapy.
  • Patient relapse is common and may necessitate long-term management.
  • Inhaled steroids may not always control the disease.

References

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

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

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

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NVA CB Sept 2020

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Endoscopy CB Sept 2020

Separation Anxiety in a Dog with Fear-Based Behavior

Leslie Sinn, CPDT-KA, DVM, DACVB, Behavior Solutions for Pets, Hamilton, Virginia

Behavior

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Separation Anxiety in a Dog with Fear-Based Behavior

A 6-year-old spayed terrier crossbreed is presented for a 2-month history of crying and barking when left at home alone. The behavior began 2 weeks after the patient was adopted from a local animal shelter. She becomes increasingly agitated (eg, panting, whining, following her owners) when her owners prepare to leave the home; when the owners return, she exuberantly greets them, engaging in marked attention-seeking behaviors (eg, standing on hindlimbs, frantically pawing at the owners) and requiring at least 15 minutes to settle.

The owners provide a video of the patient vocalizing when crated (see Video) and report that she pants, paces, vocalizes, and chews and paws at doors and window frames when not crated (Figure). These behaviors continue for the duration of the owners' absence. The owners have crated the dog, offered long-lasting chews before departures, and used verbal reprimands, none of which have impacted her behavior. The dog does not have a history of aggression toward humans or other animals.

No abnormalities are observed on physical examination. CBC, serum chemistry profile, total thyroxine, and urinalysis are unremarkable. On examination, the patient is visibly trembling, refuses food, and remains crouched on the owner’s lap with ears down, tail tucked, and eyes averted. To avoid exacerbating her fearful response to handling, temperature is not obtained.

Diagnoses of separation anxiety and fear-based behaviors in the veterinary setting are made.

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Video Video provided by client of the patient vocalizing

The patient damages door frames when not crated during owner absence.
The patient damages door frames when not crated during owner absence.

FIGURE The patient damages door frames when not crated during owner absence.

FIGURE The patient damages door frames when not crated during owner absence.

Which of the following drugs would be appropriate for this patient’s separation anxiety?

Based on the information provided, how would you grade the following drugs and why?

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.

Alprazolam

Correct ResponseSafeAlprazolam is a short-acting benzodiazepine that exerts anxiolysis by enhancing the effect of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Alprazolam should be administered 30 to 60 minutes prior to the stressful event (eg, departure of pet owners, arrival to the veterinary clinic).1,2 Because time to onset is variable and paradoxical reactions (eg, increased restlessness, hyperactivity) may be observed, the owners should be advised to administer a test dose prior to using this medication in a stressful situation. Because alprazolam is short-acting (ie, 4-6 hours), a longer-lasting maintenance medication will also be needed to treat this patient’s separation anxiety.

Acepromazine

Correct ResponseDo Not UseAcepromazine is a phenothiazine tranquilizer that blocks dopamine receptors and increases the dopamine turnover rate. It is a CNS depressant that induces sedation and muscle relaxation. Acepromazine has poor anxiolytic properties and should never be used as a sole agent when treating anxiety disorders. The only exception is when the drug is used in conjunction with an anxiolytic to prevent self-injury or trauma.

Trazodone

Correct ResponseSafeTrazodone is a serotonin antagonist and reuptake inhibitor that functions by enhancing serotonin, dopamine, and norepinephrine, resulting in antidepressant, hypnotic, and anxiolytic effects. This drug has been demonstrated to be an efficacious adjunctive medication for the treatment of separation anxiety.3 Trazodone has a mild sedative effect, which can be highly advantageous in animals that panic and/or are destructive.3 Occasionally, paradoxical reactions (eg, restlessness, hyperactivity) are observed; owners should be advised to administer a test dose before using trazodone in a stressful situation. Trazodone should be administered 2 hours prior to departures or veterinary visits. Because trazodone is short-acting, a longer-lasting maintenance medication will also be needed to treat this dog’s separation anxiety.

Gabapentin

Correct ResponseSafeGabapentin functions by inhibiting calcium channels. It is used to treat pain and epilepsy in humans and has anxiolytic and sedative properties. Sleepiness is a common adverse effect and may be advantageous in the treatment of separation anxiety. Gabapentin should be administered 1 to 2 hours prior to veterinary visits or departures. Because gabapentin is short-acting, a longer-lasting maintenance medication will also be needed to treat this patient’s separation anxiety. Of note, gabapentin remains a frequent choice as a short-acting departure medication used in the treatment of separation anxiety despite little research supporting its use.

Clonidine

Correct ResponseProceed with CautionClonidine is a selective α2-receptor agonist that blocks norepinephrine release in the locus coeruleus, which induces noradrenergic stimulation. It is short-acting and requires 1 to 2 hours to reach full effect. Clonidine has been shown to be an effective adjunctive medication for treatment of canine separation anxiety.4 Because it is a hypotensive agent, clonidine should be used with caution (ie, not as a first-choice drug) in older patients and patients with cardiovascular disease. Adverse effects may include increased water intake, incoordination, sedation, and constipation.4 Owners should be advised to administer a test dose before using this drug in a stressful situation. Because clonidine is short-acting, a longer-lasting maintenance medication will also be needed to treat this patient’s separation anxiety.

Fluoxetine

Correct ResponseSafeFluoxetine is a selective serotonin reuptake inhibitor that provides anxiolysis by increasing serotonin levels in the neurosynaptic cleft. Common adverse effects include drowsiness, loss of appetite, and occasional diarrhea. Fluoxetine is FDA-approved for the treatment of separation anxiety in dogs in conjunction with behavior modification. Although improvement may be seen as soon as the first week, in most cases, the medication must be administered daily for 4 to 6 weeks to be effective.5 Thus, a short-acting medication should be used prior to departures to provide additional needed support. Some dogs can tolerate separation once the maintenance medication is initiated, whereas others require lifelong departure drugs and maintenance medication.

Clomipramine

Correct ResponseSafeClomipramine is a tricyclic antidepressant that helps reduce anxiety by the selective inhibition of neuronal reuptake of serotonin and has lesser effects on neuronal reuptake of norepinephrine. It must be administered daily as a maintenance medication. Common adverse effects include drowsiness, loss of appetite, urine retention, and occasional diarrhea. Clomipramine is FDA-approved for the treatment of separation anxiety in dogs in conjunction with behavior modification. Improvement can be seen as quickly as 1 week, but maximum effectiveness in most cases takes 8 to 12 weeks6; a short-acting medication should therefore be used prior to departures to provide needed support. Some dogs can tolerate separation once the maintenance medication is initiated, whereas others require lifelong departure drugs and maintenance medication.

Dog-Appeasing Pheromone

Correct ResponseSafeDog-appeasing pheromone is a mimic of the pheromone released from nursing dams that provides a sense of reassurance and calm to help dogs adjust to stressful situations (eg, triggering noises, travel) and new environments. The efficacy of dog-appeasing pheromone for treatment of separation anxiety has been demonstrated.7 This product is appropriate for mild cases of separation anxiety and fear-based behaviors and when used as a component of a comprehensive treatment plan.

L-Theanine

Correct ResponseProceed with CautionThe available research on L-theanine is limited but appears promising.8,9
Theanine is an amino acid found in green tea that binds to glutamate receptors in the brain, countering neural stimulation at these sites. This effect causes a subsequent rise in GABA, thereby inhibiting neural transmission and excessive firing associated with anxiety.8 Although it can be used as a sole agent to help address mild distress due to separation, theanine is best used as part of a comprehensive treatment plan with other psychoactive medications when clinical signs of separation anxiety are escalated.

Rescue Remedy

Correct ResponseDo Not UseRescue Remedy contains extracts of rockrose, impatiens, clematis, Star of Bethlehem, and cherry plum. No research is available regarding its efficacy in animals. A double-blind, placebo-controlled study in humans demonstrated no effect.10 When discussing this product with owners, the clinician should keep in mind that the placebo effect can be as high as 45%.11

α-Casozepine

Correct ResponseProceed with Cautionα-Casozepine is a supplement derived from milk protein. It affects GABA receptors and has benzodiazepine-like properties, resulting in an anxiolytic effect. α-Casozepine can be used as a sole agent to help address mild fear and anxiety or as part of a comprehensive treatment plan in conjunction with other psychoactive medications.12,13 Although it can be used as a sole agent to help address mild distress due to separation, α-casozepine is best used as part of a comprehensive treatment plan with other psychoactive medications when clinical signs of separation anxiety are marked.

References

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

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