November 2018   |   Volume 16   |   Issue 11

Subclinical Bacteriuria

in this issue

in this issue

Management of Subclinical Bacteriuria

Top 5 Substances that Affect Blood Glucose

Iatrogenic Hypothyroidism Following Radioiodine Treatment

Subclinical Subaortic Stenosis in a Golden Retriever

Top 5 Tips for Sedation & Anesthesia in Fractious Dogs

Content continues after advertisement

Hill's Cover Tip CB Nov 2018

Content continues after advertisement

Proviable CB Nov 2018

Top 5 Substances that Affect Blood Glucose

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

Sign in to Print/View PDF

Top 5 Substances that Affect Blood Glucose

Glucose homeostasis requires that blood glucose be constrained within a narrow concentration. Homeostasis is accomplished through diverse physiologic mechanisms that work together to precisely regulate glycemia. Abnormalities in blood glucose (ie, hyperglycemia, hypoglycemia) occur when physiologic regulation is disrupted (eg, during disease states or metabolic disturbances). In some circumstances, medications and toxins may also affect blood glucose regulation; for example, many drugs produce glucose disturbances in humans and may cause similar disturbances in dogs and cats (see Drugs that Can Alter Blood Glucose in Humans).

Following are the author’s top 5 substances that exert significant effects on blood glucose regulation in dogs and cats and the clinical situations in which they may be encountered.

1

Insulin

Insulin, secreted from β cells in the pancreatic islets of Langerhans, produces a potent hypoglycemic effect through its physiologic role as a hormone or when used as a replacement hormone to manage diabetes.1 Insulin-induced hypoglycemia caused by naturally occurring disease is rare, but clinical disorders (eg, canine insulinoma) can occur.2 In contrast, pharmacologic insulin preparations are the most potent hypoglycemic agents in routine clinical use.1 Various modifications have been made to alter the pharmacologic properties of endogenously produced insulin, the mainstay for diabetes treatment in dogs and cats. These modifications, which have expanded the clinical efficacy of insulin preparations, may also produce severe hypoglycemia when administered inappropriately or after overdose. The endogenous hormone and all insulin preparations produce hypoglycemia via identical mechanisms, but pharmacologic modifications may cause the magnitude and duration of the hypoglycemic effect to be more pronounced.3

In most tissues, especially muscle and adipose tissue, insulin binds to specific insulin receptors on the surface of most cells.4 After binding, receptor activation initiates a cascade of intracellular steps that culminates with the insertion of glucose transporters into the cell membrane and activation of cellular glucose uptake. In the liver, insulin serves as a regulator of glucose storage and production. Insulin activates glycogenesis and inhibits gluconeogenesis, both of which reduce blood glucose.5 The hypoglycemic effects wane when blood insulin is low or absent.

DRUGS THAT CAN ALTER BLOOD GLUCOSE IN HUMANS*

Drugs that Induce Hypoglycemia

  • Insulin
  • Glucose-lowering drugs
    • Biguanides
    • Sulfonylureas
    • Glucagon-like peptide-1 (GLP-1) analogs
  • ACE inhibitors
  • β blockers
  • Antibiotics
    • Quinolone antibiotics
    • Chloramphenicol
  • Disopyramide
  • Ethanol
  • Salicylates

Drugs that Induce Hyperglycemia

  • Corticosteroids
  • Quinolone antibiotics
  • Antipsychotics
  • β blockers
  • Calcineurin inhibitors (eg, cyclosporine)
  • Protease inhibitors
  • Thiazide diuretics
*Hypo- or hyperglycemia has been reported as an adverse effect of many drugs used in human medicine. Some drug classes (eg, β blockers, quinolone antibiotics) appear on both lists because separate drugs within the class can cause hyper- and hypoglycemia. It is possible that these drugs exert similar actions on blood glucose in dogs and cats, although hypo- or hyperglycemic effects of many infrequently prescribed drugs are not well documented in these species.

2

Glucocorticoids

Glucocorticoids are a chemical class of hormones and synthetic drugs that includes cortisol, hydrocortisone, prednisone, dexamethasone, and less familiar hormones and drugs. They exert a wide range of effects on carbohydrate, protein, and lipid metabolism and are involved in regulation of inflammatory processes and the immune system.6 The principal glucocorticoid effect on glucose homeostasis is promotion of hyperglycemia, which can be marked in the presence of supraphysiologic or pharmacologic glucocorticoid concentrations.7

Hyperglycemia caused by glucocorticoid excess can arise as a consequence of naturally occurring endocrine disorders or exposure to exogenous glucocorticoid substances.8,9 Any condition that increases adrenal production of glucocorticoids can produce hyperglycemia, including physiologic responses. In dogs, hyperadrenocorticism (ie, Cushing’s disease) is the most common endocrinopathy associated with glucocorticoid overproduction and hyperglycemia.10 In affected dogs, hyperglycemia occurs in the presence of excess plasma cortisol and other glucocorticoids, caused by adrenal hyperplasia or functional adrenocortical neoplasia.11 Physiologic distress (eg, due to illness or fear) can result in hyperglycemia caused by activation of an adrenal hormone response (ie, stress hyperglycemia), which includes hypercortisolemia and elevations in catecholamines.12 Stress hyperglycemia can occur during illness and is a common finding in otherwise healthy dogs and cats.

Exogenous glucocorticoids may also cause hyperglycemia.13 Glucocorticoid preparations are among the most frequently prescribed drugs in small animal medicine. The potency of synthetic glucocorticoids, including prednisone and dexamethasone, is much greater than hydrocortisone. Thus, these preparations may produce substantial side effects, even when used at appropriate pharmacologic doses.14 Hyperglycemia can develop as a side effect of oral, injectable, or topical glucocorticoid administration.15

Endogenous and exogenous glucocorticoids induce hyperglycemia by the same mechanism, referred to as insulin resistance.16 Glucocorticoids reduce tissue sensitivity to insulin, which antagonizes the hypoglycemic actions of insulin. The insulin-resistant state is characterized by a subnormal biologic response to normal concentrations of insulin.16

3

Xylitol

Xylitol is a 5-carbon sugar alcohol used as an artificial sweetener in many commercial products (eg, chewing gum, drugs, candies).17 Although safe for humans and most other mammals, xylitol induces severe hypoglycemia after ingestion in dogs.17 Along with hypoglycemia, xylitol toxicity may cause hepatic necrosis that may progress to liver failure in some dogs, which may contribute to hypoglycemia via a separate mechanism.18

Xylitol appears to be a potent stimulator of insulin secretion in dogs; this effect has not been observed in other mammals.19 The increase in plasma insulin induced by xylitol stimulates tissue uptake of glucose, leading to severe hypoglycemia. The mechanism that leads to hepatic necrosis, characterized by severely increased serum alanine transaminase (ALT) activity, is not completely known but may involve adenosine triphosphate (ATP) depletion.20

4

Growth Hormone

Growth hormone (GH; ie, somatotropin) is produced and secreted by the anterior pituitary.21 In adulthood, GH is a component of the counter-regulatory response to hypoglycemia and stress.22

GH secretion disorders are uncommon causes of blood glucose disturbances in dogs and cats. The most frequently encountered clinical disorder of GH secretion is feline acromegaly.23 Acromegaly in cats is caused by excessive GH secretion from a pituitary adenoma that causes hyperglycemia through induction of insulin resistance in muscle and adipose tissue.23,24 Hyperglycemia can be severe, and affected cats often have diabetes mellitus on presentation for hyperglycemia treatment.25

5

Progestins

Progestins are a class of natural and synthetic compounds with actions that mimic those of progesterone.26 Exposure to progesterone or progestins may produce alterations in blood glucose homeostasis in dogs and cats, although the circumstance under which the aberration occurs differs between the species. In dogs, progesterone and synthetic progestins stimulate GH secretion from mammary tissue, which contributes to insulin resistance in body tissues.27 Progesterone-induced insulin resistance can be severe enough to induce diabetes mellitus in some pregnant dogs, which may resolve following pregnancy termination.28,29 In countries where long-acting progestins are used to impede estrus cycling, treated dogs may develop hyperprogestinemia and, eventually, acromegaly as a result of persistent stimulation of GH release.29

In cats treated with megestrol acetate, a synthetic progestin, hyperglycemia or even overt diabetes mellitus may develop.30 Progestin-induced hyperglycemia in cats does not have a clear link to elevated GH concentration, and the exact mechanism by which progestins induce carbohydrate intolerance in cats is unknown.31

Poll

Have you ever had a feline patient develop diabetes after treatment with methylprednisolone acetate?


GH = growth hormone

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.


Content continues after advertisement

WVC CB Nov 2018

Content continues after advertisement

Adequan Canine CB Nov 2018

Subclinical Subaortic Stenosis in a Golden Retriever

Kursten Pierce, DVM, DACVIM (Cardiology), Colorado State University

Cardiology

|Peer Reviewed

Sign in to Print/View PDF

Subclinical Subaortic Stenosis in a Golden Retriever

THE CASE

A 12-month-old intact female golden retriever is presented for a wellness examination and to discuss the pros and cons of breeding the patient versus pursuing ovariohysterectomy. The owner would like her to produce one litter of puppies prior to being spayed.

On physical examination, the patient is bright, alert, and responsive. She is extremely energetic with a good BCS (4/9) and appropriate musculature. Cardiovascular examination reveals pink mucous membranes, no obvious jugular venous distension, and a normal heart rate and rhythm with normal synchronous femoral pulses. Auscultation is difficult and brief because the patient is rambunctious and panting. Despite the panting, she is eupneic with clear bronchovesicular sounds. A grade II/VI left basilar systolic heart murmur is auscultated. A murmur had not previously been documented at her puppy wellness visits. The owner has not observed any coughing, trouble breathing, exercise intolerance, or syncope at home, and the patient appears subclinically affected.

Diagnostic investigation of the heart murmur via echocardiography is discussed with the owner but declined due to the patient’s lack of clinical signs and the costs associated with additional testing.

What are the next steps? 

THE CHOICE IS YOURS …

CASE ROUTE 1

To provide information on breeding and caring for a pregnant bitch and neonatal puppies and plan to spay the patient after the puppies have been weaned.

CASE ROUTE 2

To avoid providing additional recommendations regarding breeding and ovariohysterectomy to the owner until a diagnostic investigation with a cardiologist has been pursued.

Poll

Which option did you choose?


CHF = congestive heart failure, LVOT = left ventricular outflow tract, SAS = subaortic stenosis

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.


Content continues after advertisement

PNC CB Nov 2018

Content continues after advertisement

Drontal CB Nov 2018

Top 5 Tips for Sedation & Anesthesia in Fractious Dogs

Katherine Bennett, DVM, University of Tennessee

Christine Egger, DVM, MVSc, CVA, CVH, DACVAA, University of Tennessee

Sign in to Print/View PDF

Top 5 Tips for Sedation & Anesthesia in Fractious Dogs

FIGURE 1 A long extension set directly connected to the catheter, which is placed in the lateral saphenous vein. An injection port is accessible (out of frame).

Aggression represents over 50% of behavior-related problems in dogs,1 and fractious animals pose an inherent risk to veterinary staff. Behavior management is the ideal long-term solution for aggressive or fractious animals; however, some surgical or diagnostic procedures require relatively immediate attention and preclude most recommended behavior modifications. Precautions should be taken to ensure both patient and team safety when sedating or anesthetizing these patients.

Following are the authors’ tips for safe handling of a sedated or anesthetized fractious dog presented for diagnostic or surgical procedures. 

1

Owner Communication

Communication with the pet owner ahead of the scheduled appointment is critical. Discussion should include current medications, patient behavior at home, and whether the owner is comfortable medicating the patient at home. Owner involvement can help facilitate a team-based approach to safe and effective patient sedation.2 In addition, a thorough risk assessment should be explained to the owner, as many sedative medications can have adverse effects on patients with underlying diseases, particularly cardiovascular disease. Patients with underlying systemic disease may require dose alterations and/or alternative drug protocols to account for comorbidities.

2

Preappointment Preparation

At-home administration of one or more sedatives (eg, trazodone, clonidine, dexmedetomidine, acepromazine, alprazolam; Table 1) the day before and the day of the scheduled visit allows for multimodal anxiolysis and can facilitate delivery of additional sedatives in the clinical setting. Caution should be taken when prescribing multiple serotonin-altering medications, as serotonin syndrome is a potentially lethal side effect (see Serotonin Syndrome).3 Combining different medications or introducing new serotonin-altering medications to a dog’s treatment protocol can have deleterious effects; owners should be informed that, although uncommon, disinhibition of behavioral tendencies4 and/or development of aggression5 can occur at home. If adverse behavioral effects or signs of serotonin syndrome do not occur, the dose can be gradually increased over 1 to 2 days until the desired dose is reached or the desired effect is achieved.6 Alternatively, medications that do not alter serotonin levels (eg, α2 agonists, benzodiazepines, gabapentin) can be used.

Serotonin Syndrome

Serotonin syndrome, defined as a group of clinical signs associated with administration of serotonin-altering medications (eg, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, antidepressants), although rare in veterinary medicine, can occur when multiple serotonin-altering medications are coadministered.18 Clinical signs of serotonin syndrome include altered mental status, agitation, nervousness, myoclonus, hyperreflexia, tremors, diarrhea, incoordination, increased heart rate and blood pressure, and hyperthermia.19 If a patient is already receiving medications for behavior alteration or other reasons, slow introduction of additional medications at lower doses is recommended. Any signs of agitation, restlessness, or myoclonus may suggest serotonin syndrome, and cessation of any additional serotonin-altering medications is recommended.

Common at-home administration protocols include administering oral trazodone, gabapentin, and alprazolam the day before the appointment and on the morning of the scheduled appointment or administering oral acepromazine, gabapentin, and alprazolam, potentially coadministered with maropitant (2 mg/kg PO q24h) to decrease the risk for vomiting after later administration of injectable sedatives (especially those that contain a pure μ opioid).7

Table 1

Perioperative Anxiolytic & Sedative Dosages in Dogs15-17

Drug (Drug Category) Dosage*
Acepromazine (phenothiazine) 0.5-2 mg/kg PO q8h
Alprazolam (benzodiazepine) 0.02-0.04 mg/kg PO q6h
Clonidine (α2 agonist) 0.01-0.05 mg/kg PO q12h
Dexmedetomidine gel (α2 agonist) Refer to product insert
Diazepam (benzodiazepine) 1-2 mg/kg PO q8h
Gabapentin (anticonvulsant, neuropathic pain analgesic) 5-10 mg/kg PO q8-12h
Trazodone** (serotonin antagonist and reuptake inhibitor) 2-10 mg/kg PO q8-12h
*Some dosages are anecdotal based on those used in the authors’ facility.
**Indicates commonly prescribed medications that, when combined with other serotonin-altering drugs, may place the patient at risk for serotonin syndrome. Careful and controlled introduction of medication combinations can help mitigate risks for serotonin syndrome development.

3

Sedation Administration

Many patients may become more stressed in the hospital waiting area, making it more difficult for sedative medications to reach full efficacy. The owner should be advised to place a muzzle and/or Elizabethan collar on the patient before or just after arrival, if possible. If available, other parts of the hospital (eg, parking lot, grassy relief area, barn) can be used as an environmental distraction for the patient during handling, waiting, and/or sedative administration.8 Because dogs use multiple cues (eg, visual, auditory, olfactory) to influence their behavior and/or reactions to their environment,9 soft and calm voices and limited personnel involvement are recommended. Pheromone sprays can help reduce anxiety but have not been shown to consistently reduce aggression in dogs.10

White coat syndrome (ie, the increase in a patient’s sympathetic response to stress due to the appearance of medical personnel in white coats or similar clothing) has been well documented in human medicine.11-13 To reduce the perceived threat of medical personnel, staff members who interact with the patient should avoid wearing white coats or similar hospital clothing while initially handling the patient (ie, from arrival to administration of injectable sedation). Typically, a coat or other outerwear is recommended to be worn over hospital clothing.11,12

Administering sedation via an intramuscular injection (Table 2) is preferable and can be done while the patient is walking on a leash, provided the person handling the patient and the person administering the drugs are both experienced enough for a rapid pelvic limb injection and subsequent patient reaction. These drugs are typically used in combination to provide deep sedation and/or general anesthesia. Combining different drug classes (Table 3) allows for a dose reduction in all agents, thereby potentially limiting negative adverse effects.

Table 2

Sedative Dosages in Dogs15-17

Drug Dosage* Duration of Full Effect**
Acepromazine 0.01-0.03 mg/kg IM 6-8 hours
Alfaxalone 1-3 mg/kg IM 15-20 minutes
Butorphanol 0.1-0.4 mg/kg IM 30-60 minutes
Dexmedetomidine 1-10 µg/kg IM (not to exceed 10 µg/kg) 30-60 minutes
Hydromorphone 0.05-0.1 mg/kg IM 4-6 hours
Ketamine 3-10 mg/kg IM 30-60 minutes
Midazolam 0.1-0.5 mg/kg IM 20-40 minutes
Tiletamine/zolazepam 1-4 mg/kg IM 30-60 minutes
*Some dosages are anecdotal based on those used in the authors’ facility.
**Most drugs have a dose-dependent duration of effect (ie, higher doses usually prolong the effect); however, higher doses can also increase the frequency of adverse events.

Table 3

Sedative Combinations & Dosage Recommendations in Dogs15-17

Drug Combination* Dosage** Effect

Combination 1

Butorphanol

Dexmedetomidine

Tiletamine/zolazepam

 

0.4 mg/kg IM

5 µg/kg IM

3 mg/kg IM

 

High level of sedation with mild analgesia

Combination 2

Hydromorphone

Dexmedetomidine

Ketamine

 

0.1 mg/kg IM

5 µg/kg IM

2 mg/kg IM

 

Higher degree of analgesia with good sedation

Combination 3

Butorphanol

Alfaxalone

Midazolam

 

0.4 mg/kg IM

2 mg/kg IM

0.5 mg/kg IM

 

Dissociative anesthetics or α2 agonists are not recommended in patients with questionable cardiac disease or significant comorbidities

*Opioids can be substituted within their drug class (eg, butorphanol substituted for hydromorphone) if goals for pain management require a different opioid.
**Doses can be adjusted based on recommended dosing ranges (Table 2). Some dosages are anecdotal based on those used in the authors’ facility.
Any opioid can be substituted for hydromorphone based on availability.

Other handling techniques involve using a half-wall or chain link fence as a barrier between the patient and the injector/handler. An ideal sedative protocol, as recommended in human medicine, is rapid-acting with minimal side effects, although, without physical examination, adverse effects are difficult to predict in fractious patients.13 Of note, most anesthetic drugs are associated with some degree of risk14; this risk is increased in patients that are unable to be assessed for pre-existing comorbidities (eg, heart disease). Reversible drugs (eg, α2 agonists, opioids) are preferable, as their adverse effects can be mitigated with reversal agents if necessary.

Some patients may become sedate enough to lose airway protection. Supplies for intubation and appropriate ventilation should always be available for patients that show signs of requiring a protected airway or ventilatory support (eg, cyanosis, shallow breathing, regurgitation).

4

Patient Handling While Hospitalized

Fractious patients may require additional precautions for handling and drug administration while hospitalized. Standard monitoring procedures are recommended with the patient sedated or anesthetized. Hospitalization of fractious animals typically requires planning.

Placement of an IV catheter in a pelvic limb can be advantageous, as it provides more room between the patient’s head and the injection site. If pelvic limb catheter placement is not feasible, additional placement of long extension sets attached to the IV catheter (Figure 1, top of page) can facilitate semi-remote drug administration and provides an additional level of safety for the patient and staff.

An Elizabethan collar and/or basket muzzle can be used to provide additional safety for aggressive patients, and allowing patients to wear a harness with an attached leash while in a cage can be helpful when removing them from the confined space (Figure 2). Floor-level cages or runs are preferred, as they prevent the need for the handler to lift the patient out of the cage and onto the floor or into a carrier. Muzzles with connections suitable for oxygen delivery are also helpful for providing flow-by oxygen to aggressive patients.

To ensure patient and staff safety, an Elizabethan collar and a harness are used on the patient, with the leash attached to the harness and placed toward the cage door.
To ensure patient and staff safety, an Elizabethan collar and a harness are used on the patient, with the leash attached to the harness and placed toward the cage door.

FIGURE 2 To ensure patient and staff safety, an Elizabethan collar and a harness are used on the patient, with the leash attached to the harness and placed toward the cage door.

FIGURE 2 To ensure patient and staff safety, an Elizabethan collar and a harness are used on the patient, with the leash attached to the harness and placed toward the cage door.

5

Recovery & Discharge

For outpatient procedures (eg, outpatient surgery, diagnostic procedures) requiring sedatives/anesthetic drugs, a basket muzzle can be modified so that the endotracheal tube can be removed through the muzzle, which allows the muzzle to be placed on the patient prior to extubation and be in place at the end of the procedure (Figure 3). This facilitates safety in the recovery period while still allowing the patient to be closely monitored.

Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 
Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 

FIGURE 3 Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 

Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 
Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 

FIGURE 3 Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 

FIGURE 3 Basket muzzle modified to facilitate extubation (A). Placement of the pilot balloon and endotracheal tube ties through the end of the muzzle is necessary to avoid difficulty extubating the patient (B). 

Intravenous catheters can be removed just before discharge. With all tape removed and a bandage left over the catheter, the extension line, which is attached to the catheter hub, can be pulled, thus removing the catheter while keeping the bandage in place for hemostasis (see Step-by-Step Catheter Removal Video). Sedatives can be administered intravenously just before catheter removal at the time of discharge and can facilitate a smooth transition from the hospital to the transportation vehicle. The owner should be made aware of the expected nature and duration of the sedation protocol.

Conclusion

Careful planning, communication, and preparation can facilitate a safe and productive appointment for fractious patients that need to be sedated or anesthetized. Multimodal pharmacologic restraint, along with modified approaches to drug administration and patient handling, can mitigate most of the issues encountered with aggressive patients in the hospital setting.

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.


Content continues after advertisement

Hill's CB Nov 2018

Content continues after advertisement

Bronchi CB Nov 2018

Bordetella bronchiseptica & Mycoplasma cynos in Dogs with Inflammatory Airway Disease

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

Sign in to Print/View PDF

<em>Bordetella bronchiseptica</em> & <em>Mycoplasma cynos</em> in Dogs with Inflammatory Airway Disease

In the Literature

Canonne AM, Peters I, Roels E, Desquilbet L, Clercx C. Detection of specific bacterial agents by quantitative PCR assays in the bronchoalveolar lavage fluid of dogs with eosinophilic bronchopneumopathy vs dogs with chronic bronchitis and healthy dogs. Vet J. 2018;232:52-56.


FROM THE PAGE …

Eosinophilic bronchopneumopathy (EBP) is characterized by eosinophilic infiltration of the bronchial mucosa and the lungs of young adult dogs that leads to coughing. The cause is unknown, but evidence has suggested an immunologic or aeroallergen component may be involved, as the response may be similar to a type 1 hypersensitivity reaction.1-3 Diagnosis is based on an increased eosinophil component in tracheal or bronchial fluid collection. Testing to exclude infection from bacterial and parasitic diseases should be performed prior to treatment, and culture and PCR results should always be interpreted with cytology, as presence of oral contamination may lead to false positive results.4

Infection with certain respiratory pathogens (eg, Mycoplasma pneumoniae) has been shown to favor asthma development in human patients. This study sought to determine if similar pathogens were present in dogs with EBP and whether infection was related to the severity of respiratory signs. Healthy patients and those with chronic bronchitis were also evaluated. Bacteria evaluated included Mycoplasma canis, Mycoplasma cynos, and Bordetella bronchiseptica. M cynos and B bronchiseptica are known causative agents of respiratory signs in dogs. Quantitative polymerase chain reaction (qPCR) was used to detect these organisms in bronchoalveolar lavage fluid (BALF) samples, and the results were reported as cycle threshold (CT) values. No significant difference in qPCR detection rates for each of the bacterial agents was found between dogs with EBP and chronic bronchitis or between healthy dogs and dogs with EBP. However, in dogs that tested positive for M cynos, CT values corresponding to a very high bacterial load were found only in patients with inflammatory bronchial disease (both chronic bronchitis and EBP). CT values corresponding to a moderate-to-high load of B bronchiseptica were found only in patients with EBP; subjectively, these patients had more severe clinical signs based on the authors’ scoring system. Median neutrophil counts were also higher in BALF samples positive for either M cynos or B bronchiseptica.

Despite some study limitations, results suggest that infection with specific organisms may contribute to or worsen clinical signs of airway disease in patients with EBP. The exact role these or other organisms may play in inflammatory respiratory diseases has yet to be determined.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Culture and qPCR of BALF should always be performed when samples are collected in a coughing patient.

 

2

Collection of BALF samples should occur prior to antibiotic administration or after a washout period to decrease the risk for false negative results. Results should be interpreted with caution if oral bacterial contamination is present.

3

If clinical signs worsen acutely or do not respond to traditional therapies (ie, glucocorticoids) in patients with known EBP, infection should be considered.

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.


Content continues after advertisement

Mirataz CB Nov 2018

Content continues after advertisement

Prozinc CB Nov 2018

Content continues after advertisement

iM3 CB Nov 2018

Concurrent Canine Hyperadrenocorticism & Diabetes Mellitus

Jinelle Webb, DVM, MSc, DVSc, DACVIM (SAIM), Mississauga Oakville Veterinary Emergency Hospital, Oakville, Canada

Sign in to Print/View PDF

Concurrent Canine Hyperadrenocorticism & Diabetes Mellitus

In the Literature

Miceli DD, Pignataro OP, Castillo VA. Concurrent hyperadrenocorticism and diabetes mellitus in dogs. Res Vet Sci. 2017;115:425-431.


FROM THE PAGE …

This study of 235 dogs with pituitary- or adrenal-dependent hyperadrenocorticism (HAC) examined the co-occurrence of diabetes mellitus (DM) and HAC and evaluated risk factors for development of DM in dogs with HAC. Dogs were divided into 3 groups (ie, fasting blood glucose <100 mg/dL, fasting blood glucose between 100 mg/dL and 180 mg/dL, fasting blood glucose >180 mg/dL). Parameters assessed included triglyceride level, cholesterol, urine cortisol:creatinine ratio, age, sex, breed, neuter status, BCS, cause of HAC, and median survival time.

DM occurred in conjunction with HAC in 13.61% of study dogs. Risk for developing DM was higher in dogs with a fasting glucose >100 mg/dL, even in patients in which overt DM was not yet apparent. This suggests that dogs with HAC can experience a prediabetic state that may progress to clinical DM.

Other risk factors for development of DM included presence of pituitary-dependent HAC, urine cortisol:creatinine ratio >100 × 10-6, and intact status for female dogs. In addition, there was a trend toward increased risk in dogs with cholesterol levels >351 mg/dL or triglyceride levels >221 mg/dL. These findings support reducing hypercortisolemia as effectively as possible, as the degree of control is likely related to risk for developing concurrent DM.

In this cohort of dogs, obesity did not increase risk for developing DM. Purebred dogs were also not at increased risk as compared with crossbreed dogs. It is possible that obesity was partially corrected with treatment for HAC and resulted in improved response to endogenous insulin.

Median survival time was shorter in dogs with both concurrent HAC and DM as compared with those with HAC alone. Recognition of risk factors linked to development of DM, and early intervention to address these risk factors, may reduce the number of patients with HAC that develop overt DM.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Controlling hypercortisolemia in dogs with HAC may decrease risk for development of concurrent DM.

 

2

Obesity in dogs with HAC does not appear to increase the risk for developing DM.

 

3

Early recognition and intervention to address risk factors may reduce incidence of concurrent DM development in dogs with HAC.

 

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.


Content continues after advertisement

Vetriscience CB Nov 2018

Content continues after advertisement

Entyce CB Nov 2018

Content continues after advertisement

Dechra CB Nov 2018

Vector-Borne Diseases in Cats

Katie M. Clow, DVM, PhD, University of Guelph

Sign in to Print/View PDF

Vector-Borne Diseases in Cats

In the Literature

Lappin MR. Update on flea and tick associated diseases of cats. Vet Parasitol. 2018;254:26-29.


FROM THE PAGE …

Several vector-borne pathogens have been detected in cats. A detailed history should be obtained, and potential pathogen transmission should be considered when the patient has come in contact with vectors such as ticks and fleas, as exposure may lead to clinical disease.

Anaplasma phagocytophilum, the causative agent of feline anaplasmosis, is transmitted by Ixodes spp ticks. Fever, anorexia, and lethargy are the most common clinical signs.1 Rhipicephalus sanguineus, another tick species, can transmit Ehrlichia canis to cats but is not as well characterized in cats as in dogs.2,3 Risk for exposure to these pathogens coincides with the geographic range of these tick species.2-4

Fleas can transmit Bartonella henselae, B clarridgeiae, and B koehlerae to cats.2,5 Numerous clinical signs (eg, fever, swollen lymph nodes, uveitis, myocarditis, endocarditis, osteomyelitis) have been associated with feline bartonellosis.6 Occupational risk for exposure exists for veterinarians and support staff due to potential transmission of Bartonella spp by cat scratches and flea bites.6

Hemolytic anemia in cats can result from infection with Mycoplasma haemofelis, Candidatus M haemominutum, and/or Candidatus M turicensis.7-9 More severe feline hemoplasmosis is associated with M haemofelis or coinfection with other hemoplasmas. Transmission is believed to occur via flea bites and by direct cat-to-cat transmission via saliva (eg, from fighting).10

Feline rickettsiosis, caused by Rickettsia felis and transmitted by the flea Ctenocephalides felis, may manifest as fever in a subset of cats, but past studies have been inconclusive on the role of R felis in clinical disease.5,11

The most reliable method for detecting any of these pathogens is PCR testing using blood of acutely ill cats,4,5,10 which can be combined with serologic assays to detect antibodies, depending on the stage of infection. Clinically ill cats can be treated with doxycycline (5 mg/kg PO q12h or 10 mg/kg PO q24h). Duration of treatment varies from 7 to 10 days for hemoplasmosis and 14 to 28 days for anaplasmosis and bartonellosis.1,12-14

Prevention is recommended for any cat at risk for exposure to ticks and/or fleas. Effective ectoparasite control should be strongly recommended to reduce this risk.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Ticks and fleas can transmit Anaplasma spp, Ehrlichia spp, Bartonella spp, Mycoplasma spp, and Rickettsia spp to cats. These pathogens may be associated with disease, so it is important to determine potential exposure to these vectors when evaluating clinically ill cats.

2

PCR testing using blood of acutely ill cats is the most reliable diagnostic test for any of these pathogens. Doxycycline is the treatment of choice.

 

3

Flea and tick prevention should be considered for any cat that may come in contact with these vectors.

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.


Content continues after advertisement

Nestle CB Nov 2018

Research Note: Estradiol Effect on Bone-Marrow–Derived Mesenchymal Stem Cells

Sign in to Print/View PDF

Fracture nonunion increases patient morbidity and healthcare costs. Bone grafts are often used in these defects but have several drawbacks. Bone-marrow–derived mesenchymal stem cells (BMSCs) may be an appealing alternative due to their trophic properties and immune-suppression function. 17β-estradiol has been shown to improve the osteogenesis and proliferation potential of mesenchymal stem cells in humans. This study evaluated the effect of 17β-estradiol on exploiting autologous BMSCs for healing of radial nonunion segmental defects in 20 rabbits. Through serial radiologic assessment and histopathologic evaluation, 17β-estradiol was found to provide BMSCs with improved osteogenic capacity and an accelerated rate of bone healing.

Source

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

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

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


Research Note: Effect of Cardiomyopathy & Diabetes Mellitus on SDMA in Cats

Sign in to Print/View PDF

Considering the potential benefits of renoprotective nutritional treatment in cats in preazotemic stages of kidney disease, early diagnosis of kidney disease is critical. Symmetric dimethylarginine (SDMA) increases as glomerular filtration rates decrease, with a mean time of 17 months before serum creatinine elevations are observed. However, little is known about the influence of comorbidities on SDMA in cats. Human models have shown that SDMA may be influenced by other diseases. This study examined possible relationships between SDMA and hypertrophic cardiomyopathy and diabetes mellitus. In cats, SDMA does not appear to be affected by hypertrophic cardiomyopathy. However, diabetes mellitus appears to lower SDMA levels, making it a less predictable marker for cats with concomitant diabetes mellitus and chronic kidney disease.

Source

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.


Content continues after advertisement

Brief Summits CB Nov 2018

Feline Hemoplasmosis

Emi Barker, BSc (Hons), BVSc (Hons), PhD, DECVIM-CA, University of Bristol, Bristol, United Kingdom

Sign in to Print/View PDF

Feline Hemoplasmosis

In the Literature

Novacco M, Sugiarto S, Willi B, et al. Consecutive antibiotic treatment with doxycycline and marbofloxacin clears bacteremia in Mycoplasma haemofelis-infected cats. Vet Microbiol. 2018;217:112-120.


FROM THE PAGE …

Mycoplasma haemofelis is the most pathogenic of the feline hemoplasmas1 and can cause life-threatening hemolytic anemia in immunocompetent cats. Clinical hemoplasmosis is often successfully managed with a course of an appropriate antibiotic (eg, tetracycline, fluoroquinolone), but infection is only eliminated in a minority of cases. Clearance of infection may be desirable in cases in which the cat poses a risk to others, there is concern regarding risk for zoonotic spread to an immunocompromised owner,2 clearance of infection is a requirement of rehoming (eg, for experimentally hemoplasma-infected cats), and/or the cat is immunocompromised by concurrent infection (eg, FIV, FeLV) or following chemotherapy.

This study sought to optimize the antibiotic treatment protocol required to consistently eliminate bacteremia. Fifteen cats chronically infected with M haemofelis were included and treated with doxycycline (5 mg/kg PO q12h for 28 days), followed by marbofloxacin (2 mg/kg PO q24h for 14 days) if still bacteremic. To accurately detect bacteremia, quantitative M haemofelis real-time PCR was performed on a weekly basis. Five of the 15 cats cleared bacteremia following doxycycline therapy alone. The remaining cats cleared bacteremia following subsequent marbofloxacin administration, which was initiated up to 4 weeks following discontinuation of doxycycline. Following clearance of infection, 5 cats were immunosuppressed with steroids for 3 weeks in an attempt to induce relapse. No cats relapsed following immunosuppression.

The decision to treat should be based on a firm diagnosis and clinical requirement. Cats should be closely monitored, and the risks for adverse effects should be minimized. Administration with food is recommended, as esophagitis and esophageal stricture have been reported in cats receiving doxycycline in the management of hemoplasmosis.3 Administration of a fluoroquinolone as part of an elimination protocol should be based on the demonstration of persistent infection by real-time PCR testing following an extended course of doxycycline.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

If M haemofelis infection persists and/or poses a risk to the cat or the owner, a combination of doxycycline, followed by marbofloxacin if the patient is still bacteremic, should be considered.

 

2

It is important to note that a delay between one course of antibiotics and the next does not appear to affect patient outcome, and doxycycline alone may be sufficient in clearing infection, as a significant number of study cats (33%) did not require additional treatment with a fluoroquinolone.

3

Repeat testing on multiple occasions may be required to confirm clearance of infection.

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.


Content continues after advertisement

Jorvet CB Nov 2018

Content continues after advertisement

AVMA CB Nov 2018

Research Note: Effect of Neutering in Male Cats

Sign in to Print/View PDF

Patients with urinary obstruction are most often male and neutered. In male rats and rabbits, androgen depletion appears to result in changes to penile structures. This study examined the extracellular matrix in the penises of neutered male cats as compared with intact male cats. Results showed neutered male cats to have an increased density of fibers in the corpus spongiosum and decreased density of elastic fibers as compared with intact male cats, suggesting decreased compliance of the periurethral region that may increase risk for obstruction in neutered male cats.

Source

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

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

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


Research Note: Utility of Peripheral Pulse Palpation

Sign in to Print/View PDF

Peripheral pulse palpation is often used to assess cardiovascular stability during triage. Pulse quality is determined by the difference between systolic blood pressure and diastolic blood pressure. Strong peripheral pulses reflect normal or elevated systolic blood pressure or reduced diastolic blood pressure. Weak or absent pulses reflect low systolic blood pressure or arterial clot formation. The utility of peripheral pulse palpation, however, has been controversial. This prospective study compared peripheral pulse quality and Doppler systolic blood pressure in 93 dogs presented to an emergency center. Results indicated that absent dorsal metatarsal pulses had high specificity for hypotension but poor sensitivity (ie, dogs with palpable metatarsal pulses may still be hypotensive). This highlights the importance of evaluating multiple physical parameters to determine cardiovascular stability.

Source

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.


Content continues after advertisement

Glandex CB Nov 2018

Content continues after advertisement

WSAVA CB Nov 2018

Gait Abnormalities in Pugs

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

Sign in to Print/View PDF

Gait Abnormalities in Pugs

In the Literature

Rohdin C, Jäderlund KH, Ljungvall I, Lindblad-Toh K, Häggström J. High prevalence of gait abnormalities in pugs. Vet Rec. 2018; 182(6):167.


FROM THE PAGE …

Gait abnormalities originating from orthopedic and/or neurologic disease are commonly observed in brachycephalic breeds, and the popularity of the pug breed requires veterinarians to be aware of common diseases in pugs.

A group in Sweden, where nearly all pugs are universally registered with the national kennel club, surveyed pug owners to assess gait abnormalities. Owners were asked to assess lameness, ataxia, inability to jump, and wearing of the dorsal surface of the nails or skin on paws. Of the questionnaires sent, 26% (n = 550) were returned, and 59 videos suitable for inclusion were submitted.

Most respondents (79.6%) described their dog as having a normal gait, whereas 20.4% described short-term or chronic gait abnormalities. However, 10.3% of the owners who described their dog as having a normal gait also noted wearing of nails or dorsum of paws, increasing the total percentage of pugs with a likely abnormality to 30.76%. Most owners described a slow onset of signs. Median age of abnormality identification was 2 years; 14.3% of pugs were described as having an abnormality by 1 year of age and 46.3% by 8 years of age. There was an association between other possible neurologic signs (eg, scratching at the neck, seizures, syncope, fly biting, licking the air) and gait abnormalities. Dyspnea was also associated with gait abnormalities. Among dogs with abnormal gaits, thoracic limb involvement was more common than pelvic limb involvement (51.3% vs 17.7%); 31% of pugs with abnormal gaits were affected in all 4 limbs.

In a multivariate analysis, age, dyspnea, and scratching around the neck, ears, and head were most commonly found to correlate with owner-perceived gait abnormality. Video analysis found 23.9% of dogs classified by their owner as normal were abnormal when evaluated by a neurologist. In addition, 28.8% cited gait abnormality as the cause of euthanasia or death. This study shows that a large number of pugs have gait abnormalities and that these abnormalities are seen early in life, are significant, and worsen with age.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Gait abnormalities are common in the pug breed; owners should be made aware of this and be educated on what to look for when assessing their dog’s gait (eg, wearing of tops of nails or dorsum of paws).

2

Gait abnormalities in all 4 limbs are frequently associated with other neurologic or respiratory diseases; thus, these patients should also be assessed for such diseases.

 

3

Owners should be advised that gait abnormalities are likely to worsen with age.

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.


Content continues after advertisement

WMPB CB Nov 2018

Content continues after advertisement

PVD CB Nov 2018

Iatrogenic Hypothyroidism Following Radioiodine Treatment

Stefanie M. DeMonaco, DVM, MS, DACVIM (SAIM), Virginia–Maryland College of Veterinary Medicine

Sign in to Print/View PDF

Iatrogenic Hypothyroidism Following Radioiodine Treatment

This article describes 2 similar case presentations featuring cats that developed iatrogenic hypothyroidism following radioiodine treatment for hyperthyroidism. Each case demonstrates the importance of patient monitoring after radioactive iodine treatment.

CASE 1

Betty, a 14-year-old, spayed domestic shorthair cat, was presented for a recheck examination, urinalysis, and evaluation of CBC, serum chemistry profile, and total thyroxine concentration 3 months after receiving radioiodine treatment for hyperthyroidism. The owner had noted weight gain and resolution of previous clinical signs related to hyperthyroidism (ie, polyphagia, vocalization). Previously, at the 1-month posttreatment evaluation, a low serum thyroxine (T4) concentration had been detected (Table 1), and CBC and serum chemistry profile results were normal. Given the low T4 concentration, Betty’s thyroid-stimulating hormone (TSH) concentration was also evaluated (using the canine TSH assay*) and found to be increased above the reference range (Table 1). Because iatrogenic hypothyroidism may be transient, no treatment was initiated at that time, and re-evaluation was postponed until the recheck examination scheduled for 3 months after radioiodine treatment.

table 1

BETTY'S RELEVANT TEST VALUES

Parameter Reference Range 1 Month Postradioiodine Treatment 3 Months Postradioiodine Treatment 1 Month of Levothyroxine Treatment 3 Months of Levothyroxine Treatment
Creatinine 1.0-1.8 mg/dL (88-159 μmol/L) 1.5 mg/dL (133 μmol/L) 2.6 mg/dL (230 μmol/L) 2 mg/dL (177 μmol/L) 1.7 mg/dL (150 μmol/L)
BUN 18-32 mg/dL (6.4-11.4 mmol/L) 25 mg/dL (8.9 mmol/L) 64 mg/dL (22.8 mmol/L) 45 mg/dL (16.1 mmol/L) 30 mg/dL (10.7 mmol/L)
T4 16.0-37.7 nmol/L 15 nmol/L 11 nmol/L 18 nmol/L 29 nmol/L
TSH 0.03-0.30 ng/mL 0.7 ng/mL 1.7 ng/mL 0.9 ng/mL 0.21 ng/mL

Physical Examination

At the 3-month recheck examination, Betty was bright, alert, and responsive, and vital signs were within normal limits. Betty had a BCS of 5/9 (3/9 prior to radioiodine treatment) and was noted to have gained 1.54 lb (0.7 kg) since beginning radioiodine treatment. The rest of the physical examination was unremarkable.

Diagnosis

CBC was unremarkable. Serum chemistry profile results revealed azotemia, with a BUN of 64 mg/dL (22.8 mmol/L) (range, 18-32 mg/dL [6.4-11.4 mmol/L]) and creatinine of 2.6 mg/dL (230 μmol/L) (range, 1-1.8 mg/dL [88-159 μmol/L]; Table 1). The rest of the serum chemistry profile results were unremarkable, as were the urinalysis results, aside from a urine specific gravity of 1.014 (normal, >1.035). A thyroid profile showed a decreased serum T4 concentration and an increased serum TSH concentration (Table 1). The low serum T4 concentration was suggestive of hypothyroidism or a nonthyroidal illness related to azotemia. TSH was obtained to differentiate iatrogenic hypothyroidism from nonthyroidal illness secondary to azotemia. The combination of increased serum TSH concentration and decreased serum T4 concentration was suggestive of overt hypothyroidism.

DIAGNOSIS:

OVERT IATROGENIC HYPOTHYROIDISM

Treatment & Long-Term Management

Treatment with levothyroxine (0.1 mg PO q24h) was initiated, and serum T4 and TSH concentrations were rechecked one month after initiation of treatment. Serum T4 concentration had increased into the reference range, serum TSH concentration had decreased, and azotemia had improved. Peak T4 concentration was low-normal, and TSH concentration remained elevated; thus, the levothyroxine dose was increased to 0.15 mg PO q24h to obtain a peak T4 concentration in the middle to upper half of the reference range and a TSH concentration within the reference range. After 2 months of levothyroxine treatment at the increased dose, serum T4 and TSH concentrations were within reference range, and azotemia had resolved (Table 1; see Treatment at a Glance).

TREATMENT AT A GLANCE

Treatment of iatrogenic hypothyroidism should include administration of levothyroxine to normalize T4 and TSH values. Levothyroxine at 0.15 mg PO q24h has reportedly been successful in normalizing or improving thyroid hormone concentrations, as well as serum creatinine concentrations, in hypothyroid cats.4

CASE 2

Isabella, a 14-year-old, spayed domestic shorthair cat, was presented for recheck examination and blood work 3 months after receiving radioiodine treatment for hyperthyroidism. On presentation, the owner noted that Isabella was polyuric and polydipsic. At the time radioiodine treatment was initiated, Isabella had a slightly increased BUN (37 mg/dL [13.2 mmol/L]) and normal creatinine concentrations (1.1 mg/dL [97 μmol/L]). Two months earlier at the 1-month posttreatment evaluation, serum T4 concentration was low and serum TSH concentration was normal, with azotemia present on serum chemistry profile results (Table 2).

Physical Examination

Isabella was bright, alert, and responsive, and vital signs were within normal limits. Isabella had a BCS of 4/9 (3/9 prior to radioiodine treatment) and was noted to have gained 0.88 lb (0.4 kg) since receiving radioiodine treatment. The rest of the physical examination was unremarkable.

Diagnosis

CBC was unremarkable. Serum chemistry profile results revealed progressive azotemia, with a BUN of 43 mg/dL (15.4 mmol/L) and creatinine of 3.5 mg/dL (309 μmol/L) (Table 2). The remainder of the serum chemistry profile and urinalysis results were unremarkable, except for a urine specific gravity of 1.012 (normal, >1.035). Thyroid profile demonstrated a low-normal serum T4 concentration and an increased serum TSH concentration. Azotemia had progressed over the 2-month period since first noted at the 1-month posttreatment recheck examination. Low-normal serum T4 and high serum TSH concentrations were consistent with subclinical hypothyroidism.

TABLE 2

ISABELLA’S RELEVANT TEST VALUES

Parameter Reference Range 1 Month Postradioiodine Treatment 3 Months Postradioiodine Treatment 3 Months of Levothyroxine Treatment
Creatinine 1.0-1.8 mg/dL (88-159 μmol/L) 2.3 mg/dL (203 μmol/L) 3.5 mg/dL (309 μmol/L) 3 mg/dL (265 μmol/L)
BUN 18-32 mg/dL (6.4-11.4 mmol/L) 61 mg/dL (21.8 mmol/L) 43 mg/dL (15.4 mmol/L) 40 mg/dL (14.3 mmol/L)
T4 16.0-37.7 nmol/L <6.4 nmol/L 17 nmol/L 30 nmol/L
TSH 0.03-0.30 ng/mL 0.09 ng/mL 1 ng/mL 0.28 ng/mL

DIAGNOSIS:

SUBCLINICAL IATROGENIC HYPOTHYROIDISM

Treatment

Due to the development of subclinical hypothyroidism and progressive azotemia, treatment for hypothyroidism with levothyroxine (0.15 mg PO q24h4) was initiated. Isabella was also started on a renal diet. After 3 months of levothyroxine treatment, both serum T4 and TSH concentrations were within reference range, and azotemia had not progressed any further (Table 2). Because peak T4 concentration was within the upper half of the reference range and TSH concentration was within reference range, the levothyroxine dosage was maintained at 0.15 mg PO q24h (see Treatment at a Glance).

CASE 1 & CASE 2

Prognosis & Outcome

Both Betty and Isabella had developed azotemia and iatrogenic hypothyroidism (overt and subclinical, respectively) after radioiodine treatment. A low T4 concentration and high TSH concentration are indicative of overt hypothyroidism, whereas a low-normal T4 concentration and high TSH concentration are indicative of subclinical hypothyroidism. Cats that develop iatrogenic hypothyroidism are more likely to develop azotemia, as hypothyroidism leads to decreased glomerular filtration rate1,2; this is of particular importance in cats with preexisting chronic kidney disease (CKD). In addition, azotemic hypothyroid cats have shorter survival times as compared with nonazotemic hypothyroid cats, and hypothyroid cats that are untreated have shorter survival times as compared with treated hypothyroid cats.3,4 A study of cats with iatrogenic hypothyroidism that were treated with levothyroxine at 0.15 mg PO q24h showed improved-to-normalized serum creatinine concentrations.4 Both Betty and Isabella exhibited either stabilization or improvement of azotemia when treated with levothyroxine supplementation at 0.15 mg PO q24h, and this stabilization or improvement of azotemia should have a positive impact on their overall survival.

Conclusion

Iatrogenic hypothyroidism can occur in approximately 10% to 30% of hyperthyroid cats following radioactive iodine treatment, with studies showing considerable variations in prevalence (1%-78%; see Take-Home Messages).5-10 Considering the impact iatrogenic hypothyroidism has on kidney function and overall survival, early diagnosis is ideal. Clinical signs (eg, weight gain, lethargy) alone may not raise suspicion of hypothyroidism, as clinical signs can overlap with resolution of hyperthyroidism.4 The screening test of choice for hypothyroidism in dogs is evaluation of total T4 concentration, which is also routinely monitored in cats following treatment for hyperthyroidism. However, a total T4 concentration below reference range does not confirm hypothyroidism, as the presence of nonthyroidal illness can confound the diagnosis. This is particularly true in cats with CKD, in which serum T4 concentration is low in approximately 50% of cases.11-14 The combination of low T4 concentration and high TSH concentration is used to diagnose overt iatrogenic hypothyroidism, as seen in Betty.4 Conversely, some hypothyroid cats can have a low-normal T4 concentration; an increased TSH concentration in these cats is indicative of subclinical hypothyroidism, as seen in Isabella.4 Therefore, only monitoring T4 concentration in cats that have undergone treatment for hyperthyroidism can lead to overdiagnosis or can preclude the diagnosis of hypothyroidism. Periodic evaluations—including evaluation of T4 and TSH concentrations—at 1, 3, 6, and 12 months following radioiodine treatment are recommended. If persistent, overt iatrogenic hypothyroidism is detected, treatment with levothyroxine should be considered, particularly in cats that develop azotemia. Similarly, if hypothyroidism is detected in cats receiving methimazole therapy, the dose should be appropriately adjusted.

Pet owners should be informed of the risks and complications of iatrogenic hypothyroidism, the importance of posttreatment monitoring, and the necessity of levothyroxine supplementation in select cases following radioiodine therapy. Preventive strategies for iatrogenic hypothyroidism, particularly in cats with mild-to-moderate hyperthyroidism, can include treatment with lower doses of radioactive iodine, which has been shown to lower the prevalence of iatrogenic hypothyroidism without compromising treatment efficacy.9

Take-Home Messages

  • Cats undergoing radioiodine therapy may develop iatrogenic hypothyroidism, which can be either subclinical (ie, low-normal T4 concentration and increased TSH concentration) or overt (ie, decreased T4 concentration and increased TSH concentration).3,4,9 
  • Diagnosis of iatrogenic hypothyroidism can be complicated by the presence of nonthyroidal illnesses such as CKD.11-14 Serum TSH is highly sensitive for iatrogenic hypothyroidism, and serum TSH values can be helpful in differentiating azotemic hypothyroid cats from those with azotemic nonthyroidal illness.4
  • Cats with iatrogenic hypothyroidism are more likely to develop azotemia3,4 and have a shorter life expectancy.3 Cats that develop iatrogenic hypothyroidism with new or worsening azotemia should be candidates for treatment of hypothyroidism.
  • Restoration of euthyroidism in hypothyroid cats with azotemia may improve or stabilize kidney function and improve survival time.4,15
*All feline TSH values were measured using the canine TSH assay.

CKD = chronic kidney disease, T4 = thyroxine, TSH = thyroid-stimulating hormone

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.


Content continues after advertisement

Tonopen CB Nov 2018

Content continues after advertisement

Aesculight CB Nov 2018

Management of Subclinical Bacteriuria

David F. Senior, BVSc, DACVIM (SAIM), DECVIM-CA, Louisiana State University School of Veterinary Medicine

Urology & Nephrology

|Peer Reviewed

Sign in to Print/View PDF

Management of Subclinical Bacteriuria

Bacteria has been observed in the urine sediment and isolated from appropriately collected urine in patients that do not show clinical signs (ie, subclinical bacteriuria*). Subclinical bacteriuria is a frequent occurrence in dogs and cats, and confirming its presence can alert the clinician to a predisposing condition that may require treatment.

*The term asymptomatic bacteriuria that is used in human medicine does not apply to veterinary patients, as clinicians cannot know the symptoms animals are experiencing; rather, they can only observe their clinical signs.

Background & Pathophysiology

The clinical signs typically associated with acute bacterial UTIs (eg, hematuria, dysuria, pollakiuria, periuria, stranguria) occur when the host’s immune system responds to signals generated by bacterial attachment and invasion into the uroepithelium.1 When host defenses against bacterial invasion are replete, UTIs are typically caused by bacteria capable of expressing vital virulence factors—most notably the ability to attach to the urethral mucosa and invade tissue—that enable colonization and persistence in the urinary tract.1 In many local and systemic disease conditions, normal barriers to bacterial establishment in the urinary tract are diminished so that bacteria that either do not possess or present virulence factors normally required to establish an infection can colonize and persist.2,3 Although long-term persistent subclinical bacteriuria may have minimal detrimental effects on the urinary tract, it may serve as a sentinel for other metabolic and immunologic disorders (eg, diabetes mellitus, hyperadrenocorticism). Although many host defense mechanisms likely remain obscure, common causes or associations with subclinical bacteriuria have been identified (eg, aberrant genital conformation, systemic or concurrent disease of the urinary tract).4-11

Commonly Recognized Conditions Predisposing to or Associated with Overt UTI & Subclinical Bacteriuria

  • Vulval involution
  • Old age
  • Obesity
  • Incomplete bladder emptying resulting from:
    • Bladder atony
    • Spinal cord injury
    • Other causes of dyssynergia
  • Ectopic ureter
  • Skin disease
  • Indwelling urethral catheter use
  • Hyperadrenocorticism
    • Pharmacologic
    • Endogenous
  • Diabetes mellitus
  • Hypothyroidism
  • Immunosuppression
  • Urolithiasis
  • Bladder polyps/tumors
  • Prostatic involvement (intact male dogs)

Diagnosis

Diagnostic efforts should be made to identify causes of diminished host defenses. In immunocompromised patients, or after identification and elimination of predisposing conditions that may be negatively impacting urinary tract host defenses, a course of antimicrobial therapy based on culture and antimicrobial susceptibility results is indicated if clinical signs of UTI are apparent.

Diagnosis of subclinical bacteriuria can be based on detection of bacteria in the urine sediment in the absence of clinical signs and can be confirmed via positive culture of an appropriately collected urine specimen. Isolation of bacteria is preferably done on urine collected by cystocentesis, but quantitative bacterial culture performed on urine collected via urethral catheterization or voided urine collected by clean catch can be considered positive if the bacterial count equals or exceeds 105 CFU/mL in dogs and 104 CFU/mL in cats.12,13 Bacterial counts lower than this may suggest contamination. Although bacteria can be readily detected in a wet mount urine sediment, Gram staining significantly improves accurate diagnosis of bacteriuria.14

Subclinical bacteriuria is typically associated with geriatric patients and comorbid conditions but can be encountered on routine screening.15,16 

Treatment

Antimicrobial Treatment

When a diminished host defense or a predisposing condition cannot be identified (or can be identified but not corrected), antimicrobial treatment of subclinical bacteriuria can result in colonization of the urinary tract by highly resistant bacteria but with no real benefit due to the lack of initial clinical signs.

Left untreated, subclinical bacteriuria may leave patients at potential (but unknown) risk for developing an ascending infection that can lead to pyelonephritis and resulting progression of chronic kidney disease and—in cases of infections with urease-producing bacteria (eg, Staphylococcus pseudintermedius, Proteus spp)—risk for developing struvite urolithiasis.17 Very alkaline urine may be caused by urease-producing bacteria, which should be treated to prevent formation of struvite uroliths. Clinical suggestion of pyelonephritis includes dilute urine and the intermittent presence of WBC casts in urine sediment; accordingly, lack of casts does not definitively rule out renal involvement. In addition, dilute urine can be caused by many other physiologic and pathophysiologic conditions. Radiographs and sonograms can reveal changes associated with chronic pyelonephritis, but such changes in normal architecture tend to be permanent and may not reflect a current infection.18 If a patient’s urine is concentrated, pyelonephritis is unlikely. Presence of WBC casts in a patient’s urine sediment confirms pyelonephritis.19,20

In patients with subclinical bacteriuria with a nonurease-producing isolate and no diagnostic evidence of renal involvement, antimicrobial treatment likely is not worthwhile and could be detrimental. Colonization of the urinary tract and associated microflora by multidrug-resistant bacteria may increase the risk for similarly resistant microflora infecting humans living in the same household.21-23

Because bacteria compete for required growth factors (eg, iron) and actively produce substances that inhibit growth of other strains (eg, aerobactin), the normal genital microflora serves as a barrier to colonization by uropathogenic bacteria.24 Studies in human paraplegic patients have indicated that purposeful inoculation and colonization of the lower urinary tract with genetically altered Escherichia coli lacking the P-fibrial virulence factor that facilitates renal pelvic colonization can act as a barrier to prevent colonization with more virulent strains.25

Although expression of P-fimbria by uropathogenic E coli appears to be irrelevant to the risk for renal involvement in dogs and cats, and although virulence factors that may enhance the likelihood of pyelonephritis have not been identified, recent studies in veterinary medicine have pursued the same concept.26,27 Thus, it is possible that spontaneous presence in the urinary tract of an avirulent strain of bacteria that does not involve the upper urinary tract could provide the same protection against invasion by virulent and/or highly resistant bacteria and therefore should be left untreated.

Nonantimicrobial Treatment

Alternative nonantimicrobial therapies that might preclude colonization with multidrug-resistant bacteria after repeated antimicrobial treatments have been sought. Early studies in humans have suggested that cranberry juice and cranberry juice extract reduce the frequency of recurrent UTIs in humans, but recent reports may negate these findings.28,29 Results from experimental studies involving use of cranberry extract to prevent UTI in dogs have been mixed, and, in a recent clinical report, cranberry extract failed to reduce the risk for bacteriuria in a small number of dogs with intervertebral disk disease.30-32

Methenamine, administered as a mandelic acid or hippuric acid salt, has been used in humans as a urinary antiseptic to prevent UTI recurrence. Efficient conversion of methenamine to formaldehyde, the main bactericidal component of the drug, requires urine pH to be at or below 5.5, a level difficult and likely even detrimental to sustain on a long-term basis in dogs and cats.33

Conclusion

In many instances, subclinical bacteriuria can and should remain untreated because infected animals do not show clinical signs, and repeated antimicrobial treatment to eliminate such infections can result in establishment of multidrug resistance. Further, colonization of the urinary tract by nonpathogenic bacteria may act as a barrier to infection by more virulent microorganisms. However, treatment is indicated in patients with evidence of upper urinary tract involvement, which could lead to renal damage with reduced renal function, and in patients with urease-producing infections that could lead to struvite urolithiasis if left untreated.

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.


Content continues after advertisement

Nexgard CB Nov 2018

Content continues after advertisement

Profender CB Nov 2018

Content continues after advertisement

Orthomed CB Nov 2018

© Educational Concepts, L.L.C. dba Brief Media ™ All Rights Reserved. Privacy Policy (Updated 05/08/2018) Terms of Use (Updated 05/08/2018)