May 2018   |   Volume 16   |   Issue 5

Interpreting Culture & Susceptibility Reports

in this issue

in this issue

Clinical Reasoning

Image Gallery: Red Blood Cell Evaluation in Blood Films

External Splinting for Pectus Excavatum in Kittens

Feline Complications from Mouth Gags

Pulse Alterations

Mirtazapine

Sponsored by

Interpretation of Culture & Susceptibility Reports

Patricia Dowling, DVM, MSc, DACVIM (Large Animal), DACVCP, University of Saskatchewan

Clinical Pathology

|Peer Reviewed

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Interpretation of Culture & Susceptibility Reports

Antimicrobial stewardship programs typically recommend culture and susceptibility testing to guide clinicians in choosing optimal antimicrobial therapy; however, the majority of antimicrobial selections are made empirically,1,2 rather than based on test results from individual patients. Antimicrobial selection guided by culture and susceptibility testing is conducted mostly for chronic or recurrent infections.3,4 

Culture and susceptibility reports are often underused by veterinary practitioners because of a number of limitations, including cost and the time delay between sampling and results.4 Even after results are obtained, clinicians may lack the information necessary to interpret the reports in a meaningful way.

Culture & Susceptibility Reports

A culture and susceptibility report from a microbiology laboratory identifies the bacterial pathogen and lists antimicrobials labeled with an S, R, or I, designating Susceptible, Resistant, or Intermediate, respectively.5 These labels indicate the likelihood of a clinical response to antimicrobial treatment. Categories are determined by clinical breakpoints (ie, values that express whether specific bacterial pathogens will respond to certain antimicrobials), which are determined for specific antimicrobial/bacteria combinations based on the minimum inhibitory concentration (MIC) and the designation S, R, or I that corresponds to a specific MIC value (see Determining Breakpoints). MIC values are based on populations of the specific bacteria, the pharmacodynamic data for a specific species, and evidence from clinical use in patients treated with that antimicrobial.6 The clinical use is specific to the dose regimen (ie, dose, route of administration, frequency of administration) and disease. If any aspect of the regimen is altered (eg, the drug is administered orally instead of by injection), the predictive values of the breakpoints are no longer reliable.

DETERMINING BREAKPOINTS5-6

  • Breakpoint: The specific concentration of an antimicrobial that defines susceptibility or resistance
  • MIC: The lowest concentration of an antimicrobial required to inhibit the growth of specific bacteria
    • MIC less than local drug concentration: Associated with a high likelihood of therapeutic success, therefore susceptible (S)
    • MIC equal to local drug concentration: Associated with an uncertain effect; might be effective if concentrated at the site of infection or if the dose is increased, therefore intermediate (I)
    • MIC greater than local drug concentration: Associated with a high likelihood of therapeutic failure, therefore resistant (R)

Established Breakpoints

The Clinical Laboratory Standards Institute (CLSI) sets the standards for conducting and interpreting veterinary antimicrobial susceptibility tests.7 Breakpoints have been set only for a limited number of antimicrobial/bacteria combinations in veterinary species. If veterinary breakpoints are not available, breakpoints derived from human data are often provided on the report; this practice, however, is controversial, with some veterinary microbiologists stating that interpretation from nonveterinary breakpoints should not be performed or should only be performed with extreme caution.8,9 The CLSI recommends that microbiology laboratories should inform clinicians of the breakpoint source (ie, human or veterinary), but such designations rarely appear on culture and susceptibility reports. Thus, the report must be used in conjunction with knowledge of the pharmacokinetics and pharmacodynamics of the antimicrobial and the pathophysiology of the disease to determine if a specific drug is a reasonable treatment option (see Table).10

Diagnostic laboratories independently choose which bacterial isolates and which antimicrobial susceptibilities to report. Although laboratories recommend reporting only isolates that are clinically relevant, as reporting clinically irrelevant isolates can lead to unnecessary antimicrobial use, this would require oversight by a veterinary microbiologist with an adequate clinical background1; however, not all laboratories have the services of such specialists. It is also recommended that laboratories practice selective reporting (ie, all determined susceptibilities are not automatically reported), which helps prevent clinicians from choosing antimicrobials for cases in which they are not appropriate.1 For example, the susceptibility of an Escherichia coli isolate to nitrofurantoin should only be reported for isolates from an uncomplicated UTI, as UTI is the only clinical situation in which nitrofurantoin is an effective treatment. Susceptibilities for last resort drugs important in human medicine (eg, vancomycin, imipenem) should not be routinely reported.

Resistance & Susceptibility

It is important to recognize intrinsic resistance when interpreting culture and susceptibility reports.11 There are certain antimicrobial/bacteria combinations for which resistance should be assumed (eg, enterococci and cephalosporins). Some pathogens are intrinsically resistant to most major categories of antimicrobials. For example, Pseudomonas aeruginosa is a common secondary invader in cases of chronic otitis externa in dogs. Therefore, it is common to see resistance reported to all antimicrobials except aminoglycosides, fluoroquinolones, and antipseudomonal penicillins (eg, piperacillin). As another example, methicillin-resistant staphylococci should be reported as resistant to all penicillins and cephalosporins and imipenem; even if in vitro test results indicate susceptibility, the laboratory should report the result as resistant if there is a known intrinsic resistance. Results reported as susceptible should be questioned, as they are most likely the result of an identification or susceptibility testing error, indicating potential problems with the laboratory’s adherence to standard guidelines.

Unexpected resistance results (eg, penicillin-resistant streptococci) should also be identified and investigated (see Table). Although such results might be due to the emergence of antimicrobial resistance, it is more commonly the result of laboratory error.8,12

Rather than listing drugs in alphabetical order, it is preferable for the reporting laboratory to list drugs in groups according to class and in order of appropriate first-line, second-line, and third-line treatment choices to support prudent antimicrobial use. Cross-resistance often occurs within classes of antimicrobials and may be more difficult for the clinician to visualize if drugs are listed in alphabetical order. This order may also prevent practitioners from simply choosing the first drug labeled “S” for therapy.

Table

Breakpoint Sources for & Resistance to Common Antimicrobials

This table provides antimicrobials commonly found on small animal culture and susceptibility reports and is organized according to antimicrobial classification and a general preference for order of use. Breakpoint information is derived from CLSI performance standards for veterinary isolates.7

Penicillins

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Ampicillin

Canine: Escherichia coli in dermal, soft tissue, and urinary tract infections; Staphylococcus pseudintermedius and Streptococcus canis in dermal and soft tissue infections

 

Human: Enterococcus spp

Klebsiella spp, Proteus vulgaris, Serratia marcescens, Enterobacter spp, Pseudomonas aeruginosa
  • Susceptibility to ampicillin indicates susceptibility to amoxicillin.
  • Aminopenicillins are inactivated by most β-lactamases, but sufficient concentrations are achieved in urine to overcome low-level resistance; therefore, amoxicillin is recommended as empiric treatment for UTIs even if reported as R.13
Amoxicillin–clavulanic acid Canine and feline: E coli, Staphylococcus spp, and Streptococcus spp in dermal, soft tissue, and urinary tract infections S marcescens, Enterobacter spp, P aeruginosa
  • Resistance indicates extended-spectrum β-lactamase–producing (ESBL) bacteria, which are typically susceptible to amoxicillin–clavulanic acid but resistant to third- and fourth-generation cephalosporins.14 
  • As a result of high urine concentrations of amoxicillin, amoxicillin alone is recommended as the first-line treatment of UTIs.
  • The combination of amoxicillin with clavulanic acid is required for effective treatment of methicillin-susceptible staphylococcal superficial bacterial folliculitis/ pyoderma.15
Oxacillin Human: Staphylococcus spp Most gram-negative bacteria
  • Used solely to determine methicillin resistance in S pseudintermedius
  • Disk-diffusion (ie, Kirby-Bauer) testing is not reliable for Staphylococcus aureus; cefoxitin disks should be used to determine methicillin resistance.7
Penicillin Human: Enterococcus spp and Staphylococcus spp Most gram-negative bacteria
  • All β-hemolytic streptococci are susceptible.
  • Clinical use in small animals is limited due to available formulations.
Piperacillin Human: P aeruginosa N/A
  • An antipseudomonal penicillin
  • Clinical use is limited due to available formulations.

Cephalosporins

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Cephalothin or Cefazolin

Canine: E coli, Pasteurella multocida, S aureus, S pseudintermedius, and β-hemolytic

Streptococcus spp in dermal, respiratory, soft tissue, and urinary tract infections

 

Human: Enterobacteriaceae

Enterococcus spp, P vulgaris, S marcescens, Enterobacter spp, P aeruginosa
  • Generally indicates susceptibility to cephalexin and cefadroxil
  • Human breakpoints for cephalothin are used for other first-generation cephalosporins to treat Enterobacteriaceae infections, but cefazolin should be tested separately.
Cefoxitin Human: Staphylococcus spp Enterococcus spp, P aeruginosa
  • A second-generation human-approved cephalosporin with excellent activity against anaerobes
  • Cefoxitin resistance is an indicator of methicillin-resistance in S aureus but is not reliable for S pseudintermedius; oxacillin resistance is the preferred indicator.16
  • Indicates ESBL-producing bacteria, which are susceptible to cefoxitin but resistant to third-generation cephalosporins17
Cefpodoxime Canine: E coli, Proteus mirabilis, P multocida, S aureus, S pseudintermedius, and S canis in wounds and abscesses Enterococcus spp, P aeruginosa
  • Generally indicates susceptibility to third-generation cephalosporins, including cefovecin and ceftiofur
  • Indicates ESBL-producing bacteria, which are often resistant to these cephalosporins but still susceptible to amoxicillin–clavulanic acid18

Tetracyclines

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Doxycycline

Canine: S pseudintermedius in dermal and soft tissue infections

Human: Enterococcus spp

P aeruginosa
  • Frequently active against methicillin-resistant staphylococci9
Minocycline Proposed Canine: S pseudintermedius in dermal and soft tissue infections P aeruginosa
  • May be considered in the treatment of methicillin-resistant staphylococci when resistance to doxycycline has been documented
Tetracycline

Canine: Staphylococcus spp in dermal and soft tissue infections

 

Human: Enterococcus spp

Proteus spp, P aeruginosa
  • Susceptibility indicates susceptibility to oxytetracycline.
  • Staphylococci with reduced susceptibility to tetracycline or oxytetracycline may be susceptible to doxycycline or minocycline.9

Sulfonamides

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Sulfisoxazole

Human: Enterobacteriaceae, Staphylococcus spp

Enterococcus spp, P aeruginosa
  • Susceptibility indicates general susceptibility to all sulfonamides.11​​​​​​​
Trimethoprim– sulfamethoxazole Human: Enterobacteriaceae, Staphylococcus spp Enterococcus spp, P aeruginosa
  • Susceptibility indicates general susceptibility to sulfonamides in combination with trimethoprim.11

Macrolides/Lincosamides

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Clindamycin

Canine: β-hemolytic Streptococcus spp in dermal and soft tissue infections

Enterobacteriaceae11
  • Susceptibility indicates susceptibility to lincomycin.
  • Active against respiratory gram-negative pathogens but not gram-negative enteric bacteria
  • If staphylococci are reported as susceptible to clindamycin but resistant to erythromycin, disk-diffusion test should be performed to check for inducible resistance that renders clindamycin ineffective.19
Erythromycin Human: Staphylococcus spp Enterobacteriaceae
  • Susceptibility indicates general susceptibility to azithromycin and clarithromycin.
  • Active against respiratory gram-negative pathogens but not gram-negative enteric bacteria

Phenicols

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Chloramphenicol

Canine: P multocida in dermal and soft tissue infections

 

Human: Enterococcus spp

P aeruginosa
  • Chloramphenicol is generally active against staphylococci (including methicillin-resistant isolates), enterococci, and E coli (including ESBL-producing isolates).20,21
  • Toxicity limits treatment to only a short duration in cats.
  • Clinical use in small animals is limited due to human health concerns (eg, aplastic anemia).

Fluoroquinolones

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Enrofloxacin

Canine: Enterobacteriaceae, Staphylococcus spp, and Streptococcus spp in dermal, respiratory, soft tissue, and urinary tract infections

Feline: Enterobacteriaceae, P aeruginosa, and Streptococcus spp in dermal and soft tissue infections

Anaerobes
  • Susceptibility indicates general susceptibility to veterinary fluoroquinolones, including marbofloxacin, difloxacin, and orbifloxacin.
  • Ciprofloxacin (in humans) has the greatest activity of all the fluoroquinolones against Pseudomonas spp, but it has less ideal pharmacokinetics than veterinary fluoroquinolones.
Pradofloxacin

Canine: Enterobacteriaceae, S pseudintermedius in dermal and urinary tract infections

Feline: Enterobacteriaceae, P multocida, S pseudintermedius, S aureus, Staphylococcus felis, and S canis in dermal, respiratory, and urinary tract infections

N/A
  • Pradofloxacin is active against anaerobic bacteria.
  • Many pathogens remain susceptible to pradofloxacin while testing resistant to other fluoroquinolones.22

Aminoglycosides

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Amikacin

Canine: E coli, P aeruginosa, Staphylococcus spp, Streptococcus spp

Enterococcus spp,11 anaerobes
  • Amikacin is active against gram-negative enteric bacteria and staphylococci, including methicillin-resistant isolates.23 It is less active against streptococci but more active against Pseudomonas spp than other aminoglycosides.
  • Clinical use in small animals is limited by pharmacokinetic properties and toxicity.
Gentamicin Canine: Enterobacteriaceae, P aeruginosa Enterococcus spp,11 anaerobes
  • Gentamicin is active against gram-negative enteric bacteria and staphylococci, including some methicillin-resistant isolates.23
  • Usually active against Pseudomonas spp but is more susceptible to enzymatic resistance than is amikacin.
  • Clinical use in small animals is limited by pharmacokinetic properties and toxicity.

Limited-Use Antimicrobials

Antimicrobial

Breakpoint Source

(Canine, Feline, Human)

Intrinsic Resistance Notes
Nitrofurantoin

Human: Enterococcus spp, Enterobacteriaceae

P mirabilis11
  • Used exclusively to treat uncomplicated UTIs
  • Usually active against E coli (including ESBL-producing isolates), enterococci, and staphylococci, including methicillin-resistant isolates24
Mupirocin There are no veterinary breakpoints for topical antimicrobial product; human breakpoints are questionable. N/A
  • Topical product used for the treatment of methicillin-resistant staphylococci
  • It is assumed that drug concentrations are high at the application site; however, for most topical agents, measured drug concentrations at the site are not known, nor is the length of time for which those concentrations are maintained. The decision to use is based on clinical experience of efficacy.
Fusidic acid Human: Staphylococcus spp N/A
  • Topical product used for the treatment of methicillin-resistant staphylococci25
  • See Mupirocin for limitations in susceptibility testing.
Rifampin Human: Staphylococcus spp N/A
  • Rifampin is generally active against methicillin-resistant staphylococci.
  • Use is limited due to hepatotoxicity.
  • Should not be used as monotherapy, as resistance rapidly emerges with this type of use
Imipenem Human: Enterobacteriaceae, P aeruginosa N/A
  • Susceptibility indicates susceptibility to carbapenems, including meropenem.
  • Methicillin-resistant staphylococci are resistant to imipenem.
  • Imipenem should be a last resort treatment in human medicine; use in veterinary medicine should be strictly limited.
Vancomycin Human: Enterococcus spp, S aureus, coagulase-negative Staphylococcus spp N/A
  • Vancomycin should be a last resort treatment for gram-positive infections (eg, enterococci, methicillin-resistant staphylococci) in humans; use in veterinary medicine should be strictly limited.

CLSI = Clinical Laboratory Standards Institute, ESBL bacteria = extended-spectrum β-lactamase–producing bacteria, MIC = minimum inhibitory concentration

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.


Pulse Alterations

Elisa M. Mazzaferro, MS, DVM, PhD, DACVECC, Cornell University Veterinary Specialists

Cardiology

|Peer Reviewed

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Pulse Alterations
Clinician's Brief
Clinician's Brief

AFAST = abdominal focused assessment using sonography for trauma, SIRS = systemic inflammatory response syndrome, TFAST = thoracic focused assessment using sonography for trauma

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.


Image Gallery: Red Blood Cell Evaluation in Blood Films

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

Clinical Pathology

|Peer Reviewed

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Image Gallery: Red Blood Cell Evaluation in Blood Films

Blood film evaluation is an important part of the routine CBC, as it often provides valuable diagnostic and prognostic information regarding the patient and the disorder being investigated. Ideally, a blood film should be evaluated as a part of every CBC.  

Regular blood film evaluation can provide the practitioner with a breadth of experience, including a better understanding of normal variation among patients; an increased ability to recognize, and thus not overinterpret, the presence of common contaminants and artifacts that result from sample collection, preparation, and handling; an improved capacity to recognize morphologic abnormalities; and enhanced skill in determining when abnormal findings are clinically significant.

Even in cases when all CBC values are within the reference interval, abnormalities may be detected on the blood film. The following images and their interpretations focus on RBC morphology.

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.


Antiepileptic Drugs in Dogs

Heidi L. Barnes Heller, DVM, DACVIM (Neurology), Barnes Veterinary Specialty Services, Madison, Wisconsin

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Antiepileptic Drugs in Dogs

In the Literature

Kelly D, Raimondi F, Shihab N. Levetiracetam monotherapy for treatment of structural epilepsy in dogs: 19 cases (2010-2015). Vet Rec. 2017;181(15):401.


FROM THE PAGE …

Dogs with structural epilepsy (ie, seizures that occur secondary to an identifiable intracranial cause [eg, inflammatory, neoplastic, or vascular disease]) pose a special concern for veterinarians. These dogs may be neurologically abnormal, with a high risk for progression or worsening of neurologic signs as disease worsens. Commonly accepted first-line antiepileptic drugs (eg, phenobarbital, potassium bromide) carry dose-dependent risks for sedation, ataxia, and weakness, all of which could result in true or apparent clinical progression in neurologically compromised dogs.1 Patients receiving newer anticonvulsant drugs (eg, levetiracetam) have a reportedly lower incidence of adverse effects as compared with those receiving potassium bromide and/or phenobarbital.2 

This study evaluated seizure control and tolerability of levetiracetam monotherapy in 19 dogs diagnosed with structural epilepsy. Five of 6 dogs diagnosed with meningoencephalomyelitis of unknown origin (MUO) demonstrated improved seizure control on levetiracetam monotherapy, although phenobarbital was later added to one dog’s treatment regimen. Four of 5 dogs diagnosed with seizures secondary to vascular disease were considered to have good seizure control with levetiracetam, whereas none of the 5 dogs diagnosed with neoplasia attained good seizure control with levetiracetam. Of the remaining dogs, one with congenital hydrocephalus attained good seizure control, whereas the 2 others (one with cortical dysplasia, one with traumatic brain injury) attained poor control.

Dogs with seizures that occur secondary to intracranial neoplasia and without definitive treatment (surgery or radiation therapy) often demonstrate progression resulting in death or euthanasia. Based on the data presented, levetiracetam should not be considered appropriate monotherapy for dogs with seizures that occur secondary to intracranial neoplasia. Levetiracetam may be considered appropriate for dogs with vascular disease or MUO; however, this needs further investigation in a large number of dogs with a standardized treatment protocol for the underlying disease. The lack of a standard treatment protocol in this study was a major limitation. Managing a dog with structural epilepsy requires a balance of unwanted side effects, undesired progression of disease, quality-of-life goals for the dog, and owner financial limitations.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Levetiracetam may be useful as monotherapy for a select population of dogs with structural epilepsy, but close seizure monitoring is important.

 

2

If seizure control is not achieved, the addition of phenobarbital or potassium bromide 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.


Chronic Kidney Disease in Hyperthyroid Cats

Alex Gallagher, DVM, MS, DACVIM, University of Florida

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Chronic Kidney Disease in Hyperthyroid Cats

In the Literature

Williams TL, Elliott J, Syme HM, Archer J. Investigation of the association between serum protein concentrations and concurrent chronic kidney disease in hyperthyroid cats. Res Vet Sci. 2017;115:412-417.


FROM THE PAGE …

Hyperthyroidism is the most common endocrine disorder in cats, with prevalence ranging from 2% to 4%.1 Because of increases in glomerular filtration rate and decreased muscle mass, cats with hyperthyroidism may have masked concurrent chronic kidney disease (CKD) that does not become apparent until after treatment.2,3 It can be difficult to determine before therapy which cats may develop azotemia after restoration of the euthyroid state. A suitable biomarker has not been identified in prior reports.

In a previous study, lower plasma globulin concentrations were found to be a predictor of azotemia within 240 days of diagnosis of hyperthyroidism.4 In the present study, the investigators aimed to establish the repeatability of this finding and determine whether a particular globulin fraction, measured by protein electrophoresis, was associated with masked CKD. Fifty-six hyperthyroid cats and 26 healthy older cats were evaluated. Although differences were found between healthy and hyperthyroid cats in some variables, no differences were noted in concentrations of total globulin or any of its fractions between masked-azotemic and nonazotemic cats. 

Because a reliable biomarker to determine masked kidney disease is not available, clinicians should thoroughly evaluate kidney function in cats before and after hyperthyroidism treatment. Thyroid function should also be assessed using thyroid-stimulating hormone and total thyroxine concentrations to avoid iatrogenic posttreatment hypothyroidism, as this can contribute to azotemia and reduced survival time.5,6


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Cats with hyperthyroidism should be screened at the time of diagnosis for evidence of CKD through evaluation of serum chemistry profile and urinalysis. Blood pressure should also be measured to assess for hypertension.

2

Because there is not a reliable biomarker to determine the presence of masked kidney disease, reassessment for kidney disease should be performed once the cat is euthyroid.

 

3

A hypothyroid state after treatment can contribute to the development of azotemia and result in reduced survival time.

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.


Cyclophosphamide-Induced Sterile Hemorrhagic Cystitis

Timothy M. Fan, DVM, PhD, DACVIM (Oncology, Internal Medicine), University of Illinois at Urbana–Champaign

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Cyclophosphamide-Induced Sterile Hemorrhagic Cystitis

In the Literature

Setyo L, Ma M, Bunn T, Wyatt K, Wang P. Furosemide for prevention of cyclophosphamide-associated sterile hemorrhagic cystitis in dogs receiving metronomic low-dose oral cyclophosphamide. Vet Comp Oncol. 2017;15(4):1468-1478.


FROM THE PAGE …

Systemic chemotherapy remains a cornerstone for treating companion animals with cancer. The manner by which antineoplastic drugs are administered can be categorized in 2 therapeutic strategies: maximum-tolerated dose or metronomic chemotherapy (ie, low-dose daily oral administration).1,2 Oral cyclophosphamide, either alone or in conjunction with NSAIDs (eg, piroxicam), is the most common cytotoxic agent used for metronomic chemotherapy in veterinary patients.3,4 Although metronomic cyclophosphamide administration does not typically cause myelosuppression or GI toxicities, the metabolism of cyclophosphamide still results in production of acrolein, a potent uroepithelial irritant with the potential to cause sterile hemorrhagic cystitis (SHC).5 Strategies for mitigating the development of SHC involve reducing acrolein contact time with uroepithelial cells via drug-induced polyuria and administering furosemide or prednisolone.6

This retrospective study examined the incidence of clinically relevant SHC in pet dogs receiving long-term (>6 months) metronomic cyclophosphamide therapy with or without concurrent oral furosemide. Over a span of 6 years at a single institute, 115 dogs meeting study inclusion criteria were categorized into 2 groups and evaluated for the development of clinically relevant SHC. Among the dogs, 25 cases of SHC were either diagnostically confirmed (via urinalysis, urine culture, ultrasonography) or clinically suspected (unresponsiveness to antibiotic), amounting to an incidence of 21.7%. Significantly, the incidence of SHC was reduced in dogs treated with concurrent furosemide therapy (10.2% [5/49 dogs]) as compared with that in dogs not treated with furosemide (30.3% [20/66 dogs]). Collectively, these findings suggest that coadministration of furosemide along with long-term metronomic cyclophosphamide therapy can reduce the incidence of clinical signs associated with SHC.

Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.
Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.

Figure Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.

Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.
Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.

Figure Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.

Figure Visual (A) and chemical (B; ie, colorimetric) detection methods useful in complementing clinical signs (eg, hematuria, stranguria, pollakiuria) to support the presumed diagnosis of SHC. Visual assessments should be limited to detecting gross hematuria, whereas chemical detection (ie, urine dipstick) provides improved sensitivity for the identification of microscopic hematuria.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Oral metronomic cyclophosphamide therapy can result in uroepithelial irritation secondary to acrolein formation, even at low doses.

 

2

The overall incidence of SHC in pet dogs treated with metronomic cyclophosphamide is clinically relevant, with approximately 1 in 5 dogs being affected during long-term (>6 months) treatment.

 

3

Coadministration of furosemide (0.5-1.0 mg/kg q24h) with metronomic cyclophosphamide therapy can substantially reduce the likelihood of SHC-associated clinical signs (ie, hematuria, stranguria, pollakiuria).

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.


Rapid Assessment with Physical Examination in Dyspneic Cats

Elke Rudloff, DVM, DACVECC, Lakeshore Veterinary Specialists, Glendale, Wisconsin

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Rapid Assessment with Physical Examination in Dyspneic Cats

In the Literature

Dickson D, Little CJL, Harris J, Rishniw M. Rapid assessment with physical examination in dyspnoeic cats: the RAPID CAT study. J Small Anim Pract. 2018;59(2):75-84.


FROM THE PAGE …

The utility of clinical history and initial examination of cats presented with acute dyspnea (n = 108) to differentiate between cardiac and noncardiac causes were assessed in the present study. A study protocol was provided to participating clinicians to standardize the data collected. A triage algorithm was created using the data taken from the study participants’ clinical examination findings, which were highly specific for excluding or diagnosing cardiac dyspnea. 

One of the main statistical parameters found to be associated with cardiac-related respiratory distress was tachycardia (heart rate, >200 bpm), although this may be discordant with common clinical impressions. In addition, 10% (6/60) of the cats in the cardiac group were later definitively diagnosed with hyperthyroidism. It remains unclear whether all cats in the cardiac group were tested for hyperthyroidism and whether this might have affected the range and median heart rate used in building the algorithm.

The study essentially recommends that, if a cat with acute respiratory signs has a gallop rhythm and an increased heart rate or respiratory rate or hypothermia, furosemide should be administered before performing additional diagnostics. This approach seems benign, as long as the clinician also evaluates the respiratory pattern and auscultates the lungs and, if pleural effusion or pneumothorax is possible, performs an immediate thoracocentesis.1 Including instructions for sedation/anxiolysis in the study algorithm may also be worthwhile to reduce patient anxiety caused by dyspnea.

Of note, the term dyspnea, which in veterinary medicine refers to difficult or labored breathing, is a term derived from human medicine, in which it is used to describe a subjective, sensory experience of breathing discomfort; this is an experience rather than a clinical sign.2 Veterinarians should describe the clinical signs of respiratory distress (ie, respiratory rate, respiratory effort, breathing pattern, open-mouth breathing) to accurately convey what a nonverbal patient is showing rather than assume what it is feeling. A more valid measure of response to treatment can then be determined.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

A gallop rhythm and the presence of hypothermia or increased respiratory rate in a cat with acute respiratory difficulty should alert the veterinary team to the possibility of congestive heart failure.

 

2

Institution of therapy with furosemide before a definitive echocardiogram is obtained is reasonable when congestive heart failure is suspected.

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.


Risk Factors & Prevalence of Dystocia in Dogs

Selena L. Lane, DVM, DACVECC, University of Georgia

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Risk Factors & Prevalence of Dystocia in Dogs

In the Literature

O’Neill DG, O’Sullivan AM, Manson EA, et al. Canine dystocia in 50 UK first-opinion emergency-care veterinary practices: prevalence and risk factors. Vet Rec. 2017;181(4):88.


FROM THE PAGE …

Dystocia is a significant cause of mortality in puppies and can be a life-threatening condition in bitches at parturition. Age, size, and breed are known risk factors.1-3 Understanding more about patient-specific attributes associated with canine dystocia may help veterinary professionals educate the public about breed-specific risk factors.

Data compiled from primary care and emergency veterinary practices were used to provide epidemiologic data of dystocia in bitches in the United Kingdom. Dystocia cases were defined as bitches requiring veterinary intervention at the time of whelping with at least one puppy retained on presentation.

Among 18 758 intact female dogs seen in UK veterinary clinics, 701 dystocia cases were identified, with a 3.7% prevalence rate of emergent dystocia cases in the overall population. 

Dystocia was most common in French bulldogs, Boston terriers, pugs, and Chihuahuas. Brachycephalic breeds represented 3 of the 4 breeds at the highest risk for dystocia. Most (94%) affected dogs were purebred bitches. Purebred dogs were found to be 3.4 times more likely to develop dystocia as compared with crossbreed bitches. Identification of at-risk breeds may help veterinary professionals inform breeders and owners about responsible breeding practices and reduce the incidence of dystocia in high-risk breeds. 

Body weight also had an impact on risk, with dogs that weighed less than 22 lb or more than 88.2 lb at higher risk as compared with dogs that weighed 44.1 lb to 66 lb. Bitches between 3 and 5.9 years of age were 3.1 times more likely to experience dystocia as compared with younger intact female dogs.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Brachycephalic breeds and Chihuahuas are at increased risk for dystocia, with dogs 3 to 5.9 years of age more frequently affected than younger dogs.

 

2

Owners should be educated about responsible breeding practices and potential for dystocia in at-risk breeds.

 

3

Dystocia is always urgent and may require emergency surgical intervention, regardless of breed and age.

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.


Leflunomide & Immune-Mediated Disease

Lisa Singer, VMD, DACVIM, Veterinary Specialist Services

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Leflunomide & Immune-Mediated Disease

In the Literature

Sato M, Veir JK, Legare M, Lappin MR. A retrospective study on the safety and efficacy of leflunomide in dogs. J Vet Intern Med. 2017;31(5):1502-1507.


FROM THE PAGE …

Leflunomide is an immunomodulatory drug that has been used as primary and adjunctive therapy for naturally occurring immune-mediated and inflammatory diseases, specifically colorectal polyps in miniature dachshunds and immune-mediated polyarthritis.1,2 

This study retrospectively evaluated the safety and efficacy of leflunomide (0.8-4.3 mg/kg q24h) in 92 dogs treated between the years 1995 and 2014. Median duration of treatment was 23.5 weeks (range, 1-208 weeks). Various adjunctive therapies included prednisolone, mycophenolate, cyclosporine, and azathioprine. The most common diseases treated were immune-mediated polyarthritis, immune-mediated thrombocytopenia, and immune-mediated hemolytic anemia. Adverse events possibly attributable to this drug were observed in 11/92 dogs (12%) and included diarrhea, lethargy, unexplained hemorrhage, thrombocytopenia, and increased liver enzymes. After a 30% to 50% dose reduction or drug discontinuation, several adverse events resolved.

Previous studies have reported a starting dose of 3-4 mg/kg q24h.3 The median starting dose was higher in dogs with adverse events (2.9 mg/kg q24h) than in dogs without adverse events (1.6 mg/kg q24h). The overall drug response rate was 70.5%; for dogs receiving leflunomide as monotherapy, drug response rate was 81.8%.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Leflunomide is well tolerated when used in conjunction with prednisolone.

 

2

Leflunomide at lower starting doses (eg, 2 mg/kg q24h) when used as an adjunctive therapy may be equally clinically effective in the treatment of immune-mediated diseases as compared with its use at higher doses (3-4 mg/kg q24h).

3

Leflunomide dose reductions of 30% to 50% or drug discontinuation can resolve most adverse events. Leflunomide may rarely cause hemorrhage after 6 weeks or more of drug administration, in which case the drug should be discontinued immediately.

References

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

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

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


Research Note: Autologous Canine Skin Substitute

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This proof-of-concept study described an autologous canine skin substitute designed to treat large, deep, or delayed-healing wounds. The grafting capacity of the skin constructs were first assessed by xenografting in mice, then 2 dogs with large, deep skin wounds were recruited for the study. Keratinocytes and fibroblasts were isolated from 8-mm punch biopsy samples from each dog. Skin substitutes were constructed on a fibrin-based matrix and were ready to use within 12 to 14 days after biopsies were obtained. Full wound closure was achieved 25 days after grafting in one dog and 40 days after grafting in the second dog. Permanent epithelialization was confirmed via histology. Although the engineered skin construct did not contain hair follicles or adnexal glands, most requirements of an ideal skin substitute appeared to be fulfilled.

Source

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

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Research Note: Feline Vaccine-Associated Injection Site Sarcomas

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Feline vaccine-associated injection site sarcomas (ISSs) were first reported in 1991. Although radical surgery, radiation, and chemotherapy are all used to treat these aggressive tumors, recurrence is common. Nanoparticles can provide building blocks for therapeutic mechanisms and increase ability to visualize tissue. Gold nanoparticles (AuNP) can increase the radiation dose deposited into tissue. This in vitro study evaluated the effect of AuNP on ISS cytotoxicity and colony formation. Although AuNP alone did not apparently alter short-term viability or cell cycle of ISS cells, cellular proliferation decreased significantly. Thus, AuNP shows initial promise as a long-term therapeutic to decrease ISS growth.

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.


Prazosin Use in Feline Urethral Obstruction

Elke Rudloff, DVM, DACVECC, Lakeshore Veterinary Specialists, Glendale, Wisconsin

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Prazosin Use in Feline Urethral Obstruction

In the Literature

Reineke EL, Thomas EK, Syring RS, Savini J, Drobatz KJ. The effect of prazosin on outcome in feline urethral obstruction. J Vet Emerg Crit Care. 2017;27(4):387-396.


FROM THE PAGE …

Feline urethral obstruction is common in veterinary medicine, and recurrence rates of 14% to 57% have been reported.1-4 Although therapeutic techniques have evolved, no reliable method or medication has been proven to prevent recurrent feline urethral obstruction (rFUO). In 1971, an observational study discussed an escalating approach to therapy, which included IM injections of pancreatic extract, antibiotic administration, and digital and needle manipulation of the urethra.5 Since then, reports have documented use of intravesicular lidocaine, intravesicular and oral glycosaminoglycans, phenoxybenzamine, and prazosin in the prevention of rFUO.2,6-9

Prazosin, an α1-adrenergic blocker, acts as a smooth muscle relaxer and is labeled for the treatment of hypertension in humans. Its use in the treatment of benign prostatic hyperplasia is extra-label and, in veterinary medicine, is prescribed for the prevention of feline urethral obstruction and rFUO.9 No pharmacokinetic information on prazosin in cats has been reported, and recommended doses range from 0.25-1 mg/kg PO q12h.9 Until this study was published, there had only been weak evidence in the form of retrospective studies without control subjects describing the use of prazosin in cats with rFUO, and small studies have reported mixed information regarding prazosin’s efficacy in preventing rFUO.3,10,11 

This article prospectively examined whether prazosin at 0.25 mg/cat PO q12h affected rFUO rates. No significant side effects or reduction in rFUO rates were noted in 47 male cats (27 receiving prazosin, 20 receiving placebo) observed for one month. Studies using larger test and control groups are needed to determine statistically relevant differences.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Prazosin at 0.25 mg/cat PO q12h does not appear to have clinically relevant side effects.

 

2

Based on the study findings, prazosin does not appear to prevent rFUO.

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.


Canine Aural Hematoma Techniques

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

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Canine Aural Hematoma Techniques

In the Literature

Hall J, Weir S, Ladlow J. Treatment of canine aural hematoma by UK veterinarians. J Small Anim Pract. 2016;57(7):360-364.


FROM THE PAGE …

Aural hematomas occur commonly in dogs. Treatment can include needle drainage +/- steroid infusion or surgical drainage with suture placement. Management of the underlying cause is essential. Information on recurrence is limited, and no robust comparative data to guide initial and recurrence treatment strategies exist.

This survey investigated opinions regarding aural hematoma treatment techniques and success. A total of 251 responses were analyzed. Initial treatments included needle drainage with (43%) and without (16%) local deposition of corticosteroids, surgery (29%), Penrose drain placement (4%), or other (8%). Surgical techniques included linear incision with sutures (35%), sutures with stents (24%), S-shaped incision and sutures (23%), or other punch biopsy or stent approaches (18%). The most common rationale for treatment type provided was history of previous success (77%); less frequent reasons cited were owner preference (6%), cost (5%), practice policy (4%), convenience (4%), and other (4%). The clinicians’ perceived success of initial treatment was good to excellent with surgery (91%) as compared with needle drainage with (59%) and without (38%) steroids. Sixty-five percent of veterinarians predicted a 0% to 25% chance of recurrence; however, only 51% of veterinarians who used needle drainage and steroids expected an outcome equally as favorable as compared with the 96% who chose surgery as a first-line treatment. Recurrent hematomas were more commonly treated with surgery (67%), followed by needle drainage with (16%) or without (7%) steroids, Penrose drain placement (7%), and other (3%). Following a second treatment, 83% of veterinarians predicted a 0% to 25% chance of recurrence.

Study results suggest the most common initial treatment provided for aural hematomas is needle drainage with or without local steroids (59%). Some type of surgical intervention is more common with recurrent hematomas, and the overall perceptions of success with surgery generally are higher than with other treatment options.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Identification and management of the underlying cause of aural hematoma formation is key to successful treatment.

 

2

Treatment must be provided in a timely fashion and followed carefully in the short term.

 

3

Goals include removal of the blood clot, prevention of recurrence, and maintaining cosmetic appearance and function of the ear.

 

4

Less invasive options (drainage +/- steroids) should be considered for acute or mild cases.

 

5

Chronic or recurrent cases may require surgical drainage and tacking sutures.

 

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.


Mirtazapine

Mirtazapine

Jessica M. Quimby, DVM, PhD, DACVIM, The Ohio State University

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Mirtazapine

Mirtazapine has become widely used in veterinary medicine due to its commonly recognized effects of appetite stimulation and weight gain.

CLINICAL APPLICATIONS

  • Mirtazapine is an effective appetite stimulant in cats1-5 and is used for nutritional support in both dogs and cats with acute and chronic illness. 
    • Mirtazapine has been demonstrated in placebo-controlled trials to result in appetite stimulation in normal cats and appetite stimulation, weight gain, and improved body condition in cats with chronic kidney disease (CKD).3,4 
    • The drug’s mechanism of action is not fully understood but likely involves antagonism of the serotonin 2C (5HT2c) receptor, which is known for its appetite-inhibition activity, as well as antagonism of the histamine 1 (H1) receptor, which also plays a role in appetite regulation.6,7 
  • Mirtazapine has antiemetic properties due to its antagonism of the serotonin 3 (5HT3) receptor and has been shown to decrease vomiting in cats with CKD.4 
  • Because of its superior receptor-binding affinity, there is some evidence that concurrent administration of mirtazapine with 5HT3-receptor antagonists (eg, ondansetron) may decrease the efficacy of ondansetron in humans.8 
    • Although evidence for this interaction is not available for cats and dogs, this phenomenon should be taken into account when choosing antiemetic and antinausea regimens.
  • Mirtazapine appears anecdotally to have some appetite-stimulating properties in dogs, but no studies have been conducted to assess appetite in healthy or hyporexic dogs receiving this drug.9,10 
  • A prokinetic effect has been demonstrated in healthy dogs that received mirtazapine at 1.7-2.0 mg/kg PO once, resulting in improved gastric emptying and colonic motility.11 
    • The clinical utility of this prokinetic effect merits further investigation. 

PHARMACOKINETICS & PHARMACODYNAMICS

  • In cats, administering one-fourth of a 15-mg tablet (3.75 mg) every 3 days was initially recommended based on an early, mostly anecdotal, open clinical trial in which a dose was extrapolated from use in humans10; however, several studies have since helped determine a more appropriate starting dose for cats. 
  • Mirtazapine is amenable to transdermal administration and has been demonstrated to achieve therapeutic serum concentrations in cats.1,5 
    • Placebo-controlled pharmacodynamic studies have demonstrated that transdermal administration of mirtazapine results in increased appetite in normal cats and increased appetite and weight in cats with CKD.1,5 
    • Transdermal mirtazapine obtained from compounding pharmacies can have high variability1 among preparations and may not have the same stability and efficacy as that demonstrated in referenced studies.
  • The pharmacokinetics of mirtazapine is affected by age and several disease states.
    • As compared with humans (half-life, 20-40 hours), the half-life of oral mirtazapine in young normal cats is relatively short (9.2 hours).
    • A repeat-dosing study demonstrated little drug accumulation with daily administration of 1.87 mg/cat in young cats2,3; median peak serum concentrations were reached in one hour.
    • In contrast, the half-life of oral mirtazapine is prolonged in elderly cats (12.1 hours) and cats with CKD (15.2 hours) and/or liver disease (15.1 hours).2,12 
      • This is similar to pharmacokinetics in humans in which kidney and/or liver disease prolong half-life by 25% to 30%.13
  • In young healthy dogs, the half-life of mirtazapine is 6 hours, with peak serum concentration at 0.9 hours.9

ADMINISTRATION & DOSE INTERVAL

  • The variable pharmacokinetics of mirtazapine should be taken into account when determining the dose interval.
  • The suggested oral dose interval for cats is 1.87 mg/cat PO q24h in younger cats with normal organ function, q48h in cats with CKD, and q48-72h in cats with liver disease.2,3,12  
    • A higher dose of 3.75 mg has been associated with increased side effects, typically without any greater efficacy for appetite stimulation.3,14
      • Some cats may require titration up to this dose.3,14 
  • The suggested (anecdotal) dose interval for dogs is 0.6-1.0 mg/kg q12h. 
    • Studies evaluating dose interval in dogs with liver and/or kidney disease have not been conducted.9 

SAFETY & ADVERSE EFFECTS

  • Adverse effects in cats are dose-dependent and much more likely to occur at higher doses or with accidental administration of an entire 7.5- or 15-mg tablet.3,14 
    • Adverse effects, which appear to be more common in cats than in dogs, most commonly include vocalization, agitation, vomiting, abnormal gait/ataxia, restlessness, tremors/trembling, hypersalivation, tachypnea, tachycardia, and lethargy.3,14
    • With both the oral and transdermal formulations, the dose should be titrated to the lowest effective amount for appetite stimulation to minimize adverse effects.
  • Subclinical reversible increases in liver enzymes (eg, marked increases in alanine transaminase [possibly idiosyncratic]) may occur as a result of mirtazapine administration; discontinuation of the drug is recommended in these patients.4 
  • Concurrent administration with selective serotonin reuptake inhibitors may increase serotonin syndrome-like adverse effects.13

CKD = chronic kidney 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.


External Splinting for Pectus Excavatum in Kittens

Karen M. Tobias, DVM, MS, DACVS, University of Tennessee

Whitney DeGroot, DVM, University of Tennessee

Orthopedics

|Peer Reviewed

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External Splinting for Pectus Excavatum in Kittens

Figure 1 Pectus excavatum in a 12-week-old kitten. The caudal sternebrae are deviated dorsally, whereas the xiphoid process is pointed ventrally.

Pectus excavatum is a congenital, concave deformity of the caudal sternum that results in a reduced ventrodorsal thoracic diameter.1,2 The cause is unknown, although a hereditary component has been suggested.3 Pectus excavatum can result in compromised pulmonary and cardiac function due to decreased intrathoracic capacity and restriction of diastolic filling.2-4 Common clinical signs include a palpable concavity of the thorax, respiratory distress, exercise intolerance, tachypnea, cyanosis, and failure to thrive, although some animals may appear clinically normal.

Diagnosis is based on physical examination and thoracic radiography findings (Figure 1). Radiographs should show a sternal deformity and decreased caudal thoracic space secondary to dorsal deviation of the sternum.3,5 The severity of the deformity can be graded using 2 indices (ie, vertebral or frontosagittal; see Deformity Indices), although these indices may not correlate with the severity of clinical signs.4 Severity can also be evaluated with CT. A study in kittens found CT to be useful in identifying midline sternal deviation that could potentially cause more severe clinical signs, despite relatively mild skeletal deformity, because of diastolic restriction.4

DEFORMITY INDICES4,8

  • Frontosagittal index: The ratio of thoracic width at T10 measured on a dorsoventral radiograph and the distance from the center of the ventral surface of the vertebra overlying the deformity to the nearest point on the sternum (normal, 0.7-1.3) 
  • Vertebral index: The ratio of the distance from the center of the dorsal surface of the vertebral body overlying the deformity to the near point of the sternum and the dorsoventral diameter of the centrum of the same vertebra measured on a lateral radiograph (normal, 12.6-18.8)

Three types of surgical repair have been described in cats: external splinting, internal splinting (using plates or rods), and sternebral pinning combined with external splinting.1,6,7 Reports have suggested that external splinting can be attempted in kittens (typically those less than 4 months of age) if the sternebrae are still pliable.6,8 

The brace should be created from a moldable (preferably radiolucent) material and should be U-shaped to fit around the ventral thorax, extending approximately three-fourths of the way to the spine. Surgical scrub sponges can be used to pad the edges of the brace to prevent pressure sores, and holes can be created along the ventrolateral aspects of the brace to allow for suture passage. Percutaneous sutures should be placed around the sternum (ie, circumsternal) and through, around, or over the brace. The sutures should be tightened and secured so the sternum is pulled outward. To allow evaluation and cleaning of the region, the sutures can be secured by tying in a bow or with replaceable split shot fishing sinkers to allow for loosening and/or retightening. After placement of the circumcostal sutures and brace, lateral radiographs should be obtained to evaluate the position of the sternebrae and verify improvement in the thoracic width as compared with pretreatment measurements (Figure 2). The brace should be kept in place for several weeks until the sternum is sufficiently stiff to prevent inward displacement.

Patient in Figure 1. The sternum has been pulled ventrally and secured by circumsternal sutures to an external brace with removable split shot fishing sinkers.
Patient in Figure 1. The sternum has been pulled ventrally and secured by circumsternal sutures to an external brace with removable split shot fishing sinkers.

FIGURE 2 Patient in Figure 1. The sternum has been pulled ventrally and secured by circumsternal sutures to an external brace with removable split shot fishing sinkers.

FIGURE 2 Patient in Figure 1. The sternum has been pulled ventrally and secured by circumsternal sutures to an external brace with removable split shot fishing sinkers.

Potential complications of external splinting include inadvertent lung or heart puncture, pneumothorax, re-expansion pulmonary edema, infection associated with the sutures, moist dermatitis from the splint, sinus tracts around the sutures, and deformity recurrence. While the brace is in place, patients must be strictly exercise-restricted and, preferably, kept away from other cats. Prying or scratching at the brace—by the kitten itself or other cats during play—must be prevented, as this can result in suture loosening and/or loss of reduction.

Weekly rechecks are recommended to ensure the brace has not loosened and that there is no evidence of infection at the suture sites. If infection is suspected, the replaceable split shot sinkers can be opened and matching suture ends can be clamped with hemostats until the brace can be elevated from the patient’s chest enough to examine the suture sites and facilitate wound care. Sedation is recommended any time the sutures are to be loosened.

Radiography every 2 weeks is recommended to ensure the defect remains reduced. The brace should remain in place for 4 to 8 weeks, depending on patient age, until the sternum feels palpably noncompliant after splint removal.3,6 If reduction fails with external splinting, partial sternectomy, or sternal wedge resection and internal splinting, may be required. Recurrence of clinical signs4 and evidence of recompression6,9 have not been reported in follow-up data for kittens treated with external splinting alone. 

There have been no controlled studies to determine whether all kittens with pectus excavatum require correction. The authors primarily perform external splinting on kittens showing clinical signs (eg, respiratory difficulty, exercise intolerance, poor growth). In some of these kittens, final indices after splint removal are not much improved over initial measurements, but clinical signs have resolved. It is possible that the splint prevented the condition from worsening while the kittens grew or that other, unmeasured indices (eg, diastolic volume) were improved by splinting. 


STEP-BY-STEP

EXTERNAL SPLINTING IN KITTENS


WHAT YOU WILL NEED

  • Moldable splint material (preferably radiolucent)
  • Nonabsorbable suture (0 or 2-0) material on a taper needle
  • Hemostats and needle drivers
  • Split shot fishing sinkers
  • Adhesive tape

STEP 1

Anesthetize the patient and position in dorsal recumbency. Aseptically prepare the ventral thorax. 

Clinician's Brief

STEP 2

Place the first suture, passing the needle underneath the xiphoid or the palpable caudal-most aspect of the sternum and keeping it adjacent to the dorsal surface of the cartilage. Place a hemostat at the suture ends to maintain them as stay sutures.

Clinician's Brief

STEP 3

Place gentle upward traction on the first suture, and place a second suture around the sternum, just cranial to the first, in the same fashion. The needle must be directed to pass dorsal to and circumferentially around the sternum. Exercise caution to avoid damaging essential intrathoracic structures, including the heart and lungs.

Clinician's Brief

STEP 4

With an index finger underneath the sternum, apply upward pressure to reduce the sternal defect and isolate the sternum from the lung and heart. While the sternum is secured in this position, additional sutures can be preplaced, as described above, until the sternal deformity is spanned.

Clinician's Brief

STEP 5

Separate the paired suture ends and pass them through the holes in the brace to either side of the midline. Resecure the sutures with hemostats.

Clinician's Brief

STEP 6

Once all circumcostal suture pairs have been passed through the brace, pull the sutures tight to reduce the sternal defect and secure them together by tying in a knot or bow or by clamping them with a removable split shot fishing sinker.

Clinician's Brief

STEP 7

Secure the suture ends with adhesive tape; do not cut them. The chest and brace can be covered with a bandage or small cloth (ie, t-shirt) to prevent self-trauma.

Clinician's Brief

References

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

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

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


Feline Complications from Mouth Gags

Justin Fraser, BSc (DVM Candidate), University of Tennessee

Shelly J. Olin, DVM, DACVIM (SAIM), University of Tennessee

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Feline Complications from Mouth Gags

A cat recovering from general anesthesia

THE CASE

A 7-year-old spayed female domestic shorthair cat is presented for routine dental cleaning and extraction of the left maxillary premolar. The patient is bright and alert with a normal energy level. Physical examination is unremarkable, with the exception of grade 3 periodontal disease. Preoperative CBC, serum chemistry profile, total thyroxine, urinalysis, and blood pressure are normal. 

The cat is premedicated with butorphanol (0.2 mg/kg IM) and tiletamine–zolazepam (3 mg/kg IM) before sedation is induced with propofol (6 mg/kg IV to effect). The patient is intubated, and anesthesia is maintained with isoflurane (1.5%) in 100% oxygen. Intravenous fluid rate during anesthesia is 10 mL/kg/hr. Monitoring includes pulse oximetry reading (peripheral capillary oxygen saturation [SpO2]), systolic blood pressure, and electrocardiography. SpO2 is maintained above 95%, blood pressure ranges from 100 to 110 mm Hg, and heart rate is stable between 160 and 170 bpm with no arrhythmias. 

With the patient positioned in lateral recumbency, dental radiographs are obtained. The patient is stable under anesthesia, and the team prepares to begin the procedure. 

What are the next steps?

THE CHOICE IS YOURS …

CASE ROUTE 1

Maintain good visualization with a spring-loaded mouth gag, which may be most convenient, for maximal opening of the jaw.

CASE ROUTE 2

Maintain good visualization with a small mouth gag crafted from a hypodermic needle cap cut to 20 mm in length and use your fingers to retract the lips during the procedure.

Poll

Which option did you choose?


Sounding Board

BAER = brainstem auditory evoked response, ERG = electroretinography, OU = both eyes, SpO2 = peripheral capillary oxygen saturation

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.


Clinical Reasoning

Jill Maddison, BVSc, DipVetClinStud, PhD, SFHEA, MRCVS, Royal Veterinary College, London, United Kingdom

Internal Medicine

|Peer Reviewed

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Clinical Reasoning

Veterinarians make decisions every day about diagnostic and treatment options for their patients. Clinical reasoning, along with a sound and relevant knowledge base, forms the cornerstone of these decisions.

Undergraduate and continuing education tend to focus on acquisition of knowledge; however, knowledge is only useful if it can be accessed, formulated, and applied to the problem at hand. Thus, successful case assessment requires knowledge, understanding, and clinical reasoning.

Case Example

Sheba, a 3-year-old spayed rottweiler located in New York, is presented with an acute history of melena and collapse overnight. She had vomited bile once a few hours prior, had been active and normal the preceding day, and had eaten well the preceding afternoon. On physical examination, she is overweight and weak with pale mucous membranes, a prolonged capillary refill time (>2 seconds), a heart rate of 160 bpm, and a normal rectal temperature. A systolic heart murmur (grade 2/6) is auscultated on the left-hand side. Her spleen appears large on abdominal palpation. She is up-to-date on vaccinations and parasite preventives and has not recently traveled.

Clinical Reasoning Models

Clinical reasoning is a complex process that varies widely depending on the clinician’s preferred thinking and learning style, past experiences and expertise, the clinical problem itself, and the context in which the problem is encountered. Clinical reasoning used by clinicians can be broadly classified as Type 1 (nonanalytic) or Type 2 (analytic). A blended approach or triangulation of both types (to cross-check clinical reasoning and diagnostic conclusions) is advocated for successful diagnostic decision-making.1

Nonanalytic Clinical Reasoning

Nonanalytic reasoning, often referred to as pattern recognition, occurs quickly and subconsciously and primarily relies on the clinician accessing knowledge and patterns from past experiences that can be applied to the present case. Thus, limited previous case exposure may hinder pattern recognition in students and new graduates, veterinarians returning to practice after a prolonged break, or veterinarians changing their area of practice. Nonanalytic reasoning based on pattern recognition can be also be flawed if the clinician recognizes only a small number of salient factors in the case. 

Use of pattern recognition as the primary mode of clinical reasoning works well for many common disorders and has the advantage of being quick and cost-effective, provided that the diagnosis is correct. Pattern recognition is also effective in cases for which: 

  • A disorder has a unique and recognizable pattern of clinical signs
  • There are only a few diagnostic possibilities that can be easily remembered or ruled in or out by routine tests 
  • The clinician has extensive experience (and thus a rich bank of illness scripts to recall), is well read and up-to-date, reviews all diagnoses made regularly and critically, and has an excellent memory

Alternatively, pattern recognition as the primary clinical reasoning process can be problematic: 

  • For uncommon diseases
  • For common diseases that present atypically
  • When the patient is exhibiting multiple clinical signs that are not immediately associated with a specific disease and may or may not be related to a single diagnosis
  • If the pattern of clinical signs is suggestive of certain disorders but not specific for them 

For an experienced clinician, the success of pattern recognition relies on a correct diagnosis for the previously observed pattern. In general practice, the clinician must often form a provisional diagnosis and make treatment decisions in the absence of complete knowledge or data and without confirming the diagnosis.2 These decisions will likely be reinforced by the presumption that the diagnosis was correct if the patient clinically improves with treatment.

Even experienced clinicians are vulnerable to bias (Table) in nonanalytic reasoning. Such bias is generally subconscious, although some authors suggest that an awareness of bias can help avoid such errors. Diagnostic error can involve a combination of biases. Cognitive skill errors (ie, processing biases) are reported to be a more common reason for diagnostic error as compared with errors caused by knowledge gaps.1 Overconfidence is believed to be a major factor contributing to diagnostic error and bias, even among specialists.3

TABLE

Diagnostic Biases in Clinical Medicine

Bias Description
Availability bias A tendency to favor a diagnosis because of a case the clinician has seen recently
Anchoring bias An initial diagnosis is favored but is misleading. The clinician persists with the initial diagnosis and is unwilling to change his or her mind.
Framing bias Features that do not fit with the favored diagnosis are ignored.
Confirmation bias When information is selectively chosen to confirm—not refute—a hypothesis. The clinician only seeks or takes note of information that will confirm his or her diagnosis and does not seek or ignores information that will challenge it.
Premature closure Narrowing the choice of diagnostic hypotheses too early

 

In Sheba’s case, the range of diagnoses that will be suggested by veterinarians based on pattern recognition may include an acute GI disease, a bleeding disorder, acute cardiac failure, splenic torsion, splenic hemangiosarcoma, hypoadrenocorticism, and hemolytic anemia. All of these are feasible and all require different diagnostic and treatment strategies.

The Minimum Database

Routine diagnostic tests (eg, hematology, serum chemistry profile, urinalysis) can be useful and often essential in understanding a patient’s clinical condition. Relying on a minimum database to provide more information about the patient before clinical reasoning is engaged may be reasonable for some diseases but unhelpful for others. Serious, even life-threatening, disorders of the GI tract, neuromuscular system, pancreas (especially in cats), and heart rarely cause significant diagnostic changes in the routine hematologic and biochemical parameters measured in general practice. In addition, diagnostic tests are rarely 100% sensitive or specific. Using blood testing to screen for diagnoses can therefore be misleading, as the positive and negative predictive value of any test is influenced by the prevalence of a disorder in the population. 

Abnormal results in an unwell patient can create confusion if not critically reviewed as an integral part of the clinical assessment of all data relevant to the patient and related to the presenting problem(s). Veterinarians may overestimate the information gained from laboratory and imaging results,1 especially if the fundamentals (ie, comprehensive history, thorough clinical examination) are bypassed in favor of tests. It is recommended to avoid performing a test if not looking for a specific disease, as results can be misleading. For example, total thyroxine and fecal panels are tests that are requested frequently but that may be misinterpreted.

Analytic Clinical Reasoning

For cases in which nonanalytic reasoning is not helpful, analytic reasoning is required. An analytic approach to clinical reasoning is also needed to double-check presumptive diagnoses that are based on pattern recognition. 

In contrast to nonanalytic reasoning, analytic reasoning is reflective and systematic, permitting hypothesis formation and abstract reasoning. 

Analytic reasoning is less prone to bias than nonanalytic reasoning2 but is limited by working memory capacity, unless strategies are developed to provide the clinician with a logical, methodical, and memorable process through which to problem-solve any case presentation. 

Problem-Based Inductive Reasoning

In problem-based inductive reasoning, also described as logical clinical problem-solving, each significant clinicopathologic problem is assessed before being related to the patient’s other problems. Using this approach, the pathophysiologic basis and key questions for the most specific clinical signs the patient is exhibiting are considered before a pattern is sought. This ensures that the clinician’s mind remains more open to other diagnostic possibilities beyond the most obvious based on pattern recognition and thus helps prevent diagnostic bias.

The Problem List

The initial step in problem-based inductive reasoning is to clarify and articulate the patient’s clinical signs by constructing a problem list. Constructing a problem list (either mentally, orally, or in written form) helps make the clinical signs explicit to the clinician’s current level of understanding, transforms vague presenting information to specific problems, and helps the clinician determine the key clinical problems (ie, hard findings) versus the “background noise” (ie, soft findings). Most importantly, it helps prevent the clinician from overlooking less obvious, but nevertheless crucial, clinical signs and becoming overwhelmed with information. Incidental findings can mislead the clinician, particularly in older patients (eg, by focusing on the chronic diseases present instead of recognizing that it may be an acute disease that is responsible for the current clinical signs). Constructing and critically assessing a problem list can help prevent this. Problems should be prioritized, and those that are most specific and/or diagnostically useful can act as “diagnostic hooks.”4

Sheba’s problem list would include:

  • Profound weakness
  • Melena
  • Pale mucous membranes
  • Systolic murmur and tachycardia
  • Vomiting
  • Splenomegaly
  • Obesity (which would not contribute to the diagnostic plans but would need to be addressed at a later stage)

Each acute problem is important, and answering key questions related to each can provide important clues to guide diagnosis.

Problem Assessment

Problem-based inductive clinical reasoning provides steps to bridge the gap between the problem list and the list of differential diagnoses via a structured format. Once the problem list has been formulated, it can be used as the foundation for problem-based reasoning. After the key problems have been assessed as below, rather than listing every possible differential diagnosis for every problem on the problem list, a list of feasible differential diagnoses based on the problem list as a whole should be made.  

The specific problems identified should be investigated through rigorous use of key steps:

  • Define and refine the problem (What is the problem?).
  • Define and refine the system (What system is involved and how is it involved?). 
  • Define the location (Where in the system is the problem located?).
  • Define the lesion (What is the lesion?).

This structured approach to defining and refining the problem and system in particular will help determine the appropriate questions to ask when obtaining the history. The owner responses may alert the clinician to pay particular attention to aspects of the physical examination, indicate the most appropriate diagnostic test(s) to use, and prepare the clinician intellectually to assess the results of the chosen tests.

Define & Refine the Problem

When assessing a patient’s clinical signs, it is essential to define the problem as accurately as possible. Considering whether there is another clinical sign with which the problem could be confused is a vital first step, as failure to define the problem correctly can derail a clinical investigation that might otherwise have been relatively straightforward.

In Sheba’s case, melena in particular requires careful problem definition, as digested blood in the GI tract can be a result of either GI bleeding or swallowed blood (eg, from eating raw red meat, a bleeding lesion in the mouth or nasopharynx, coughing up then swallowing blood, licking a bleeding wound). It should be confirmed that the melena is due to GI bleeding by ruling out possible sources of ingested blood.

Define & Refine the System

Once the problem is defined, the body system that is malfunctioning should be considered. For every clinical sign, there is a system(s) that must be involved or that “creates” the clinical sign. However, the most important question is how it is involved. The key specific questions are what system could be involved in causing this clinical sign and is it a primary (ie, structural) problem of a body system or a secondary (ie, functional) problem whereby the system involved in creating the particular clinical sign is secondarily affected in the pathophysiologic process. An alternative, although closely related, question for some problems is if the problem is local or systemic.

In Sheba’s case, the key questions related to system definition include:

  • Is her profound weakness due to primary or secondary neuromuscular disease? Given the other clinical signs, secondary (eg, cardiovascular, hematopoietic) is most likely. 
  • Is her melena a result of GI bleeding due to local disease (eg, parasites, foreign body, neoplasia, drug damage [eg, NSAIDs]) or systemic disease, such as coagulopathy or GI ulceration due to nonGI disease (eg, hypoadrenocorticism, mast cell tumor, hepatic disease, uremia, gastrinoma)?
  • Are her pale mucous membranes due to anemia or decreased peripheral perfusion?
  • Are her systolic murmur and tachycardia due to primary cardiac disease or secondary noncardiac disease (eg, anemia)?
  • Is her vomiting a result of primary or secondary GI disease?

The range of diagnoses to consider, diagnostic tools used, and potential treatment or management options for primary structural problems of a body system are often very different from those relevant to secondary functional problems of that system. Investigation of primary structural problems often involves imaging (eg, radiology, ultrasonography, advanced trans-sectional imaging, endoscopy, surgical exploration) and/or biopsy. Routine hematology, serum chemistry profile, and urinalysis are often of little value in confirming the diagnosis but can be helpful in assessing the consequences of the underlying pathology (eg, anemia from GI bleed, metabolic perturbations as a result of vomiting and diarrhea in primary GI disease). 

In contrast, for secondary functional disorders, hematology and serum chemistry profile are often critical in reaching a diagnosis.

In Sheba’s case, the problem-based approach has clarified that there are several key questions that need to be answered:

  • Are the pale mucous membranes due to anemia or poor peripheral perfusion? This signals that packed cell volume (PCV) and total protein values should be obtained.  
  • Is the systolic murmur due to cardiac disease or anemia? 
  • Is the melena due to GI ulceration (primary or secondary) or a coagulopathy? This signals that platelet count and rapid assessment of clotting capability (eg, activated clotting time) should be obtained. Coagulation status should be established before any invasive diagnostic procedures (eg, endoscopy) are performed (if needed). 
  • Is the vomiting due to primary or secondary GI disease? Serum chemistry profile and hematology should help identify whether secondary (ie, metabolic) GI disease is present.

For some cases, once the system and its involvement are defined, the location within the system may need to be determined. For all problems, once the system and its involvement are determined, the lesion should be defined (ie, the differential diagnosis list).

In Sheba’s case, the key findings include:

  • Significant anemia (PCV, 18%); it should now be determined whether anemia is due to decreased RBC production (ie, bone marrow disease), hemolysis, or hemorrhage.
    • The acute onset of the clinical signs suggest that hemorrhage or hemolysis is more likely than bone marrow failure. 
  • A total plasma protein level of 7.8 g/dL (78 g/L), signaling that external hemorrhage from the GI tract was not the sole cause of the anemia. Loss of at least 50% of RBCs through the gut (for the PCV to drop to 18%) would result in a plasma protein in the lower reference range. Thus, the patient has either internal (abdominal) hemorrhage or hemolysis. 
  • Profound thrombocytopenia (10 × 106/mL [10 x 109/L]); it should be determined whether this is due to decreased platelet production (ie, bone marrow disease), platelet consumption (eg, disseminated intravascular coagulation), platelet destruction (eg, immune-mediated disease), or infectious causes. Of note, bleeding alone will reduce platelet numbers but rarely below about 50 × 106/mL (10 x 109/L); thus, melena is likely a result of the thrombocytopenia and not vice versa.

Helpful diagnostic tools would include a full hemogram and blood smear examination to assess RBC, WBC, and platelet morphology; a full coagulation profile; assessment for infectious diseases if in an endemic area; and abdominal imaging to check for abdominal hemorrhage and assess the liver and spleen. 

Sheba’s final diagnosis is primary immune-mediated anemia and thrombocytopenia (ie, Evan’s Syndrome). She is treated successfully with corticosteroids and azathioprine.

Conclusion

As with all skills, it takes time to develop the knowledge base and mental discipline required for successful logical clinical problem-solving. However, once the logical clinical problem-solving approach is embedded (and, ideally, becomes part of the clinician’s nonanalytic reasoning), it can save time by quickly eliminating extraneous information and helping the clinician focus on the information that is truly important for patients and owners.

PCV = packed cell volume

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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