July 2018   |   Volume 16   |   Issue 7

Emerging Infectious Diseases

in this issue

in this issue

Top 5 Zoonotic Disease Concerns in Hospital Visitation Dogs

Lameness & Osteomyelitis in a Cat

Hypocobalaminemia

Pulmonary Barotrauma & Pneumothorax During Anesthesia

Nutrition Assessment in a Dog with Sarcoma & Anemia

Fungal Cultures

Alternatives to Opioids for Perianesthetic Analgesia Management

Differential Diagnosis: Regurgitation

The Veterinary Significance of Emerging Infectious Diseases

J. Scott Weese, DVM, DVSc, DACVIM, Ontario Veterinary College, Ontario, Canada

Infectious Disease

|Peer Reviewed

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The Veterinary Significance of Emerging Infectious Diseases

Emerging infectious diseases pose a significant threat to humans and animals but are inherently unpredictable. Although historical trends and disease patterns can provide insight, determining which diseases are likely to emerge and the impact they will have on human and animal populations is an educated guess at best. Of additional concern is the estimate that 60% to 80% of emerging diseases are zoonotic,1 which emphasizes the importance of veterinarians in the identification, prevention, and control of emerging infectious diseases.

An ecosystem approach to health considers disease occurrence to be at the intersection of the microbial agent, the host (human or animal), and the environment.1 Any alterations in the agent, host, or environment can alter the risk for disease. Thus, new infectious disease threats can emerge from a variety of sources.

Emergence of New Pathogens

Emergence of new pathogens is uncommon but continues to occur. If highly transmissible, new pathogens can have profound effects, as the worldwide population would be immunologically naïve to the emerging pathogen. For example, the emergence of canine parvovirus in the 1970s2 became a worldwide epidemic, with rapid international transmission and high morbidity and mortality rates.

Canine influenza is a more recent example of the threats posed by emerging pathogens. The emergence of equine-origin canine influenza H3N8 in the United States in the early 2000s3 demonstrated the potential impact of antigenic shift of influenza on the canine population. The more recent emergence of avian-origin canine influenza H3N2 caused—and continues to cause—widespread illness and disruption in parts of Asia, the United States, and Canada.4,5

Change in Existing Pathogens

Alterations in existing pathogens can impact a pathogen’s virulence (eg, acquisition of new virulence factors) and the ability to treat (eg, acquisition of antimicrobial-resistant genes or antiviral resistance) or prevent disease (eg, alterations in vaccine efficacy, resistance to heartworm prophylaxis). The worldwide epidemic of antimicrobial resistance, particularly methicillin-resistant staphylococci6 and extended-spectrum β-lactamase production in gram-negative bacteria, has had tremendous impacts on human and animal populations.7 Multidrug-resistant pathogens cause large numbers of infections every year and can be associated with higher morbidity and mortality rates; the need for more expensive, toxic, or cumbersome treatments; and the risk for transmission to other humans or animals. Economic impacts are similarly profound; the World Bank has estimated that by 2050 the global burden of antimicrobial resistance could surpass that of the 2008 financial crisis.8 New resistance mechanisms, including resistance to “last-resort” drugs such as colistin,9 continue to be identified and will continue to pose a problem to the veterinary profession as bacterial evolution outpaces antimicrobial development.

Development of Virulence

Virulence may develop through an existing but typically nonpathogenic microbe. Elizabethkingia anophelis is an example of such virulence development in humans; the risk in animals is unknown. This gram-negative bacterium is widespread in the environment and was considered innocuous until clusters of serious infections were identified in humans, primarily immunocompromised humans in hospitals, in various countries.10 The reasons for this change are unclear. Although E anophelis infection has not been reported in animals, it is possible that there is some degree of risk for infection. Regardless, E anophelis highlights the potential for organisms that were previously considered to be ubiquitous and innocuous to cause disease. 

Change in the Range of Existing Pathogens

Many pathogens have well defined ranges that may be limited by geography and control measures (eg, rabies), vector ranges (eg, Borrelia burgdorferi), reservoir host ranges (eg, Cytauxzoon felis), and climate (eg, various parasites). Changes in any of these limiting factors can result in the potential for range expansion. Range expansion can also occur through human activities (eg, international movement of humans and animals) and accidental international transportation of pests and, thus, the pathogens they carry. Although of limited consequence in dogs and cats, introduction of West Nile virus through a route that is still unknown resulted in establishment of this foreign mosquito-borne virus in North America, and the impacts of this disease on humans and some animal populations are ongoing.11-15

Expanding ranges of various vector-borne diseases are particularly noteworthy. In North America, tick ranges have been expanding due in part to climate change.16 When reservoir hosts move in parallel with vectors or when competent hosts are already present in the expansion regions, vector-borne pathogens may spread with the vectors, as shown by the steady movement of Lyme disease into the northern and western United States and into Canada.17 Such movement highlights the need for predictive modeling to identify new threats and the need for awareness of disease threats in adjacent regions.

New Human Encounters in Remote Endemic Ranges

Various pathogens presumably exist in remote sites where there is little human presence. There are still regions of the world that have had limited human exposure, particularly parts of sub-Saharan Africa and regions of the Amazon basin. With the remarkable biodiversity in these areas, expansion of humans and their animals into these areas may result in exposure to pathogens considered new to the region.

Ability to Diagnose

Apparent emergence of a disease may sometimes simply reflect advances in diagnostic testing. For example, Bartonella spp can be difficult to identify. As new methods for detection have become available, members of this genus have been increasingly implicated in a variety of diseases.18 

Advances in laboratory methods that allow for rapid, cost-effective detection of all microorganisms in a sample, including previously unknown bacteria and viruses, have made it possible to identify unknown microorganisms rapidly and at low cost. This has led to identification of myriad “new” viruses.19-21 Humans and animals have extensive commensal virome populations, and the ability to identify new viruses currently outpaces the ability to interpret the relevance of these discoveries. A high-profile example is the identification of canine circovirus. After reports of this virus and the subsequent ability to test for it first emerged, there was widespread concern about canine circovirus as a cause of serious enteric disease in dogs; however, proof of its role as a primary pathogen is still lacking.22-24 This highlights the potential confusion that can be associated with availability of new diagnostic tests when the clinical relevance of the results is unclear. 

Change in Host Susceptibility

A change in host susceptibility has been exemplified in medicine early in the era of human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS). Before effective HIV management approaches were available, progression to end-stage AIDS resulted in profoundly immunocompromised individuals, which led to identification of a range of previously rare or unknown infectious diseases caused by organisms that were predominantly or only pathogenic in these highly compromised hosts (see Suggested Reading).25-29 Such a severely compromising and widespread disease is not currently recognized in animals; however, emergence of new secondary pathogens in humans with AIDS demonstrates the potential for disease caused by a range of novel or overlooked microorganisms associated with the emergence of new, highly susceptible patient populations. It also emphasizes the challenges that might be posed by advances in veterinary care (eg, treatment of cancer or immune-mediated disease) that can prolong the life of patients but increase their risk for infection from existing and emerging pathogens.

The Future

Logical estimations and models for emergence can be developed, but emergence is ultimately unpredictable. New infectious disease issues will pose threats to animal and, potentially, human populations. Infectious diseases of current significance may not have been recognized or considered important 5 to 10 years ago, and infectious diseases that will be significant 10 years from now may not be currently recognized or considered important, illustrating the dynamic nature of disease.

AIDS = acquired immune deficiency syndrome, HIV = human immunodeficiency virus

References & Author Information

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

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

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


Differential Diagnosis: Regurgitation

Shanna Hillsman, LVMT, University of Tennessee

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

Internal Medicine

|Peer Reviewed

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Differential Diagnosis: Regurgitation

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

  • Esophagitis
  • Focal or generalized megaesophagus 
    • Focal
      • Vascular ring anomaly
      • Esophageal stricture
    • Generalized
      • Esophageal stricture (if close to lower esophageal sphincter)
      • Hypoadrenocorticism
      • Myasthenia gravis 
      • Lead poisoning
      • Botulism
      • Tetanus
      • Hypothyroidism
      • Polyradiculitis
      • Thallium toxicity
  • Structural esophageal disease
    • Foreign body
    • Extra- or intraesophageal neoplasia
    • Diverticula
    • Granuloma
      • Fungal
      • Spirocerca lupi
  • Polymyopathy
  • Polyneuropathy
  • Organophosphate toxicity
  • Hiatal hernia
  • Distemper
  • Neospora caninum

References & Author Information

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

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

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


Lameness & Osteomyelitis in a Cat

Lauren Chapman, DVM, VCA North Coast Animal Hospital, Encinitas, California

Ryan Taggart, DVM, MS, DACVS-SA, Adelaide Veterinary Specialist & Referral Centre, Adelaide, Australia

Infectious Disease

|Peer Reviewed

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Lameness & Osteomyelitis in a Cat

History

A skeletally mature (age unknown), 8.6-lb (3.9-kg) spayed domestic shorthair cat was evaluated for acutely worsening left pelvic limb lameness. Mild lameness had been observed for approximately 4 weeks before presentation. The patient was not receiving any medications and had been adopted in New Mexico 4 years prior. The owner reported no travel history since adoption; however, limited prior medical records indicated that the patient had been vaccinated in Northern California prior to adoption.

Physical Examination

The principal physical examination finding was a firm, painful, circumferential swelling of the left proximal metatarsal/tarsal region accompanied by a nonweight-bearing lameness on that limb. The remainder of the physical examination was unremarkable. Rectal temperature was 101.8°F (38.8°C), heart rate was 200 bpm, and respiratory rate was 36 breaths/min with no increased respiratory effort observed.

Diagnostics

Serum chemistry profile, urinalysis, and CBC were unremarkable, and the patient was negative for FIV antibodies and FeLV antigen. 

Radiographs of the left proximal metatarsal/tarsal region revealed multiple foci of osteolysis within the distal tarsal and proximal metatarsal bones, as well as marked soft tissue swelling of the area (Figure 1). Periosteal reaction was noted on the dorsal and plantar surfaces of the distal tarsal and proximal metatarsal bones.  

Multiple foci of osteolysis and surrounding marked soft tissue swelling in the distal tarsal and proximal metatarsal bones
Multiple foci of osteolysis and surrounding marked soft tissue swelling in the distal tarsal and proximal metatarsal bones

Figure 1 Multiple foci of osteolysis and surrounding marked soft tissue swelling in the distal tarsal and proximal metatarsal bones

Figure 1 Multiple foci of osteolysis and surrounding marked soft tissue swelling in the distal tarsal and proximal metatarsal bones

Radiographs of the thorax revealed a diffuse, finely granular interstitial pulmonary infiltrate with prominent bronchial markings with indistinct nodules in the middle and caudal lung lobes (Figure 2). 

Diffuse, finely granular interstitial pulmonary infiltrate (A) with prominent bronchial markings with indistinct nodules in the middle and caudal lung lobes (B)
Diffuse, finely granular interstitial pulmonary infiltrate (A) with prominent bronchial markings with indistinct nodules in the middle and caudal lung lobes (B)

Figure 2 Diffuse, finely granular interstitial pulmonary infiltrate (A) with prominent bronchial markings with indistinct nodules in the middle and caudal lung lobes (B)

A fine-needle aspirate was collected from the proximal metatarsal/tarsal swelling (Figure 3). Cytologic evaluation revealed a granulomatous inflammatory infiltrate and abundant capsulated yeast organisms  demonstrating occasional narrow-based budding. The morphology of these organisms was consistent with Cryptococcus spp infection.

Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa
Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa

Figure 3 Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa

Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa
Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa

Figure 3 Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa

Figure 3 Cytology of the fine-needle aspirate from swollen tarsus with numerous Cryptococcus spp yeast organisms featuring thick clear capsules (A). Narrow-based budding is displayed by some of the organisms (B; arrow). 100× and 500× magnification, Wright-Giemsa

A Cryptococcus spp antigen agglutination test was positive (titer 1:3688). Because of the uncommon presentation of fungal osteomyelitis, biopsies of the tarsal swelling were submitted for histopathologic analysis and fungal identification by genetic sequencing. Histopathologic analysis confirmed the organisms were consistent with Cryptococcus spp and described severe, focally extensive, granulomatous osteomyelitis and cellulitis with intralesional encapsulated yeast organisms. DNA-based analysis matched that of Cryptococcus gattii type V, molecular type VGIII.

Treatment & Outcome

Treatment was initiated with fluconazole (12.8 mg/kg PO q12h) and buprenorphine (0.015 mg/kg transmucosal q8h) for pain.1,2 Fluconazole was used for about one month. Following a discussion with a veterinary mycosis specialist, treatment was changed to itraconazole (12.8 mg/kg PO q12h; later reduced to 9 mg/kg PO q12h) and amphotericin B (0.55 mg/kg as a diluted [in 350 mL of 0.45% NaCl with 2.5% dextrose] twice-weekly SC infusion) based on the results of diagnostic testing that further classified the Cryptococcus spp strain.

Clinical signs resolved within 2 months and did not return. A total of 20 doses of amphotericin B were administered to reach a cumulative dose of approximately 10 mg/kg. Hepatic and renal parameters were monitored. Renal values remained within the reference interval, but a mildly elevated alanine aminotransferase persisted (162-249 U/L [2.71 - 4.16 μkat/L]; reference range, 10-100 U/L [0.17 - 1.67 μkat/L]). Based on intolerance (ie, inappetance, vomiting) to the initial dose of itraconazole, the dose was reduced to 8.5 mg/kg PO q12h, and treatment was continued for approximately 2 years after initiating therapy until the patient was seronegative on 2 occasions one month apart. At the final follow-up, the patient appeared healthy with no signs of illness. Lengthy, possibly lifelong, treatment may be required for some patients.3 Even when clinical signs resolve, relapse is still possible.4 A better prognosis has been observed in animals treated early or those with only localized disease without CNS or systemic involvement.5

Discussion

C gattii was long considered an organism of tropical and subtropical climates. However, C gattii-endemic areas now include western Canada and the Pacific Northwest region of the United States.6 

Unlike infection with other Cryptococcus spp organisms, Cryptococcus gattii infection tends to occur in immunocompetent individuals.3 In cats, infection typically occurs after basidiospore entry into the patient from the environment via inhalation and colonization of the nasal cavity, followed by tissue invasion of structures in the sinonasal cavity. Extension occasionally occurs into the CNS, oral cavity, and/or orbit by penetration of bones surrounding the sinonasal cavity.

This patient’s presentation is more consistent with human infection, in which the lung is typically the primary site of infection, with subsequent hematogenous dissemination to brain, bone, skin, and/or other tissues.6 C gattii is not considered to be zoonotic, except in immunocompromised humans.4 Rather, humans and animals acquire the organisms from the same environmental sources. Animals may serve as important sentinels, which indicates the potential for human exposure from the environment.5 The incubation period between exposure and clinical signs is variable and reported to be 1 to 12 months or longer.5

Young to middle-aged cats are most often diagnosed with cryptococcosis, but all ages can be affected.4 Distinguishing among species of Cryptococcus has become important in epidemiologic studies, but there is no difference between the clinical presentations of infections caused by different members of the C neoformans/gattii species complex.4 

Cats are reportedly 6 times more likely than dogs and 3 times more likely than horses to become clinically affected.4 Lesions are most often noted in the nasal, maxillary, or frontal regions of the head.3 Fungal granulomas or lesions involving the lymph nodes and skin of the head and neck are common.5 CNS and/or ocular involvement is suspected if blindness, retinal (chorioretinitis), or optic disc lesions accompany a diagnosis.4 Almost any organ system, including the lungs, kidneys, bone, and periarticular tissues, can be affected.4 Treatment typically consists of antifungal therapy, with close monitoring of liver and renal values.

References & Author Information

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

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

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


Fungal Cultures

Selene A. Jones, DVM, University of Tennessee

Elizabeth R. May, DVM, DACVD, University of Tennessee

Dermatology

|Peer Reviewed

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Fungal Cultures

Fungal cultures are an important diagnostic tool that can be easily performed in a general practice setting.1-3 It is essential to include dermatophytosis in the differential diagnoses for patients with clinical signs consistent with fungal skin infection (eg, multifocal patchy alopecia, crusts, scales, pustules, papules), as well as for patients with similar clinical signs (ie, demodicosis, pyoderma) that fail to respond to appropriate therapy.1-7 Yorkshire terriers, working dogs, hunting dogs, and Persian cats may be predisposed to dermatophytosis.3,4,7

Sample collection for fungal cultures typically involves a hair pluck, which is best performed at lesional margins,1-4,7 or a sterile toothbrush.1,2,4,6,7 A sterile toothbrush is recommended for cats and to detect subclinical carriers that lack obvious lesions (eg, cats passively carrying infectious fungal elements that pose a risk to human health and environmental contamination).1-4,6 Any commercial toothbrush in its original packaging is considered mycologically sterile for this use. 

Flat culture plates represent the best medium to use, ideally when divided into 2 compartments: dermatophyte test medium, which selects for dermatophytes, and Sabouraud dextrose agar, which encourages sporulation and thus facilitates identification via microscopy.1,2,4,7 The shape of other collection containers (eg, jars, tubes) can make inoculation of organisms challenging. In addition, these containers have tight-fitting lids that can encourage bacterial growth by trapping moisture,1,2,4 and obtaining samples from these containers to identify fungal macroconidia can be difficult.4 

Dermatophytes grow best in media slightly above room temperature (ie, 75°F-86°F [24°C-30°C]).1-4,7 Ultraviolet light and low humidity prevent growth on culture media.1,2,4 Cultures should be kept in a dark drawer or cabinet with a small dish of water nearby.4 Most dermatophytes grow within 2 to 7 days; however, culture plates should be kept for 21 days in case slow-growing variants (eg, Trichophyton spp) are present or if antifungal therapy was initiated prior to sampling.1-3

Although certain culture media are selective for dermatophytes, contaminant saprophytes can develop and be mistaken for dermatophytes.1,2,4,5,7 Colony morphology, media color change, and microscopic morphology are the best indicators to differentiate pathogens from contaminants.1-4 Dermatophyte colonies are white-to-pale in color and fluffy in appearance; saprophytes are often pigmented.1-3 Color change is caused by a pH indicator within the medium that modifies the color during protein metabolism.1,2,4 Because dermatophytes prefer protein (eg, keratin), a color change to red should correspond with colony growth consistent with the expected pathogen.1,2,4 Saprophytes prefer carbohydrates and only use protein if carbohydrates are depleted1,2,4; therefore, color change can still occur, but not alongside initial colony growth.4 Daily observation during prolonged incubation (ie, >10 days) is imperative because saprophytic fungi will eventually cause the distinctive color change to red.1,2,4 

Microscopic evaluation of macroconidia is the definitive technique for confirming dermatophytosis.4 There is a high likelihood of misdiagnosis if microscopy and macroscopic characteristics are not considered.7 The most common dermatophytes that infect small companion animals are Microsporum canis, Microsporum gypseum, and Trichophyton mentagrophytes.1-3,5,6

PCR is currently being investigated as a means of diagnosing dermatophytosis, with results available in 1 to 3 business days versus the 1 to 3 weeks required for final dermatophyte culture results; panels include more than one dermatophyte species and demonstrate high sensitivity and high specificity.5 Research into the value of PCR as a sole diagnostic tool is ongoing, and fungal culture is still considered the gold standard.


STEP-BY-STEP

FUNGAL CULTURES1-4,7


WHAT YOU WILL NEED

  • Sterile hemostat (ie, hair pluck) or new sterile toothbrush
  • Divided dermatophyte test medium or Sabouraud dextrose agar plate
  • Warm (ie, 75°F-86°F [24°C-30°C]), dark area
  • Small dish of water
  • Clear acetate tape
  • Lactophenol cotton blue or new methylene blue stain
  • Light microscope

STEP 1

Use a sterile hemostat (ie, hair pluck) or a new sterile toothbrush to obtain culture samples.    

Hair-Pluck Technique (Recommended in Animals with Active Lesions)

Using a sterile hemostat, pluck hairs (≈10-20) from the periphery of lesional skin; the hair bulb and root must be intact. Gently place plucked hair on the culture medium. Ensure the plucked hair remains in place and in contact with the agar by applying gentle pressure with the sterile hemostat (A).

Toothbrush Technique (Recommended  in Cats & Animals without Obvious Lesions)

Brush a sterile toothbrush through the animal’s hair coat, against the direction of growth, for approximately 30 strokes. Lightly press the bristles onto the culture medium (B).

Clinician's Brief
Clinician's Brief

Author Insight

Broken or misshapen hair and/or hair from inflamed, scaled, or crusted areas are preferred for sampling. Avoid areas that have been recently medicated.


STEP 2

Incubate the closed culture plate in a warm (ie, 75°F-86°F [24°C-30°C]), dark area for 21 days. Place a small dish of water nearby to provide humidity and prevent the medium from drying out. Check the medium daily for fungal growth.

Grossly, colonies of M canis are typically white with a cotton-like texture. As they age, they can become powdery and develop a centrally depressed area with radial folds (A; colony on split dermatophyte test medium and Sabouraud dextrose agar plate). 

Grossly, colonies of M canis are typically white with a cotton-like texture. As they age, they can become powdery and develop a centrally depressed area with radial folds (A; colony on split dermatophyte test medium and Sabouraud dextrose agar plate). 

M gypseum appears pale-to-light-brown with a flat-to-granular texture. White mycelia can also form (B; colony on split dermatophyte test medium and Sabouraud dextrose agar plate).

M gypseum appears pale-to-light-brown with a flat-to-granular texture. White mycelia can also form (B; colony on split dermatophyte test medium and Sabouraud dextrose agar plate).

The colony morphology of T mentagrophytes is variable. Most zoophilic forms will be white to cream in color with a powdered appearance, whereas the anthrophilic forms typically appear white with a cotton-like texture (C; colony on split dermatophyte test medium and Sabouraud dextrose agar plate). 

The colony morphology of T mentagrophytes is variable. Most zoophilic forms will be white to cream in color with a powdered appearance, whereas the anthrophilic forms typically appear white with a cotton-like texture (C; colony on split dermatophyte test medium and Sabouraud dextrose agar plate). 

Author Insight

Contaminant fungi can cause color change, usually after prolonged incubation (ie, >10 days). Correct interpretation happens when a red color change occurs simultaneously with colony growth; however, making a premature diagnosis based on color change alone can lead to misdiagnosis and unnecessary treatment and potentially delay the ability to render a definitive diagnosis.


STEP 3

Identify growth on the culture to rule out erroneous results. While wearing gloves, collect macroconidia by gently applying the sticky side of a piece of clear acetate tape to the top of the colony. Place several drops of lactophenol cotton blue stain (as used in the samples shown) or new methylene blue stain on a microscope slide, then place the tape, sticky side down, over it. After placing a coverslip on top, evaluate the sample under the microscope. Alternatively, the entire culture plate can be sent to a diagnostic or commercial laboratory for dermatophyte identification.

M canis forms spindle-shaped macroconidia with thick walls and a knob at the terminal end; 6 or more cells per macroconidia are present (A, 20×; B, 100× oil immersion).
M canis forms spindle-shaped macroconidia with thick walls and a knob at the terminal end; 6 or more cells per macroconidia are present (A, 20×; B, 100× oil immersion).
M canis forms spindle-shaped macroconidia with thick walls and a knob at the terminal end; 6 or more cells per macroconidia are present (A, 20×; B, 100× oil immersion).
M canis forms spindle-shaped macroconidia with thick walls and a knob at the terminal end; 6 or more cells per macroconidia are present (A, 20×; B, 100× oil immersion).

M canis forms spindle-shaped macroconidia with thick walls and a knob at the terminal end; 6 or more cells per macroconidia are present (A, 20×; B, 100× oil immersion).

M gypseum forms spindle-shaped macroconidia with thin walls and lacks a knob at the terminal end; 6 or fewer cells per macroconidia will be present (C, 20×; D, 100× oil immersion).
M gypseum forms spindle-shaped macroconidia with thin walls and lacks a knob at the terminal end; 6 or fewer cells per macroconidia will be present (C, 20×; D, 100× oil immersion).
M gypseum forms spindle-shaped macroconidia with thin walls and lacks a knob at the terminal end; 6 or fewer cells per macroconidia will be present (C, 20×; D, 100× oil immersion).
M gypseum forms spindle-shaped macroconidia with thin walls and lacks a knob at the terminal end; 6 or fewer cells per macroconidia will be present (C, 20×; D, 100× oil immersion).

M gypseum forms spindle-shaped macroconidia with thin walls and lacks a knob at the terminal end; 6 or fewer cells per macroconidia will be present (C, 20×; D, 100× oil immersion).

T mentagrophytes macroconidia are often cigar-shaped with thin walls; some isolates will have spiral hyphae. Globoid microconidia arranged singly or in clusters along hyphae can also be seen (E, 20×; F, 100× oil immersion). 
T mentagrophytes macroconidia are often cigar-shaped with thin walls; some isolates will have spiral hyphae. Globoid microconidia arranged singly or in clusters along hyphae can also be seen (E, 20×; F, 100× oil immersion). 
T mentagrophytes macroconidia are often cigar-shaped with thin walls; some isolates will have spiral hyphae. Globoid microconidia arranged singly or in clusters along hyphae can also be seen (E, 20×; F, 100× oil immersion). 
T mentagrophytes macroconidia are often cigar-shaped with thin walls; some isolates will have spiral hyphae. Globoid microconidia arranged singly or in clusters along hyphae can also be seen (E, 20×; F, 100× oil immersion). 

T mentagrophytes macroconidia are often cigar-shaped with thin walls; some isolates will have spiral hyphae. Globoid microconidia arranged singly or in clusters along hyphae can also be seen (E, 20×; F, 100× oil immersion). 

References & Author Information

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

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

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


Atypical Hypoadrenocorticism in Dogs

Andrew Bugbee, DVM, DACVIM, University of Georgia

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Atypical Hypoadrenocorticism in Dogs

In the Literature

Wakayama JA, Furrow E, Merkel LK, Armstrong PJ. A retrospective study of dogs with atypical hypoadrenocorticism: a diagnostic cut-off or continuum? J Small Anim Pract. 2017;58(7):365-371.


FROM THE PAGE …

Atypical hypoadrenocorticism (AH) is an uncommon veterinary endocrinopathy that is classically considered to be an isolated deficiency of cortisol production with normal electrolyte concentrations. Recent evidence suggests that insufficient aldosterone production is frequently present on AH diagnosis, regardless of measured electrolyte concentrations.1 Because AH can present with various clinical signs or biochemical abnormalities, it is said to mimic many disease states, thereby obscuring consideration of AH as a differential. Confirmation is obtained generally by documenting a post-ACTH stimulated cortisol concentration of less than 2 µg/dL (55 nmol/L). However, suboptimal stimulation (>2 µg/dL [>55 nmol/L] but below the laboratory reference interval) provides equivocal diagnostic information.

This study retrospectively reviewed approximately 10 years’ worth of medical records to extract clinical and biochemical data in dogs with confirmed AH (n = 40; stimulated cortisol concentration, 1-1.2 µg/dL [<28-33 nmol/L]) and suspected AH yielding suboptimal ACTH stimulation test results (n = 9; stimulated cortisol concentration, 3.4-8.1 µg/dL [94-223 nmol/L]).

Unlike previous reports in which female dogs were primarily affected, neutered male dogs comprised 57.5% of the AH group, with Labrador retrievers and standard poodles disproportionately affected. Clinical signs of both groups were nonspecific and chronic (present for >3 weeks), with lethargy and GI upset (eg, anorexia, vomiting, diarrhea) observed in most cases. 

Hypoalbuminemia and hypocholesterolemia were the most common biochemical abnormalities detected in both groups and were encountered more frequently in confirmed AH dogs as compared with dogs suspected of having AH. Imaging was performed in only a minority of dogs in both groups, and small adrenal gland size was documented only in dogs with confirmed AH. Only 5 of 35 AH dogs developed a low sodium:potassium ratio (≤25.7) within 51 months of diagnosis. Daily physiologic glucocorticoid supplementation resolved clinical signs (30/31), hypoalbuminemia (25/27), and hypocholesterolemia (23/25) in AH dogs. At follow-up for 7 of the 9 dogs with suspected AH, none developed an electrolyte disorder. Several dogs with suspected AH (4/7) were eventually diagnosed with inflammatory bowel disease; clinical signs resolved for 2 of these dogs with no sustained therapy. One dog had persistent signs with no diagnosis obtained.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

AH screening is warranted for patients presented with chronic lethargy or vague GI signs, hypoalbuminemia, and/or hypocholesterolemia.

 

2

Although electrolyte levels are commonly normal on AH diagnosis, assessment of pre- and post-ACTH stimulated aldosterone concentrations may more accurately reflect the patient’s mineralocorticoid status.

3

Suboptimal ACTH stimulation test results may suggest the presence of another occult nonadrenal disease state (eg, enteropathy).

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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Cat-to-Human H7N2 Infection

J. Scott Weese, DVM, DVSc, DACVIM, Ontario Veterinary College, Ontario, Canada

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Cat-to-Human H7N2 Infection

In the Literature

Marinova-Petkova A, Laplante J, Jang Y, et al. Avian influenza A(H7N2) virus in humans exposed to sick cats, New York, USA, 2016. Emerg Infect Dis. 2017;23(12):2046-2049.


FROM THE PAGE …

Influenza poses a tremendous public health burden, and extensive surveillance is used to detect emerging influenza threats. 

Although influenza in cats is rare, a previous 2016 case report identified a large influenza outbreak in cats in a New York animal shelter.1 The strain involved in this outbreak was an H7N2 avian influenza virus that had been identified in birds and a small number of humans in the early 2000s but had not been identified as part of large-scale testing (ie, 132 000-212 000 tests per day) in birds in the United States between 2007 and 2014.

The case report highlighted here discusses a veterinarian who had collected oropharyngeal samples from clinically normal cats at the shelter during the outbreak and subsequently developed influenza-like illness (eg, sore throat, muscle pain, cough).1 When the virus was sequenced, human and feline isolates were found to be closely related to H7N2 strains that had been circulating in birds in the northeastern United States in the early 2000s. Although H7N2 is considered an avian influenza strain, feline and human isolates had changes in their genomes that enhanced the ability of the virus to attach to the mammalian respiratory tract and increase the risk for intramammal transmission. Although this strain had not been identified in the United States between the early 2000s and 2016, the genetic changes (ie, drift) present as compared with older strains suggest that it has continued to circulate, likely in wild birds.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

Veterinarians may be at the forefront of exposure to new infectious disease risks.

 

2

Without testing of sick cats, this situation would have likely gone unidentified, as specific testing of the veterinarian occurred only because of the history of exposure to infected cats.

 

3

Veterinarians should be aware of zoonotic disease risks and ensure their healthcare providers are informed of any situations that might increase the likelihood of a zoonotic 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.

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Research Note: Intralymphatic Immunotherapy in the Treatment of Canine Atopic Dermatitis

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The study authors hypothesized that intralymphatic immunotherapy induces a better, more rapid response than do other types of immunotherapy for treating canine atopic dermatitis. Alum-precipitated allergen extract was injected into the popliteal lymph nodes of 51 participants. Twenty-two dogs completed the study and were included in a per-protocol analysis of results; all 51 participants were included in a separate intention-to-treat analysis. Pruritus and quality-of-life scores improved significantly in the intention-to-treat analysis; however, Canine Atopic Dermatitis Extent and Severity Index (CADESI) scores showed significant improvement only in the per-protocol analysis. Given the limited adverse effects, evaluation of intralymphatic immunotherapy as a safe, feasible, long-lasting treatment for canine atopic dermatitis is warranted.

Source

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Research Note: High-Intensity Focused Ultrasound for Canine Solid Tumors

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High-intensity focused ultrasound (HIFU) attacks cancer cells by using heat to cause thermal damage, coagulative necrosis, and cell death, leading to creation of a fibrous scar. In a clinical study, dogs received one to 3 treatments for solid tumors that were nonresectable and/or refractory to conventional chemotherapy. Tumor size decreased in 4 of 10 dogs; 2 of 10 dogs exhibited partial remission. All 4 dogs with bleeding from hemorrhagic tumors had alleviated clinical signs. Side effects (ie, hyperthermia, erythema, enteritis, skin ulceration) were mild and self-limiting. This study suggests that veterinary HIFU is a viable alternative treatment for dogs with solid tumors.

Source

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Canine Leptospirosis Update

Sandra Sawchuk, DVM

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This update discusses the current epidemiology, diagnosis, treatment, and prevention of canine leptospirosis in the United States. Infection typically results in acute severe multisystemic renal and hepatic disease, and is caused by the Leptospira spirochete bacteria. Clinical disease can be nonspecific and difficult to diagnose. Some dogs can be subclinical carriers, and serology is the most accurate diagnostic tool. Supportive care and antibiotic therapy are the cornerstones of treatment, and antibiotic therapy is used to treat the carrier state. Human and canine infection results from direct or indirect contact of skin or mucous membranes with an infected animal's urine or by direct organism ingestion, and therefore has great public health implications. Serovars frequently associated with infection include Grippotyphosa, Pomona, Bratislava, and possibly Autumnalis. Reservoirs for infection include rodents, cattle, swine, raccoons, opossums, and several other animal species. The zoonotic risks to veterinary employees and owners must be emphasized, and infectious disease control must be implemented to decrease zoonotic transmission. Prevention is imperative. Dogs should receive Leptospira bacterin vaccines based on circulating endemic bacterial strains and should also undergo lifestyle modification to prevent infection. Although rural dogs are at greatest risk, urban and suburban dogs are at increasing risk because of encroachment of humans into rural areas. Current bacterin vaccines include the serovars Icterohaemorrhagiae, Canicola, Pomona, and Grippotyphosa, and vaccination may elicit some limited cross-protection to serovars not included in the vaccine.

COMMENTARY: Leptospira vaccine is classified as a noncore vaccine for dogs. Puppies, especially small breeds (with dachshunds appearing to be overrepresented), are at greater risk for acute anaphylaxis when given this vaccine. The vaccine is recommended for dogs that are over 12 weeks of age and are considered to be at risk for exposure to the organism. Risk can be difficult to assess because even urban dogs can be exposed to wildlife reservoirs. Although it is a treatable disease (with ampicillin, doxycycline, and aggressive supportive care), treatment can be costly and diagnosis can be difficult-in the acute phase of the disease, for example, results of serologic testing may be negative.

Canine leptospirosis update. Guptil L. PROC NAVC 2009, pp 644-646.

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Nonopiate Alternative to Analgesia in Rabbits

Adolf K. Maas, III, DVM, DABVP (Reptile & Amphibian), CertAqV, ZooVet Consulting, Bothell, Washington

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Nonopiate Alternative to Analgesia in Rabbits

In the Literature

Schnellbacher RW, Divers SJ, Comolli JR, et al. Effects of intravenous administration of lidocaine and buprenorphine on gastrointestinal tract motility and signs of pain in New Zealand White rabbits after ovariohysterectomy. Am J Vet Res. 2017;78(12):1359-1371.


FROM THE PAGE …

Opiates can have a number of adverse effects; ileus1,2 and respiratory depression3 are the most disconcerting of these effects in rabbits, making nonopiate-based analgesia desirable in this species.

This study provided a direct comparison of efficacy of buprenorphine versus lidocaine for both intraoperative and postoperative analgesia. All rabbits were administered ketamine and xylazine for induction and supplemental analgesia for ovariohysterectomy. Because pain can be difficult to assess in rabbits, a behavior-based system4 to score comfort, similar to validated behavior-based systems in dogs,5 was used in addition to traditional biochemical and physiologic pain assessment methods. Seven rabbits received buprenorphine (0.06 mg/kg IV q8h) for 2 days, and seven other rabbits received lidocaine as an intravenous bolus (2 mg/kg over 5 minutes) followed by a constant-rate infusion (100 µg/kg/min) for 2 days.

Intravenous lidocaine was found to provide significant improvement in pain control as compared with buprenorphine. Rabbits treated with lidocaine had decreased heart rates, lower serum glucose concentrations, and higher postoperative food intake and fecal production than did buprenorphine-treated rabbits, which suggests improved analgesia through lidocaine infusion. Levels of activity (play and exploring) and degree of observed comfort were also markedly improved in the lidocaine-treated group; recoveries were overall improved and patients appeared comfortable.

Results suggest that lidocaine provides an excellent alternative to buprenorphine analgesia in rabbit surgery. It may also provide means for controlling pain and inflammation, as well as the secondary consequences of both, in nonsurgical cases that require analgesia and control of ileus. Because post-operative ileus is common in rabbits, improved appetite and fecal production are good indicators of improved comfort. Based on this study and earlier publications, lidocaine administered as a constant-rate infusion would be a good first-line treatment protocol for GI stasis,6 endotoxemia/dysbiosis,7 and other causes of moderate-to-severe pain.


… TO YOUR PATIENTS

Key pearls to put into practice:

1

In rabbit medicine and surgery, adequate analgesia is a critical part of providing standard-of-care treatment; lidocaine can be a valuable tool in the application of nonopiate-based analgesia protocols.

2

Lidocaine provides a number of additional benefits for rabbits, including anti-inflammatory activity, free-radical scavenging, GI prokinetic function, and inhibition of endotoxin-related damage.8-11

3

Administration of lidocaine via a constant-rate infusion is a safe and effective analgesic method with fewer adverse effects than opiates in rabbits.

 

4

Intravenous lidocaine may be administered as part of a balanced therapy in nonsurgical cases of GI pain and ileus.

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.


Alternatives to Opioids for Perianesthetic Analgesia Management

Khursheed Mama, DVM, DACVAA, Colorado State University

Morgan Oakleaf, DVM, Colorado State University

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Alternatives to Opioids for Perianesthetic Analgesia Management
Editor's Note (2019): An earlier version of this article incorrectly stated the dosage for oromucosal dexmedetomidine. The dosage has been corrected.
Editor's Note (2018): While the underlying circumstances vary from place to place, a shortage of opioids due to manufacturing delays or government restrictions is an almost global issue, which makes this guide to alternative analgesics universally germane.

The current opioid shortage has resulted in challenges providing perioperative analgesia to dogs and cats. Although direct substitution is not appropriate for all situations, many alternatives are available. 

To calm patients before and/or after anesthesia, gabapentin (5-10 mg/kg PO1) or trazodone (3-5 mg/kg PO2) may be used in cats and dogs, respectively. To the author’s knowledge, serotonin syndrome has not been reported with trazodone use in veterinary medicine. 

Oromucosal dexmedetomidine may also be considered for prearrival sedation (125 µg/m2 oromucosal).3 Oral acepromazine tends to have inconsistent effects, but injectable acepromazine (0.01-0.05 mg/kg IV, IM, or SC) is more reliable and may be used in patients that cannot receive oral medications.4 Other options, including alprazolam (0.01-0.02 mg/kg PO5), may be viable for some animals.

Oral Analgesia

Although popular, tramadol (5-10 mg/kg PO) has not been consistently reported to have good efficacy for pain management in dogs, as it has only weak opioid effects.6 However, it may provide a sense of well-being based on its nonopioid (serotonergic- and norepinephrine-based) actions.7,8 A serotonin-like syndrome has not been well documented in animals but the possibility remains especially when this drug is combined with similar medications (eg, trazodone, fluoxetine) or certain opioids (most notably meperidine).7

Perioperative NSAIDs (eg, carprofen [2.2-4.4 mg/kg PO or SC9], meloxicam [0.1-0.2 mg/kg PO or SC10], robenacoxib [1-2 mg/kg PO or SC11]) may also be considered in animals with no GI or renal disease and in the absence of steroid administration. The sooner in the course of anesthesia they can be administered so that tissue levels are reached, the more effective these medications are likely to be for postoperative pain management. It is important to remember, however, that hypotension under anesthesia may adversely affect renal blood flow and compound renal side effects.12 Grapiprant (2 mg/kg PO13) is a newer noncyclooxygenase prostaglandin-receptor antagonist that has been shown to have efficacy in treating osteoarthritis pain in dogs. Its utility as a perioperative analgesic is not well studied, but an improved side effect profile may prove advantageous.13

Injectable Analgesia

Many µ-opioid agonists (eg, morphine, hydromorphone, oxymorphone, methadone, fentanyl, alfentanil, remifentanil, sufentanil) have been sporadically available. In addition to analgesia and variable degrees of sedation, they provide anesthetic-sparing effects while maintaining cardiovascular safety. For premedication and intraoperative use by infusion, these drugs are largely interchangeable, provided the clinician has knowledge of their relative potency, onset and duration of action, and side effect profile.6 

Buprenorphine (20-30 µg/kg IV, IM, or buccal), a partial µ agonist, may be used alone or in combination with other medications as a substitute for other µ agonists in dogs and cats for mildly- to-moderately painful procedures.6,14 It may also be used with other drugs for more complex and painful surgical procedures to minimize pain. A dosing interval of approximately 6 to 8 hours has been suggested in the perioperative period.14 Salivation, bradycardia, and respiratory depression may be observed with use; drug effects are generally not thought to be reversible. Sustained-release or long-acting formulations of buprenorphine for subcutaneous administration are available and are reported to provide between 24 and 72 hours of analgesia.15,16

Butorphanol (0.1-0.5 mg/kg IV, IM, or SC), a κ agonist and µ antagonist, is best used as a sedative and analgesic for presumed mildly painful procedures (eg, gastroduodenoscopy, colonoscopy, subcutaneous mass removal) or with adjunct analgesic techniques (eg, as a nerve block).6

Premedication with dexmedetomidine (3-10 µg/kg IM) can be considered in healthy dogs and cats to provide sedation and analgesia. Cardiovascular side effects may occur and present challenges with monitoring. If these effects are significant, partial reversal with atipamezole can lessen them; however alternative analgesia should be provided prior to reversal. Dexmedetomidine may also be administered as a constant-rate infusion in healthy dogs and cats; an initial maintenance dose of 1 µg/kg/hr IV has been suggested to provide analgesia and anesthesia-sparing effects.17

Infusion Analgesia

Ketamine is an N-methyl-D-aspartate–receptor antagonist that, at subanesthetic doses, has been shown to mitigate or prevent spinal facilitation of pain (ie, the wind-up effect). Although the drug is administered during anesthesia, the greatest benefit is thought to occur postoperatively.18 However, even at low doses (eg, 10-20 µg/kg/min IV after a loading dose of 0.5 mg/kg IV), ketamine can reduce anesthetic requirements up to 25%.19 Higher doses in dogs and cats have been reported to further reduce inhaled anesthesia requirements but exhibit a ceiling effect.20 Although reports of benefits are largely anecdotal, ketamine infusions may be continued into the postoperative period in conscious animals. Doses of 1-3 µg/kg/min IV have been suggested to minimize behavior changes.18 In patients for which preventing or reducing spinal facilitation is desirable but for which oral administration is preferred, amantadine (3 mg/kg PO q24h) may be considered.21

Intravenous lidocaine (2%) may be a cost-effective source of background analgesia and inhaled anesthetic dose reduction.22 Side effects include seizures but are rare if clinically appropriate doses are used. Nausea may also be noticed at high doses in conscious patients. Anesthetic dose reduction with 50 µg/kg/min CRI IV (low end of the antiarrhythmic dose range) has been reported in dogs19; however, the authors’ experience suggests that doses as low as 20-30 µg/kg/min IV are beneficial in clinical patients. Lidocaine is not routinely recommended for use in cats, as, despite a reduction in isoflurane dose, cardiovascular depression is greater with a combination of lidocaine and isoflurane than with an equivalent dose of isoflurane alone.23 

Combinations of an opioid, lidocaine, and ketamine (opioid and ketamine for cats) may be used for their anesthesia-sparing effects to provide analgesia and reduce spinal facilitation of pain in dogs. When morphine, lidocaine, and ketamine are combined in dogs, the isoflurane dose is reduced by approximately 45%.19 Respiratory depression is generally less than with high doses of opioids alone.

Regional Anesthesia

Because of the shortage of drugs available for systemic administration, use of regional techniques (eg, injecting lidocaine [2%; up to 2 mg/kg] into the testicle prior to castration, providing a line block to the abdominal wall during an ovariectomy/ovariohysterectomy) when possible can be of significant benefit. Targeted nerve blocks and intra-articular or epidural administration provide other options for localized pain relief. Longer-acting local anesthetics (eg, ropivacaine, bupivacaine) may be used as warranted by the procedure and with consideration to duration of motor effects and toxicity. 

Liposomal bupivacaine recently became available as another alternative for long-acting pain relief following surgery when injected into tissues at the surgical site.24 Label directions should be followed if this drug is being used with other regionally or systemically administered local anesthetics.

References & Author Information

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

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

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Nutrition Assessment in a Dog with Sarcoma & Anemia

Nutrition Assessment in a Dog with Sarcoma & Anemia

Donna M. Raditic, DVM, DACVN, CVA, Nutrition and Integrative Medicine Consultants, Athens, Georgia

Gregg K. Takashima, DVM, WSAVA Global Nutrition Committee Series Editor

Kara M. Burns, MS, MEd, LVT, VTS (Nutrition), Olathe, Kansas

Nutrition

|Peer Reviewed

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Nutrition Assessment in a Dog with Sarcoma & Anemia

THE CASE

Kelsey, an 11-year-old spayed Maltese, was referred to a nutrition service for inappetence and weight loss one week post-splenectomy following a diagnosis of splenic histiocytic sarcoma. She was being treated postoperatively with lomustine (CCNU; 70 mg/m2   PO q4wk). Before surgery, Kelsey weighed 12.1 lb (5.5 kg), but on presentation to the nutrition service, she weighed 11 lb (5 kg) and had a BCS of 3/9 (ideal BCS, 5/9) and a muscle condition score of moderate muscle loss (on a scale of normal, mild, moderate, to marked muscle wasting or loss). Historic medical records showed the patient’s weight typically ranged from 13.2 lb to 15.4 lb (6-7 kg), with an average BCS of 5/9; no muscle condition score had previously been documented.

Dietary History

Kelsey had reportedly been fed a variety of commercial dog foods until age 7. However, she reportedly did not appear to enjoy any of the commercial diets and was transitioned to a mixture of cooked tofu or cooked white fish with steamed vegetables offered ad libitum 3 times a day. The homemade diet did not contain any animal or human vitamin-mineral supplements. The owner reportedly did not offer treats or other human foods. Water intake was reported to be normal.  

Preoperative serum chemistry profile and urinalysis results were normal, but CBC revealed microcytic hypochromic anemia and thrombocytosis. CBC with a reticulocyte count performed 2 weeks postsurgery (ie, 1 week after presentation to the nutrition service) showed further decrease in hematocrit and nonregenerative, microcytic hypochromic anemia (Table: CBC Value Results of Importance). 

TABLE

CBC VALUE RESULTS OF IMPORTANCE

Test Preoperative 2 Weeks Postsurgery 4 Weeks Postsurgery 2 Months Postsurgery 3 Months Postsurgery Reference Range
Hematocrit 33% 27% 41.8% 41.6% 46% 41%-60%
Mean corpuscular volume 60 fL 59 fL 62 fL 73 fL 72.9 fL 62-74 fL
Mean corpuscular hemoglobin 22.3 pg/cell 20.8 pg/cell 23.6 pg/cell 23.9 pg/cell 24.6 pg/cell 22-26.2 pg/cell
Platelets 789 × 103/mL (789 × 109/L) 939 × 103/mL (939 × 109/L) 906 × 103/mL (906 × 109/L) 707 × 103/mL (707 × 109/L) 453 × 103/mL (453 × 109/L) 147 - 423 × 103/mL (147-423 × 109/L)
Reticulocytes N/A 30.8 × 103/mL (30.8 × 109/L) 149.6 × 103/mL (149.6 × 109/L) 80.4 × 103/mL (80.4 × 109/L) 106.3 × 103/mL (106.3 × 109/L) 12.5-93 × 103/mL (12.5-93 × 109/L)

 

DIAGNOSIS:

Splenic Histiocytic Sarcoma & Nonregenerative Anemia

Because Kelsey had been consuming an unbalanced homemade diet and had undergone surgical splenectomy, a serum iron panel was ordered and sent to a veterinary diagnostic laboratory to better characterize the nonregenerative, microcytic hypochromic anemia (Table: Serum Iron Panel Results).1-4 Serum iron and total iron-binding capacity supported a diagnosis of iron deficiency anemia, although serum ferritin was slightly elevated. Serum ferritin is typically low in patients with iron deficiency anemia, as it correlates with body iron stores, but serum ferritin is an acute phase protein and may be elevated in patients with underlying disease such as neoplasia, liver disease, or hemolytic disease.2-4 Hyperferritinemia has specifically been reported in dogs with histiocytic sarcoma and hemangiosarcoma.5,6 Kelsey’s discordant serum ferritin, although increased, was not as high as the values that have been reported with neoplastic disease and perhaps indicated concurrent disease effects.4-6 It was postulated that Kelsey may have both anemia of chronic disease (secondary to neoplasia) and iron deficiency anemia (secondary to diet).2,3,7

TABLE

SERUM IRON PANEL RESULTS

Test Result Reference Range
Serum iron 30 µg/dL (5.4 µmol/L) 33-147 µg/dL (5.9-26.3 µmol/L)
Total iron-binding capacity 298 µg/dL (53.3 µmol/L) 282-386 µg/dL (50.5-69.1 µmol/L)
Serum ferritin 811 ng/mL (1822 µmol/L) 80-800 ng/mL (180-1798 µmol/L)

 

Treatment & Follow-Up

Two iron dextran injections (20 mg/kg IM) were administered approximately one month apart at 2 weeks and 2 months postsplenectomy (Table: CBC Value Results of Importance), and a nutrition plan was instituted. The nutrition plan was formulated by a boarded veterinary nutritionist and included a complete and balanced homemade diet of cooked skinless chicken breast, sweet potato, vegetables, canola oil, and a vitamin-mineral supplement. The owner was given specific instructions for preparing the diet using cooked gram weights of each ingredient and was educated on the importance of adding the vitamin-mineral supplement. To ensure adequate intake of the homemade diet by the patient, the owner was given a computerized spreadsheet food journal to record daily gram intake. Three times a day, the owner offered the recommended gram amount of the recipe, weighed any food remaining, recorded the gram intake of each meal, then calculated total gram intake per day. The nutritionist reviewed the food journal weekly to ensure Kelsey was not only consuming the homemade diet but consuming adequate kcals for weight gain. Body weight was also reported to the nutritionist biweekly. Follow-up examination was conducted at 2 weeks and 1, 2, and 3 months after diet implementation to assess patient and owner compliance with the homemade diet. Food intake gradually increased, and at the 3-month recheck, the patient weighed 14.3 lb (6.5 kg) and BCS had improved to 4/9, although MCS remained at 2/3.

Follow-up CBCs showed a marked regenerative response and resolved anemia. The owner declined a repeat serum iron panel due to financial constraints but reported that the dog’s appetite had improved after the iron injections and implementation of the nutrition plan.  

Repeat diagnostics and imaging after 9 months of lomustine therapy showed no evidence of histiocytic sarcoma; thus, the oncology service recommended discontinuing treatment. The owner was counseled to continue the homemade diet as outlined and to contact the nutrition service if there were any changes in the patient’s medical condition. Two and half years after cancer diagnosis, Kelsey was euthanized for poor quality of life with no specific diagnosis.

Conclusion

This case illustrates the importance of nutritional assessment and management in veterinary cancer patients. Veterinary patients can often sustain a reasonable quality of life on an unbalanced diet, but in patients with neoplasia, inadequate nutrient intake can impact patient outcomes and quality of life. Anemia is common and is most often assumed to be anemia of chronic disease. An in-depth dietary history and further laboratory assessment of nutritional status can help identify dietary factors that can affect quality of life in cancer patients. This case also illustrates the importance of providing nutritional follow-up when prescribing a homemade diet, as nutritional follow-up can help ensure owner compliance and that the nutritional goals—in this case, weight gain and resolution of anemia—are met. 

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Anemia of chronic disease is typically represented by:

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Iron deficiency anemia is best described as:

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Diet in Disease is a series developed by the WSAVA, the Academy of Veterinary Nutrition Technicians, and Clinician’s Brief.

References & Author Information

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

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

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


Top 5 Zoonotic Disease Concerns in Hospital Visitation Dogs

J. Scott Weese, DVM, DVSc, DACVIM, Ontario Veterinary College, Ontario, Canada

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Top 5 Zoonotic Disease Concerns in Hospital Visitation Dogs

A variety of animals may be encountered in human healthcare facilities, including service animals, patients’ pets, therapy animals for animal-assisted therapeutic activities, and visitation animals.1 The latter category, typically pets of volunteers brought to facilities to interact with patients, is the most common and the focus of this discussion.

Animal visitation programs, also referred to as pet therapy or animal-assisted activities, can have various positive impacts on patients2-5; however, any human–animal contact poses some degree of risk for transmission of zoonotic pathogens. Healthcare facilities contain large numbers of individuals with increased susceptibility to disease, heightening zoonotic disease concerns.  

Most animals used for animal visitation programs are dogs, a relatively low-risk species for which there is a good understanding of pathogen carriage rates and risk factors and an ability to test temperament. Therefore, this article focuses on zoonotic concerns pertaining specifically to dogs. 

A variety of bacteria, viruses, and fungi pose some degree of zoonotic risk, but the primary concerns typically involve opportunistic bacterial pathogens. The incidence of dog-associated disease in healthcare facilities is unknown, possibly because it is rare. However, it is likely that infections occur, at least sporadically, and are undiagnosed. This is particularly true for pathogens that are common in hospitalized individuals (eg, multidrug-resistant bacteria), as identification of an infection might not trigger much investigation or consideration of potential animal sources. A collection of basic infection control and visitation practices can presumably reduce the risks that may be encountered.1 

Following are the author’s top 5 zoonotic disease concerns in hospital visitation dogs. Because evidence is empirical, this list is based on conjecture rather than data.

1

Methicillin-Resistant Staphylococcus aureus

Methicillin-resistant Staphylococcus aureus (MRSA) is a leading cause of hospital-associated infection in humans. This multidrug pathogen can colonize the nose, throat, skin, and GI tract of dogs and humans in the absence of disease. MRSA colonization has been identified in a small percentage of dogs and typically involves the same strains that infect humans.6-9 These cases presumably occurred predominantly from human–dog transmission, but colonized dogs could be sources for subsequent infection of humans. 

Hospital visitation dogs have been shown to be at elevated risk for MRSA colonization, presumably from contact with colonized patients.10 Transient contamination of the haircoat can also occur during patient contact.11 

Screening of visitation dogs for MRSA carriage is not recommended (see Pathogen Screening).1 MRSA prevention should be focused on practicing good hand hygiene before and after animal contact. Because antibiotic exposure increases the risk for MRSA colonization in dogs,10 short-term exclusion of dogs that are receiving or have recently received antibiotics is recommended.1 Dogs that participate in hospital visitation programs are more likely to encounter MRSA than are nonparticipating dogs; thus, culture and susceptibility testing of wound infections and other bacterial infections is warranted. Dogs with any wound infections should be excluded from visitation because of the potential involvement of pathogens such as MRSA, as well as the risk for exposure to other pathogens that could complicate the wound infection.

Pathogen Screening

In general, pathogen screening is not considered useful because it shows a result from a single point in time and uses tests that are not 100% sensitive and cannot test for the wide array of potentially zoonotic pathogens. A negative result would show that the dog was “probably” negative (for the tested pathogens only) at the time of sampling but could have been exposed any time thereafter. A negative result would not show that the dog is not carrying a pathogen, that it poses no risk, or that precautions such as hand hygiene are not needed because of the range of other pathogens. Because pathogen screening does not modify required practices and can be expensive, the benefit is limited.

2

Clostridium difficile

Clostridium difficile is an important cause of morbidity and mortality in hospitalized humans. This fecal–oral pathogen can also be found in the GI tract of healthy dogs and humans.12-15 Zoonotic transmission from dogs has not been clearly established, but the same strains have been found in dogs and humans.16-18 

Hospital visitation dogs are at significantly elevated risk for C difficile shedding,10 likely acquired through ingestion of C difficile spores from the hospital environment and patient hands. Risk reduction involves limiting exposure of dogs (eg, not visiting patients who are under enhanced precautions for C difficile infection, encouraging patients to practice good hand hygiene before contact with a dog, limiting contact with patients’ living spaces) and reducing dog–human transmission (eg, through good fecal handling, preventing fecal accidents, and practicing good hand hygiene). As with MRSA, short-term exclusion of dogs that are receiving or have recently received antibiotics is recommended.1 Screening of animals for C difficile shedding is not recommended (see Pathogen Screening).

3

Extended-Spectrum β-Lactamase–Producing Enterobacteriaceae

A variety of multidrug-resistant gram-negative bacteria are important causes of infection in healthcare facilities, with some strains being near pan-resistant (ie, resistant to all available antimicrobials). Extended-spectrum β-lactamase (ESBL)–producing bacteria are widely distributed in healthy dogs, and strains that cause disease in humans are often identified in dogs,19,20 which suggests the potential for both human–dog and dog–human transmission in healthcare facilities. Other resistant gram-negative bacteria that may be encountered include carbapenemase-producing Enterobacteriaceae, which may be extensively drug resistant. Colonization or infection of dogs with carbapenemase-producing Enterobacteriaceae is rare but possible,21,22 and because these pathogens are increasingly found in human healthcare facilities, the potential for exposure and colonization in the GI tract is increased.

Because ESBL-producing bacteria are fecal–oral pathogens, preventive measures are similar to those described for C difficile, and screening of visitation animals is not recommended (see Pathogen Screening). Exclusion of dogs actively or recently (ie, within the past month) treated with antimicrobials is recommended,1 as antimicrobial exposure is a risk factor for ESBL acquisition23,24 and, presumably, acquisition of other resistant gram-negative enteric pathogens.

4

Salmonella spp

Salmonellosis can be life-threatening in compromised dogs and humans. Although the prevalence of Salmonella spp shedding tends to be low in healthy adult dogs, higher rates can be found in some subpopulations, particularly dogs fed raw meat-based diets or treats.25-27 Risk reduction involves prohibition of raw meat and/or raw animal-based treats to visitation dogs and exclusion of dogs with active or recent (ie, within the past week) diarrhea.1 Good fecal handling practices and attention to hand hygiene can help further reduce the risk. Routine testing for Salmonella spp is not recommended (see Pathogen Screening); however, culture or PCR testing of diarrheic therapy dogs may be useful in identifying animals that require a longer exclusion period after resolution of diarrhea.

5

Exposure to Pathogens from Bites & Scratches

Although often overlooked in discussion of zoonotic diseases, bites and scratches may be the most common and potentially serious hazards associated with visitation dogs. The incidence of bites and scratches in healthcare facilities has not been reported, but they have been observed.28 Bites are of particularly high risk because of the myriad opportunistic pathogens found in a dog’s mouth, such as Pasteurella spp and Capnocytophaga canimorsus. Bites can also inoculate pathogens (eg, MRSA) that might be residing on a human’s skin.29 Scratches from dogs pose a lower risk for infection as compared with bites but can cause pain, and any disruption of the protective skin barrier may increase the risk for infection in high-risk individuals.

ESBL = extended-spectrum β-lactamase, MRSA = methicillin-resistant Staphylococcus aureus

References & Author Information

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

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

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Hypocobalaminemia

Leonard E. Jordan, DVM, University of Tennessee

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

Internal Medicine

|Peer Reviewed

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Hypocobalaminemia

Background & Pathophysiology

Cobalamin (ie, vitamin B12) is a water-soluble vitamin that plays an important role in DNA and RNA synthesis, amino acid (eg, cysteine, homocysteine) metabolism, and energy production. Following ingestion of cobalamin-rich nutrients (eg, fish, poultry, eggs, red meat, dairy products), cobalamin first binds to haptocorrin, which is produced in both the salivary gland and the stomach. In the duodenum, cobalamin is bound to intrinsic factor—a protein produced primarily in the pancreas of dogs and cats—and is later absorbed in the distal small intestine. 

Any disease that affects the production of intrinsic factor or interferes with the intestinal absorption of cobalamin can cause cobalamin deficiency (Table). Dogs and cats with exocrine pancreatic insufficiency (EPI) may have decreased production of intrinsic factor. Intestinal diseases (eg, inflammatory bowel disease, food-responsive enteropathy, intestinal lymphoma, dysbiosis, lymphangiectasia) can result in compromised ileal function and inadequate absorption of cobalamin.1,2 Familial cobalamin deficiency resulting from a loss-of-function mutation in the receptor responsible for intestinal cobalamin absorption is an uncommon cause of hypocobalaminemia but should be considered in young patients presented with GI and neurologic signs, especially in predisposed breeds such as giant schnauzers, Australian shepherd dogs, border collies, beagles, shar-peis, and Komondors.3,4

TABLE

Diseases Associated with Low Cobalamin

Disease Diagnostic Test(s)
Exocrine pancreatic insufficiency Trypsin-like immunoreactivity
Pancreatitis Pancreatic lipase immunoreactivity, abdominal ultrasonography
Inflammatory bowel disease Intestinal biopsy and histopathologic examination
Intestinal lymphoma Intestinal biopsy and histopathologic examination ± immunophenotyping, PCR for antigen receptor rearrangements (PARR)
Lymphangiectasia Abdominal imaging, intestinal biopsy and histopathologic examination
Selective cobalamin malabsorption Genetic testing for some patients (eg, evaluation for cubilin [CUBN] gene mutation), urine MMA testing

 

History & Clinical Signs

Common signs of cobalamin deficiency in dogs and cats include GI signs (eg, anorexia, weight loss), which often mimic those observed in animals with chronic GI disease; thus, the clinician may not immediately consider cobalamin deficiency as a contributing factor. Additional clinical signs of hypocobalaminemia can include failure to thrive, immunodeficiency, and neuropathies. These clinical signs may be more commonly observed in dogs with familial cobalamin deficiency. Unlike those occurring with pancreatic and GI disease, clinical signs induced by familial hypocobalaminemia are responsive to cobalamin supplementation alone.5 In one case report, a border collie with selective cobalamin malabsorption was presented with hepatic encephalopathy secondary to hypocobalaminemia, which resolved following cobalamin supplementation.6 In another report, a Yorkshire terrier with selective cobalamin malabsorption was presented with seizures that also resolved with parenteral cobalamin supplementation.7 Thus, cobalamin deficiency should be considered in any animal presented with chronic GI signs, especially when in combination with neurologic signs.

Diagnosis

Hypocobalaminemic cats often do not respond as readily as normocobalaminemic cats to treatment of the primary disease unless supplemented with cobalamin; this is unproven but, in the authors’ clinical experience, is also suspected in hypocobalaminemic dogs. Thus, cobalamin deficiency is an important clinical consideration in any patient presented with signs of chronic enteropathy or pancreatic disease. Diagnosis of hypocobalaminemia requires measurement of serum cobalamin concentrations. However, patients may have serum cobalamin levels that are low-normal (250-350 ng/L) and still have critically low tissue cobalamin concentrations. In these cases, evaluating biomarkers of tissue cobalamin deficiency (eg, methylmalonic acid [MMA], homocysteine) may provide more insight, as these biomarkers often increase with tissue cobalamin deficiency in dogs.4,8-10 In cats, MMA may be a better indicator of tissue cobalamin deficiency as compared with homocysteine.6

Treatment & Management

Cobalamin therapy (see Suggested Reading for dose, frequency, and administration information) should be instituted when serum concentrations fall below 250 ng/L. Additional consideration for supplementation is recommended in patients with a low-normal serum cobalamin (250-350 ng/L) and/or signs of intestinal or pancreatic disease. Hypocobalaminemia secondary to GI disease has anecdotally been thought to require parenteral supplementation of cobalamin until the intestinal or pancreatic disease was appropriately treated because of the inability to absorb cobalamin or produce intrinsic factor, respectively. However, recent research has suggested that oral administration of cobalamin in dogs and cats with chronic enteropathies11,12 and dogs with EPI13 is effective in restoring normal cobalamin concentrations. This may be secondary to enhanced passive absorption of cobalamin along the length of the small intestine.

Prognosis & Prevention

The prognosis for hypocobalaminemic patients depends largely on the underlying disease process and how the patient responds to treatment of the primary disease. Low cobalamin concentration is associated with shorter survival with some diseases, including EPI and multicentric lymphoma.13,14 Lack of recovery for dogs with chronic diarrhea due to inflammatory idiopathic or neoplastic disease may also be more likely when severe hypocobalaminemia (<200 ng/L) is present.15 The benefit of supplementation in these disease states has not been definitively proven; however, it is recommended to evaluate the patient’s serum cobalamin concentration and provide supplementation when hypocobalaminemia is identified. Prognosis for familial cobalamin deficiency is good with long-term supplementation.

Clinical Follow-Up & Monitoring

Daily oral cobalamin supplementation or a 6-week course of weekly parenteral supplementation followed by a single injection 30 days later and retesting after 30 days is recommended.1,16 Some patients, especially those with EPI or ongoing intestinal disease, may require continued monthly cobalamin supplementation. If resolution of the primary disease cannot be achieved, more frequent cobalamin administration may be required. If remission of the underlying disease (eg, food-responsive enteropathy) is achieved, long-term supplementation may not be necessary; however, re-evaluation of the patient’s serum cobalamin concentration is recommended if disease relapse occurs.

EPI = exocrine pancreatic insufficiency, MMA = methylmalonic acid

References & Author Information

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

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

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Pulmonary Barotrauma & Pneumothorax During Anesthesia

Marlis Rezende, DVM, PhD, DACVAA, Colorado State University

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Pulmonary Barotrauma & Pneumothorax During Anesthesia

In anesthesia, the term barotrauma is used to describe lung tissue trauma resulting from excessively high airway pressure associated with excessive inflation of the lungs and alveolar overdistension, which can result in alveolar and pleural rupture.1,2 When alveolar rupture occurs, air leaks into the pleural space and creates a closed pneumothorax, which in turn can rapidly evolve into a tension pneumothorax, especially if mechanical ventilation is being used. The resulting excessively high intrathoracic pressure impairs venous return to the heart, severely compromising stroke volume and cardiac output. If not quickly recognized and corrected, life-threatening cardiovascular collapse can occur.2

Causes of Barotrauma

Although an inadvertently closed pop-off valve is regarded as the most common cause for pulmonary barotrauma and pneumothorax during anesthesia, clinicians should be aware of other potentially dangerous scenarios that could lead to alveolar overdistension and rupture. Equipment-related barotrauma is typically caused by either excessive gas inflow into the breathing circuit and airway or restriction/obstruction of the gas outflow pathway.3,4

Excessive Inflow of Gas

Excessive inflow can occur from improper use of the oxygen flush valve, aggressive ventilator settings (high airway pressures and tidal volumes), and/or inappropriate connection of oxygen tubing (meant for oxygen insufflation via open mask) to a cuffed endotracheal tube, laryngeal mask airway, or other airway device without the ability to allow excess gas to vent. 

The oxygen flush valve allows oxygen at high pressure and volume into the breathing system (35-70 L/min with a pressure of 45-60 pounds per square inch gauge [PSIG] [310-414 kPa gauge], which becomes approximately 1 L/s into the breathing system).3,4 A nonrebreathing system (eg, Bain breathing system) has a relatively small inner volume and little compliance. Therefore, use of the flush valve while a patient is connected to a nonrebreathing system transmits excess volume and pressure directly to the patient’s airway and lungs. Similarly, if the oxygen flush valve is used during the inspiratory phase of mechanical ventilation, the patient’s lungs may be exposed to excessive pressure and overdistension. During the inspiratory phase, the ventilator’s driving pressure actively compresses the bellows to deliver a breath, and the ventilator’s exhaust valve is closed. Because the ventilator’s driving pressure (65-75 cm H2O) prevents the expansion of the bellows until breathing system pressures overcome the driving pressure, activation of the flush valve at this time (eg, to reinflate the bellows after a brief disconnection) would direct all the volume and resulting pressure to the breathing circuit.3 

Aggressive Ventilator Settings

Inappropriately performed or overly aggressive mechanical ventilation can also cause barotrauma. In contrast to spontaneous ventilation, in which inspiration relies on the negative intrathoracic pressure generated by chest expansion to passively inflate the lungs, mechanical ventilation actively inflates the lungs using positive pressure. If excessive high tidal volumes and/or peak inspiratory (and plateau) pressures are used, barotrauma may occur. Overzealous manual breaths can have similar effects, when high tidal volumes and/or airway pressures are generated.

Outflow Restriction or Obstruction

Any form of significant breathing circuit outflow restriction or occlusion can lead to excessive airway pressures and lung overinflation, as there is no path to release the excess gas from the breathing system. Common examples include pop-off valve obstruction, compression or kinking of the scavenger hose, obstruction of the F/AIR anesthesia gas filter canister vents, and kinking of the hose that connects the ventilator to the breathing circuit. Additional care should be taken when using nonrebreathing systems, as the combination of the required high fresh gas flow rates with the relatively small inner volume of the breathing circuit allows airway pressures to rise very quickly in the case of an obstruction.

Safety Devices to Prevent Barotrauma

Most anesthesia-associated barotrauma events (and resulting pneumothorax) can be avoided through both a functional understanding of the anesthesia machine and the presence of safety features designed to prevent harmful conditions or alert the team if such conditions arise, including:

  • Pop-off occlusion valve (Figure 1). This device can be attached to the outflow port of the anesthesia machine’s original pop-off valve. When the top button of the valve is pushed, flow out of the pop-off valve is occluded and a manual breath can be administered. Once the button is released, flow through the valve is automatically re-established, minimizing the risk for forgetting to reopen the original pop-off valve, as it will always be left open. Although this can be useful during spontaneous ventilation, it does not completely eliminate the risk, as the original pop-off valve will still need to be closed (and opened afterward) if mechanical ventilation is to be used or during the process of pressure checking the anesthesia machine for leaks.
  • High-pressure alarm (Figure 2). This device provides an audible alarm when the breathing circuit pressure reaches a set level (typically 20 cm H2O). In addition, it can be used with both rebreathing and nonrebreathing systems with spontaneous or mechanical ventilation. The device will alarm when a dangerous breathing circuit pressure occurs (independent of cause), providing the clinician time to intervene.

Patients at Increased Risk

Pre-existing lung disease (eg, pulmonary bullae, pneumonia, acute respiratory distress syndrome, feline asthma) may predispose animals to barotrauma and pneumothorax under anesthesia.2 Other pre-existing conditions, although not a consequence of true barotrauma, may increase the risk for a pneumothorax due to pulmonary tissue fragility or injury. This is especially notable in patients that have undergone trauma to the chest (eg, hit by a car, kicked by a horse), as the pulmonary contusions create areas of alveolar fragility.5 Patients with pulmonary neoplastic masses, cysts, abscesses, or foreign body migration can be similarly predisposed to pneumothorax despite appropriate ventilation settings.

Pneumothorax

Pneumothorax is a life-threatening complication of barotrauma. Awareness and early recognition are key to a successful outcome. During anesthesia, a closed pneumothorax can rapidly evolve to a tension pneumothorax. In a one-way valve mechanism, air leaks out during lung inflation. As the lung tissue recoils during exhalation, air cannot escape via its entry path and becomes trapped outside the lungs in the thoracic cavity. The high-pressure intrathoracic environment that soon develops limits lung expansion and, most importantly, prevents venous return to the heart, leading to cardiovascular collapse. 

As the lungs’ ability to expand decreases and atelectasis increases, a change in breathing pattern typically occurs, followed by dyspnea and a decrease in oxygen saturation. As the pneumothorax evolves to a tension pneumothorax and venous return is compromised, severe hypotension and hypoxemia occurs. Reflex tachycardia may be present. The patient becomes more difficult to ventilate as lung compliance decreases and chest wall movement is diminished. On auscultation, lung sounds may be absent or significantly diminished.

Early recognition of clinical signs can be hindered in cases in which the patient’s overall condition is already compromised (eg, patient in shock, with hypovolemia, and/or with significant intraoperative blood loss). Pneumothorax may only become evident on cardiopulmonary collapse. It is therefore important that the clinician is aware of the potential risk for a pneumothorax based on the patient history and potential predisposing conditions.

If a pneumothorax is suspected, positive pressure ventilation should be immediately discontinued and thoracocentesis performed for emergency decompression of the chest. Once the intrathoracic pressure is relieved, arterial blood pressure and oxygen saturation will improve. A thoracostomy tube should then be placed to allow air to be continuously removed until the ruptured alveoli can seal to prevent the reoccurrence of a tension pneumothorax. (For a detailed description of how to perform a thoracocentesis or place a thoracostomy tube, see Suggested Reading.) 

Conclusion

Understanding and ensuring the proper functioning of the anesthesia machine before each use, adding safety features to help prevent and/or recognize mistakes, and having a dedicated individual to monitor anesthesia who is able to rapidly recognize equipment issues and adverse events are key to increasing patient safety.

References & Author Information

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

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

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


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