Download Small Animal Medicine and Feline Chapters

2012 ANZCVS Science Week
Small Animal Medicine and Feline Chapters
Proceedings are also available online at www.samedicine.acvs.org.au
Small Animal Medicine and Feline research abstracts
1. Asymptomatic bacteriuria Escherichia coli strain 83972 in competition with
emerging, highly virulent multidrug-resistant escherichia coli strains in canine urine
..................................................................................................................................................................... 4
MF Thompson1, JS Gibson1, PC Mills1, MA Schembri2, JL Platell1, DJ Trott3
2. Incidence of sterile haemorrhagic cystitis in dogs undergoing metronomic
chemotherapy with cyclophosphamide ........................................................................................ 4
SP Hagley
3. Retrospective study of 180 cats presenting with anaemia .................................................5
RM Korman1, N Hetzel1, TG Knowles1, AH Harvey2, S Tasker1
4. Congenital methaemoglobinaemia due to methaemoglobin reductase enzyme
deficiency in a six month old pomeranian puppy...................................................................... 5
C Yudelman
5. Serological survey of leptospiral antibodies in dogs in New Zealand ............................6
AL Harland1, NJ Cave1, BR Jones1, J Benschop 1, JJ Donald 2, AC Midwinter 1, RA Squires 5, JM
Collins-Emerson4
6. Indications and patient factors affecting the outcome of mechanical ventilation in
dogs and cats: 73 cases (2002-2012) ............................................................................................. 6
KA Worthing, JM Angles
7. Factors affecting hospitalisation duration in cases of canine tick paralysis Ixodes
holocyclus ................................................................................................................................................. 7
EL Neagle
8. Clinicopathological signs of red belly black snake envenomation of dogs in the
Sydney basin area ................................................................................................................................. 7
IH Goodman, JM Angles
9. Comparisons of biochemical results between three in-house biochemistry
analysers and a commercial laboratory analyser for feline plasma................................... 8
RM Baral1, JM Morton2, NK Dhand3, MB Krockenberger3, M Govendir3
10. Survey of owners’ perceptions of radioiodine treatment of feline
hyperthyroidism ................................................................................................................................... 8
LA Boland1, JK Murray1, CPV Bovens1 and A Hibbert2
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
11. Diabetic cats in remission have mildly impaired glucose tolerance ............................9
S Gottlieb1,2, JS Rand1, RD Marshall2
12. Gastrointestinal microbiota of cats with diabetes mellitus .............................................9
ET Bell1, JS Suchodolski2, L Fleeman3, A Cook2, JM Steiner2, CS Mansfield1
Joint session of the Small Amimal Medicine and Radiology Chapters
Pericardial disease of the dog and cat ......................................................................................... 10
Rita Singh
Bronchoscopy – What’s it good for?.............................................................................................. 13
Mike Coleman
Computed tomography use in respiratory medicine ............................................................. 15
Marjorie Milne
CT use in respiratory medicine ...................................................................................................... 19
Cathy Beck
CT use in respiratory medicine – Case discussions ................................................................. 22
Steven Holloway, Margorie Milne, and Cathy Beck
Joint session of the Small Animal Medicine and the AECC Chapters
The approach to the patient in respiratory distress .............................................................. 23
Dez Hughes
The diagnostic approach to the dog or cat with cyanosis ..................................................... 27
Niek J. Beijerink
Pyothorax............................................................................................................................................... 30
Trudi McAlees
Advanced cardiopulmonary monitoring .................................................................................... 33
Lisa Smart
The airways in crisis .......................................................................................................................... 35
Bruce Mackay
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
Small Animal Medicine Chapter
Canine nasal disease .......................................................................................................................... 38
Lynelle Johnson
Cor pulmonale ...................................................................................................................................... 41
Richard Woolley
Canine bronchial disease ................................................................................................................. 44
Lynelle Johnson
Small Animal Medicine and Feline Chapters
Mediastinal masses in cats..............................................................................................................47
Sue Bennett
Identification of cats with cardiac disease I - Sound advice before the echo ................. 48
Richard Woolley
Airway obstruction in cats ............................................................................................................... 51
Lynelle Johnson
Identification of cats with cardiac disease II - Echoing what has gone before .............. 54
Fiona Campbell
Exudative pleural disease ................................................................................................................ 56
Lynelle Johnson
Medical management of feline cardiac diseases ...................................................................... 60
Niek J. Beijerink
Feline upper respiratory aspergillosis: How different is it from canine sinonasal
aspergillosis? ........................................................................................................................................ 62
Vanessa R. Barrs
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
1. ASYMPTOMATIC BACTERIURIA ESCHERICHIA COLI STRAIN 83972 IN
COMPETITION WITH EMERGING, HIGHLY VIRULENT MULTIDRUG-RESISTANT
ESCHERICHIA COLI STRAINS IN CANINE URINE
MF Thompson1, JS Gibson1, PC Mills1, MA Schembri2, JL Platell1, DJ Trott3
1
The University of Queensland, Gatton, QLD, 2The University of Queensland, St Lucia, QLD, 3The University of
Adelaide, Roseworthy, SA
Background: Deliberate colonisation of susceptible dogs with the human asymptomatic bacteriuria Escherichia coli
strain 83972 may represent a viable alternative for management of recurrent urinary tract infection (UTI). The strain
out competes human uropathogenic E. coli (UPEC) in human urine in vitro, likely underpinning its success in
prevention of recurrent UTI. We examined the growth of E. coli 83972 in competition with isolates representing
three successful emerging multidrug-resistant (MDR) E. coli clonal groups in canine urine.
Methods: Mixed cultures were grown in pooled canine urine inoculated 1:1 with freshly grown pre-cultures of E.
coli 83972 and one of three previously published successful MDR UPEC isolates cultured from canine UTIs
(QUC07 [O75:ST1193]; QUC13 [ST131]; QUC18 [O15:K52:H1]). The cultures were grown aerobically at 37 oC
for 17 hours and viable counts were obtained. All experiments were performed in duplicate.
Results: In two competition experiments (QUC07 vs. 83972 and QUC13 vs. 83972), there was no significant
difference in mean viable counts at 17 hours. In the remaining competition experiment (QUC18 vs. 83972), E. coli
83972 was present in significantly lower numbers than the MDR E. coli strain after 17 hours (P < 0.05).
Conclusions: Given that the starting ratio in dogs following prophylactic bladder colonisation would favour E. coli
83972, it is feasible that it will outcompete MDR UPEC strains. Investigation of variables such as alternative
bacterial concentrations, resistance, colicin production and virulence characteristics will enhance our understanding
of the mechanisms by which E. coli 83972 grows in urine and its suitability for use in prophylactic treatment.
2. INCIDENCE OF STERILE HAEMORRHAGIC CYSTITIS IN DOGS UNDERGOING
METRONOMIC CHEMOTHERAPY WITH CYCLOPHOSPHAMIDE
SP Hagley
Veterinary Specialist Services, Brisbane, QLD
Background: Metronomic chemotherapy with cyclophosphamide has been demonstrated to inhibit tumour
angiogenesis, suppress regulatory T cells and reverse immunosuppression, preventing or delaying tumour recurrence
in canine cancer patients. Cyclophosphamide, at the maximally tolerated dose, is known to cause sterile
haemorrhagic cystitis (SHC) however the incidence is uncertain when utilised metronomically.
Aim: To determine the incidence of SHC in dogs receiving long-term metronomic cyclophosphamide.
Materials: Twenty-one client-owned dogs receiving metronomic cyclophosphamide as adjuvant therapy for various
neoplasms, for a period exceeding 30 days. Doses of cyclophosphamide ranged from 10 mg/m2 every other day to
20mg/m2/day with variations in between.
Methods: The development of SHC in patients following metronomic cyclophosphamide chemotherapy for greater
than 30 days was examined retrospectively. The only selection criterion was the duration of treatment and all dogs
were enrolled at the same clinic. Conclusive evidence, such as haematuria and a negative urine culture or
appropriate ultrasonographic findings, was required for the diagnosis of SHC to be sustained.
Results: The incidence of SHC identified in dogs receiving metronomic cyclophosphamide for greater than 30 days
was 28.5%. This occurred on average 216 days after initiating treatment. There was no association with gender nor
the dose of cyclophosphamide received.
Conclusions: The incidence of SHC with this protocol was higher than previously reported. Since some participants
had not reached the average day for development of SHC, the true incidence could be greater. Further studies are
required to identify methods of reducing this incidence and thoroughly investigate factors associated with the
development of SHC.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
3. RETROSPECTIVE STUDY OF 180 CATS PRESENTING WITH ANAEMIA
RM Korman1, N Hetzel1, TG Knowles1, AH Harvey2, S Tasker1
1
University of Bristol, Langford, UK, 2International Society of Feline Medicine, Feline Advisory Bureau, Wiltshire,
UK
Background: Feline anaemia occurs frequently, yet common underlying diseases or prognostic factors remain
undetermined.
Aims: Aims were to identify presenting findings, underlying diseases and prognostic factors in anaemic cats.
Methods: Records were reviewed and classified by aetiology of anaemia development, DAMNITV category and
anaemia severity.
Results: Criteria identified 180 cats. Lethargy (118; 65.6%) and inappetence (87; 48.3%) were common. Sixty-four
(35.6%) cats had mild anaemia (packed cell volume (PCV) /haematocrit (HCT) 20-24.9%), 58 (32.2%) moderate
(PCV/HCT 14-19.9%), 23 (12.8%) severe (PCV/HCT 11-13.9%) and 35 (19.4%) very severe (PCV/HCT < 10.9%)
anaemia. Bone marrow (BM) abnormalities were more common (95; 52.8%) than haemorrhage (37; 20.6%) or
haemolysis (19; 10.6%) by aetiology. Infectious diseases were more frequent (39; 21.7%) than neoplasia (36; 20%),
metabolic (21; 11.7%), trauma (15; 8.3%), miscellaneous (14; 7.8%), inflammatory (11; 6.1%) or immune-mediated
(11; 6.1%) by DAMNITV category. Anaemia severity was significantly associated with aetiology (χ2 = 19.9, P =
0.003), with BM abnormalities having more severe anaemia, but not with DAMNITV category (χ2 = 33.852, P =
0.153). Most cats (112, 62.2%) survived to discharge; 55 (30.6%) were euthanased, and 13 (7.2%) died. Survival
was not significantly associated with anaemia severity (χ2 = 4.15, P = 0.248) but was with aetiology (χ2 = 6.070, P =
0.046) and DAMNITV category (χ2 = 19.998, P = 0.010); cats with haemolysis or immune-mediated disease were
more likely to survive. DAMNITV category (P = 0.011) and age (P = 0.082) were associated with survival on Cox
regression analysis.
Conclusions: Anaemia arose mostly from infection or neoplasia. Anaemia severity didn’t affect survival. Younger
cats or cats with immune-mediated disease or haemolysis were more likely to survive.
4. CONGENITAL METHAEMOGLOBINAEMIA DUE TO METHAEMOGLOBIN REDUCTASE
ENZYME DEFICIENCY IN A SIX MONTH OLD POMERANIAN PUPPY
C Yudelman
Advanced Vetcare, Melbourne, VIC
Congenital methaemoglobinaemia (metHb) is an extremely rare condition reported in dogs with only four published
papers comprising six cases in total. The condition results from a deficiency in the enzyme cytochrome b5 NADH
reductase (methaemoglobin reductase). Haemoglobin is normally oxidised to form metHb on a daily basis as a result
of oxidant production from homeostatic metabolic pathways. MetHb levels are maintained at less than 1% by
conversion back to haemoglobin via the enzyme metHb reductase. High levels of metHb are characterised by
cyanosis due to the inability of the iron moiety (Fe3+) in metHb to transport oxygen. Therapy is generally not
instituted due to a lack of effective and convenient chronic treatment.
A six month old entire male Pomeranian puppy presented for signs of chronic colitis. On physical examination it
was noted that the mucous membranes appeared cyanotic. The puppy was anaesthetised and placed on 100% oxygen
however the cyanosis persisted. Echocardiography and a thoracic CT scan excluded a right to left shunt, arteriovenous fistula and pulmonary parenchymal disease. Co-oximetry performed on a venous blood sample from the
puppy measured 31% metHb (normal < 1%). Blood samples from the puppy and his littermate, which was clinically
normal, were analysed for metHb reductase. The blood of the affected dog demonstrated a very low level of 4.8 IU/g
Hb compared to his littermate 12.3 IU/ gHb. The dog showed minimal response to treatment with vitamin C. This is
the first report of this condition in an Australian dog.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
5. SEROLOGICAL SURVEY OF LEPTOSPIRAL ANTIBODIES IN DOGS IN NEW ZEALAND
AL Harland1, NJ Cave1, BR Jones1, J Benschop 1, JJ Donald 2, AC Midwinter 1, RA Squires 5, JM
Collins-Emerson4
1
Massey University, Palmerston North, NZ, 2New Zealand Veterinary Pathology Ltd, Hamilton, NZ, 3James Cook
University, Townsville, QLD
Background: Antibodies to Leptospira interrogans serovars Copenhageni and Pomona and Leptospira
borgpetersenii serovars Hardjo and Ballum have been identified in New Zealand dogs. Infections of dogs with
Copenhageni have been reported in the northern North Island, however, there is evidence that antibodies to
Copenhageni occur in dogs resident further south. There are no data available on the prevalence in South Island
dogs. Dog vaccines available contain serovar Icterohaemorrhagiae, and confer protection against Copenhageni.
Aims: To investigate the prevalence of leptospiral titres in dogs from the lower half of the North Island, and the
South Island, and explore associations between seropositivity and risk factors.
Methods: Serum from 655 dogs from the lower North Island and the South Island were screened by the microscopic
agglutination test against serovars Copenhageni, Pomona, Hardjo and Ballum. Titres > 96 were considered positive.
Variables investigated included serovar, breed, island, age and sex.
Results: Titres to Copenhageni were most common; found in 10.3% of dogs. Small breeds did not have a lower
prevalence of titres to Copenhageni than other breeds. Titres to Hardjo were associated with working breeds. No
association could be made with island or sex. Dogs greater than 12 years were less likely to have positive titres than
younger dogs.
Conclusions: Working breeds were at greater risk of exposure to Hardjo. Small breed dogs did not have a lower risk
of seropositivity to Copenhageni. The risk of dogs being exposed to Leptospira spp. and requirement for vaccination
cannot be determined by geographical location or breed group.
6. INDICATIONS AND PATIENT FACTORS AFFECTING THE OUTCOME OF MECHANICAL
VENTILATION IN DOGS AND CATS: 73 CASES (2002-2012)
KA Worthing, JM Angles
The Animal Referral Hospital, Sydney, NSW
Aim: To describe the indications for dogs and cats undergoing mechanical ventilation in Sydney, Australia and to
identify factors associated with survival to discharge.
Methods: Patient signalment, underlying disease, duration of ventilation and outcome (death or survival to
discharge) were retrospectively reviewed for animals that underwent mechanical ventilation for more than 12 hours.
Group 1 (37 animals) were ventilated due to hypoventilation resulting from tick paralysis or snake bite; group 2 (13
animals), for hypoventilation due to other central nervous system diseases; and group 3 (10 animals), for inadequate
oxygenation due to pulmonary disease. Multivariable logistic regression was used to determine which factors were
significantly associated with outcome.
Results: Seventy three animals underwent mechanical ventilation, of which 43 survived to discharge (59%). Patient
age and indication for ventilation were significantly associated with outcome (P = 0.02). Older animals were
significantly less likely to survive to discharge (P = 0.03). Animals in group 2 were significantly less likely to
survive than animals in group 1 (38% vs 72% survival; P = 0.03). Animals in group 3 were also less likely to
survive, but this result was not significant (40% survived, P = 0.14). Body weight, species, sex and duration of
ventilation were not significantly associated with outcome.
Conclusions: Animals with tick paralysis and snake bite have better survival rates than animals undergoing
mechanical ventilation for other conditions.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
7. FACTORS AFFECTING HOSPITALISATION DURATION IN CASES OF CANINE TICK
PARALYSIS (IXODES HOLOCYCLUS)
EL Neagle
Veterinary Specialist Services, Brisbane, QLD
Background: Tick paralysis (TP) caused by Ixodes holocyclus affects approximately 10 000 dogs and cats along the
eastern coast of Australia each year.
Aim:The aim of this study was to investigate and evaluate variables associated with canine TP and hospitalisation
time.
Materials and Methods: A retrospective study of medical records of all patients being hospitalised for TP at two
referral hospitals over three years (2009-2012) was performed to identify possible variables that lead to prolonged
hospitalisation.
Results: A total of 121 cases were included. Aspiration pneumonia significantly increased hospitalisation time
compared to patients without aspiration pneumonia (≥ 2.2 days, P < 0.001). Hospital duration was increased in
patients requiring respiratory support (oxygen P < 0.001, temporary tracheostomy P < 0.001, or ventilation P =
0.003). Respiratory grade ‘A-D’ also influenced hospitalisation time, with grades ‘B-D’ being hospitalised for > 1.4
days longer compared to grade ‘A’ (P = 0.01). Significant differences in hospitalisation time (P = 0.01) were noted
with ambulatory grades. Patients with an ambulatory grade ≤ ‘2’ were hospitalised for 2.8 days versus 3. 8 days for
grades ≥ ‘3’. Tick anti-serum (TAS) dosage (mL/kg), weight, age, and duration of clinical signs prior to presentation
did not affect hospitalisation time.
Conclusion: Retrospective analysis of hospitalised dogs treated for TP has identified prolonged hospitalisation
times in animals having aspiration pneumonia, requiring respiratory support, and presenting paralysed. Initial
findings suggest that TAS dosage, weight, age, and duration of clinical signs before treatment did not significantly
affect hospitalisation time.
8. CLINICOPATHOLOGICAL SIGNS OF RED BELLY BLACK SNAKE ENVENOMATION OF
DOGS IN THE SYDNEY BASIN AREA
IH Goodman, JM Angles
The Animal Referral Hospital, Sydney, NSW
Aim: To characterise the frequency of presenting clinicopathological signs of dogs bitten by red bellied black
snakes (RBBSs) Pseudechis porphyriacus, presented to a specialist referral centre in Sydney, Australia.
Method: The medical records of one hundred dogs diagnosed with RBBS envenomation were retrospectively
analysed.
Results: Twenty of 100 dogs had a history of sudden collapse after being bitten followed by a brief recovery then
relapse. Seventy-eight of 100 dogs showed neurological signs such as weakness, flaccid paralysis or muscle
fasciculation. Fifty of 100 dogs showed gastrointestinal signs including vomiting and/or diarrhoea, 64/100
developed gross pigmenturia. Fifty five of 76 (72%) bite sites were located on the head, 59/76 (78%) of all bites
were swollen and oedematous. Haemolysis was noted in the serum of 30/100 of the dogs, 10 of which required a
blood transfusion. Prolonged clotting times were noted in 45/64 (70%) dogs where clotting times were measured and
the creatine kinase (CK) level was elevated in 52/74 (70%) of dogs where CK was measured. Of the dogs that had
pupil size recorded: 17/27 (63%) had dilated pupils with poorly responsive pupillary light reflexes, 3/27 (11%) had
pinpoint miotic pupils and 3/27 (11%) presented with hyphaema.
Conclusions: Rhabdomyolysis and haemolysis were major clinical features associated with gross pigmenturia.
Close monitoring of haematocrit, clotting times and CK are recommended to ascertain the severity of envenomation
and to direct appropriate therapy.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
9. COMPARISONS OF BIOCHEMICAL RESULTS BETWEEN THREE IN-HOUSE
BIOCHEMISTRY ANALYSERS AND A COMMERCIAL LABORATORY ANALYSER FOR
FELINE PLASMA
RM Baral1, JM Morton2, NK Dhand3, MB Krockenberger3, M Govendir3
1
Paddington Cat Hospital, Paddington, NSW, 2Jemora Epidemiology Consultancy, Geelong, VIC, 3The University
of Sydney, Sydney, NSW
Background: In-house plasma biochemistry analysis is commonplace in veterinary practice but there are few
independent published studies assessing the results from such instruments. Current practices for method comparison
are rarely followed in veterinary clinical pathology; there are no prior studies following these principles to assess inhouse analysers.
Objectives: To determine the clinical acceptability of plasma biochemistry results found on three commonly used
in-house analysers (Abaxis, Idexx and Heska) in comparison to a commercial laboratory analyser by assessing the
percentage of results falling within predetermined ranges.
Methods: Clinical acceptability of in-house biochemistry analysers was assessed by determining the percentage of
results (from clinical feline plasma samples) within coverage ranges (acceptable total error [TEa], calculated total
error [TEc] and expanded measurement uncertainty [EMU]). The American Society of Veterinary Clinical
Pathology (ASVCP) determined TEa ranges were used: TEc and EMU ranges were calculated from prior quality
control material analyses. Results were also assessed by percentage of results falling within ranges determined by
(1) reference intervals (RI’s) provided and, (2) standard deviation from the mean of results found.
Results: Approximately 90% of results fell within ‘acceptable total error’ ranges: this rose to 95% of results on the
Abaxis and Idexx analysers when only results outside reference intervals were assessed. There was close alignment
of results falling within ranges determined by mean and standard deviation. Discrepancies were found with
percentage of results falling within RI’s suggesting errors with provided RI’s
Conclusions: Overall, this study suggests that in-house analysers provide acceptable results; few clinical decisions
would be affected by the results found on the three in-house analysers compared to the commercial laboratory
results.
10. SURVEY OF OWNERS’ PERCEPTIONS OF RADIOIODINE TREATMENT OF FELINE
HYPERTHYROIDISM
LA Boland1, JK Murray1, CPV Bovens1 and A Hibbert2
1
University of Bristol, Bristol, UK, 2The Feline Centre, Langford Veterinary Services (LVS), Bristol, UK
Aims: To examine factors that influence treatment choices of owners of hyperthyroid cats and their opinions
following radioiodine (I131) treatment.
Methods: Surveys were sent to owners of hyperthyroid cats referred for I131 at LVS between 2002-2011 (I131; 264
cats) and owners of non-I131 treated hyperthyroid cats seen at local first opinion practices (control; 199 cats).
Results: The response rate was 67.0% (310 returned; 175 I131, 135 control). Of 135 controls, 72 (53.3%) were
unaware of I131 as an option. Considering factors that influenced owners decision to pursue I131; 139/234 (59.4%)
had no concerns regarding human health risks of I131, for 119/232 (51.3%) cost had no impact and for 115/231
(49.8%) travel distance had no impact. Of 156 respondents, 32 (20.5%) were extremely concerned about
hospitalisation length. Owner concerns regarding hospitalisation included the possibility of the cat being unhappy
130 (82.3%), owner missing the cat 102 (64.6%), inappetence 50 (31.6%), other pets missing the cat 32 (20.3%),
development of co-morbid disease 28 (17.7%) and side effects 25 (15.8%). Owners assessed their cat’s quality of
life on a scale of 1 (very poor) to 10 (excellent), as 4 [1-10] (median [range]) pre-I131 (134 respondents), and 9 [1-10]
post-I131 (131 respondents). Of 132 respondents, 121 (91.7%) were happy with their decision to choose I131.
Conclusions: Owners are often unaware of I131 as a treatment option. Costs, travel distance and human health risks
had low impact on treatment choice. Common concerns about hospitalisation for I131 were for the cat to be unhappy
and that the owner would miss the cat.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
11. DIABETIC CATS IN REMISSION HAVE MILDLY IMPAIRED GLUCOSE TOLERANCE
S Gottlieb1,2, JS Rand1, RD Marshall2
1
The University of Queensland, St Lucia, QLD,2The Cat Clinic, Brisbane, QLD
Background: With appropriate therapy, up to 90% of newly diagnosed diabetic cats are able to achieve remission. It
is unknown if these cats are truly in diabetic remission or should be classified as prediabetic.
Aim: The aim of this study was to determine glucose tolerance status of cats in remission.
Methods: Eighteen diabetic cats in remission with insulin withheld a minimum of two weeks, and fourteen matched
non-diabetic cats were enrolled in the study. Glucose concentration was measured using a meter calibrated for feline
blood (Abbott AlphaTRAK). A simplified glucose tolerance test was performed after food was withheld for 24
hours. Blood glucose was measured at time 0 and then 2 h after 1g/kg of glucose administered intravenously.
Further blood glucose measurements were made hourly until glucose was < 6.5 mmol/L.
Results: In all control cats, fasting glucose was < 6.5 mmol/L, and following glucose administration, glucose had
returned to < 6.5 mmol/L by three hours. Fasting glucose in remission cats was < 6.5 mmol/L in 14/18 cats, and >
6.5 mmol/L in 4/18 cats. Following glucose administration, glucose was < 6.5 mmol/L at three hours (n = 3/18), four
hours (n = 9/18), five hours (n = 5/18), and one cat did not reach < 6.5mmol/L by nine hours. Five (28%) cats
relapsed.
Conclusion: Fasting glucose > 6.5 or glucose > 6.5 at 4 h after glucose challenge are predictive of relapse.
Therefore the majority of cats, while no longer diabetic, have mildly impaired glucose tolerance, and a minority
have impaired fasting glucose.
12. GASTROINTESTINAL MICROBIOTA OF CATS WITH DIABETES MELLITUS
ET Bell1, JS Suchodolski2, L Fleeman3, A Cook2, JM Steiner2, CS Mansfield1
1
The University of Melbourne, Werribee, VIC,2Texas A&M University, College Station, Texas, USA,3Animal
Diabetes Australia, Boronia, VIC
Background: The mammalian gastrointestinal tract harbours 1012-1014 bacterial organisms, which have significant
influences on host metabolism and immunity. Studies in humans and laboratory rodents have reported variability in
the composition of gastrointestinal microbiota associated with metabolic diseases including obesity and type 2
diabetes mellitus. This suggests a potential role of microbiota in the pathogenesis of these diseases, as well as a
novel therapeutic strategy. No studies of the gastrointestinal microbiota of diabetic cats have been previously
published.
Aim: To compare the gastrointestinal microbiota of diabetic and non-diabetic cats, to determine if there is a
difference in microbiota composition associated with feline diabetes mellitus.
Methods: Faecal samples were collected from diabetic and non-diabetic cats. The faecal microbiota of individual
cats was determined by pyrosequencing of the 16S rRNA gene. Microbiota of diabetic and non-diabetic cats was
compared using Wilcoxon Rank Sum tests and the phylogeny-based UniFrac analysis.
Results: Faecal samples were obtained from 10 diabetic and 12 non-diabetic cats. Microbiota comprised
predominantly Firmicutes, Bacteroidetes and Actinobacteria phyla; Actinobacteria, Clostridia, Bacteroidia, Bacilli,
Gammaproteobacteria and Erysipelotrichi classes; and Coriobacteriales, Clostridiales, Bifidobacteriales,
Bacteroidales, Lactobacillales, Enterobacteriales and Erysipelotrichales orders. There was no significant difference
in the proportion of any of these phyla, classes or orders between diabetic and non-diabetic cats. Unifrac analysis
showed that the faecal microbiota of diabetic cats was not significantly different to that of non-diabetic cats.
Conclusion: The faecal microbiota composition was not different between diabetic and non-diabetic cats in this
study. Clinical trials of probiotics as an adjunctive therapy for feline diabetes do not appear to be warranted at this
time.
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Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
PERICARDIAL DISEASE OF THE DOG AND CAT
Rita Singh BSc BVMS DipVetClinStud FANZCVS Dip ACVIM (Cardiology)
Small Animal Specialist Hospital, Sydney, NSW
The heart is encased within the pericardium, a fibrous sac that is divided into fibrous and serous layers. The fibrous
pericardium is the tough outer covering attaching to the great vessels at the base of the heart. At the apex, it extends
to the diaphragm to form the phrenopericardial ligament. The serous pericardium (epicardium) directly overlies the
heart. It is composed of a thin layer of mesothelial cells overlying an elastic lamina propria. The part of the
epicardium lining the fibrous pericardium is the parietal layer, while that overlying the heart is the visceral layer.
These layers are in contact with each other and contain a small amount of fluid that lubricates the heart. The
pericardium is very distensible when initially filled but becomes less so when full. However, there is an adaptive
response to chronic increases in volume in which an increase in compliance occurs. Part of this is due to stretch but
most is a result of pericardial hypertrophy. Normal intrapericardial pressure parallels intrapleural pressure so
remains sub-atmospheric throughout most of the cardiac cycle.
The pericardium serves several important functions including fixation of the heart in the thoracic cavity,
maintenance of optimal cardiac shape, prevention of excess movement of the heart with changes in body position,
reduced friction between the beating heart and surrounding organs, a physical barrier to infection and malignancy of
adjacent structures and to prevent over dilation of the heart. Despite these many functions it is not essential and there
are no adverse effects to removal or congenital absence.
PATHOPHYSIOLOGY OF CARDIAC TAMPONADE
Cardiac tamponade is an impairment of cardiac filling due to increased intrapericardial pressure caused by fluid in
the pericardial cavity. This can be acute or chronic. The result is elevated intracardiac diastolic pressures, reduction
in ventricular filling and reduced cardiac output. Signs of right congestive heart failure predominate in chronic
disease while low output signs and shock predominate in acute tamponade. The pericardium of the dog normally
contains 2.5-15 mL/fluid. It can accommodate rapid accumulation of an additional 50-150 mL (20 kg dog) without
significant consequences. If additional fluid accumulates slowly, the pericardium stretches and hypertrophies such
that it can than accommodate several hundred mL.
When the intrapericardial pressure equilibrates with right atrial and right ventricular diastolic pressures, the
transmural distending pressure is zero and cardiac tamponade begins. Further accumulation of fluid causes
intrapericardial pressure, right atrial pressure and right ventricular diastolic pressure to rise to the level of left atrial
and ventricular diastolic pressures. Subsequently all pressures rise together. Systemic capillaries leak at pressures of
10-15 mm Hg while pulmonary capillaries do not leak till pressures are ~ 30 mm Hg. Thus, chronic tamponade
always presents as right heart failure (usually ascites) rather than left heart failure.
CAUSES OF PERICARDIAL DISEASE
In dogs, the vast majority of pericardial disorders are due to pericardial effusion from idiopathic pericarditis or
cardiac neoplasia. Most of the effusions in dogs are haemorrhagic, regardless of cause. Clinically significant
pericardial disease is uncommon in cats. The most common cause of pericardial effusion in cats is congestive heart
failure.
Congenital disorders
Peritoneopericardial diaphragmatic hernia (PPDH)
PPDH is a communication between the pericardial and peritoneal cavities, allowing abdominal contents to enter the
pericardial space. This is usually considered an abnormality of fusion of the septum transversum with the
pleuroperitoneal folds during embryological development, however trauma in the post natal period may cause
acquired disease. The liver herniates most frequently and may range from absence of clinical signs to herniation of
the small intestines, spleen and stomach with gastrointestinal signs, respiratory signs or shock if abdominal organs
strangulate. Most cases are identified incidentally when radiographs are taken for other reasons. The diagnosis is
confirmed with echocardiography. Surgical correction is usually indicated with good outcome, however, in the older
patient, without clinical signs, treatment is not necessarily required.
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Pericardial cyst
Pericardial cysts are rare developmental abnormalities in dogs and have not been reported in cats. They are thought
to be a result of incarcerated omentum or abnormal development of mesenchymal tissue during foetal development.
Pericardial cysts are usually found at the costophrenic angle and attach to the parietal pericardium with the
remainder of the cyst in the pericardial space. In dogs they can be unilocular or multilocular and usually contain
bloody/brown tinged fluid. The clinical signs are similar to that of other pericardial disease and range from no
clinical signs to fatigue, abdominal distension and dyspnoea. Cardiomegaly is seen on thoracic radiographs and
echocardiography is necessary for definitive diagnosis although CT or MRI may also be useful. Surgical removal of
the cyst, its pedicle and subtotal pericardectomy results in resolution of clinical signs.
Pericardial defects
Pericardial defects are communications between the pericardial cavity and the pleural space. A portion of the heart
may be herniated through the defect. They are rare in dogs and cats. While thought to be congenital, trauma cannot
be ruled out in the majority of cases. Most are asymptomatic and are noticed when an abnormal bulge is seen
adjacent to the cardiac silhouette on thoracic radiographs. They can easily be mistaken for a tumour and
echocardiography is required to rule this out. If the part of the heart that is herniated strangulates, severe clinical
signs may be seen. Congenital complete absence of the pericardium is rare and asymptomatic.
Acquired disease causing pericardial effusion
Pericardial effusion is, by far, the most common pericardial disorder seen in dogs and cats and is the most likely
disorder to cause cardiac tamponade and clinical signs. Almost any disease affecting the pericardium can lead to
pericardial effusion however there are only a few diseases that are commonly encountered. Just like any other body
cavity effusion the potential fluid composition can be a transudate, modified transudate, exudate, chylous or
haemorrhagic. More than 90% of dogs with pericardial effusion have haemorrhagic effusion secondary to idiopathic
pericarditis or cardiac neoplasia. Other reported causes in dogs include atrial rupture secondary to severe chronic
mitral valve disease, rodenticide toxicity, trauma, cardiac masses other than neoplasia, fungal infections, migrating
foreign material and uraemia. In cats, the most common causes of pericardial effusion are congestive heart failure,
feline infectious peritonitis and neoplasia (lymphoma).
Cardiac neoplasia
Cardiac neoplasia represents the largest group of pericardial disorders. As with any neoplastic process, these are
commonly seen in middle aged to older patients but occasionally young animals can be affected. The most common
cardiac tumours in dogs are haemangiosarcoma of the right atrium and chemodectoma or ectopic thyroid carcinoma
at the base of the heart. These are rarely seen in cats, with lymphoma being the most common cardiac tumour
reported in this species. Other less commonly encountered tumours include mesothelioma, myxoma, fibrosarcoma,
carcinomatosis, chondrosarcoma and rhabdomyosarcoma. While large tumours may be suspected with radiography,
echocardiography by an experienced operator is usually needed for a definitive diagnosis and characterisation of
origin.
Idiopathic pericarditis
Idiopathic inflammation of the pericardium is the second most common cause of pericardial effusion in dogs. While
the aetiology remains unknown, viral or immune mediated causes are suspected. This disease appears to affect
middle aged larger breed dogs. While the process is considered inflammatory, the effusion is haemorrhagic.
Histologically the blood vessels and lymphatics of the pericardium are the target of a mononuclear inflammatory
process with fibrosis. The disease may be self-limiting and resolvecompletely, or recur years later. Pericardectomy
is usually curative. Constrictive pericarditis may, uncommonly, occur as a late sequela.
Pericardial infection
Infectious agents causing an exudative effusion are rare. Reported causes include fungal infections such as
coccidioidomycoses and mycobacterial infection such as tuberculosis, neither of which are present in Australia.
Actinomyces, Nocardia and various mixed bacterial infections have been reported secondary to migrating grass awns
in certain regions. Sterile exudative effusions have been reported secondary leptospirosis and distemper in dogs and
feline infectious peritonitis in cats.
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Left atrial split
Chronic, severe mitral regurgitation due to myxomatous mitral valve degeneration is being increasingly recognised
as a cause of pericardial effusion in dogs. Elevated left atrial pressure and severe enlargement leads to endocardial
splitting which may progress on to full thickness tears. Acute tamponade resulting in signs of collapse and shock or
sudden death occurs from severe haemorrhage into the pericardial space.
Constrictive and constrictive-effusive pericarditis
Restriction of cardiac filling may occur as a result of reduced pericardial compliance involving the parietal
pericardium, the visceral pericardium or both. In some, a small amount of effusion which is not enough to cause
cardiac tamponade if the pericardium is normal, may also be present (constrictive-effusive disease). Constrictive
pericarditis occurs because of thickening and fibrosis of the parietal pericardium due to an inflammatory process.
With time, the visceral pericardium also becomes affected and may fuse to the parietal pericardium. Reported causes
in dogs include idiopathic pericarditis, septic pericarditis, neoplasia and trauma. At presentation, the cause is often
not able to be determined. Most dogs present with severe, refractory ascites. Diagnosis of constrictive pericarditis in
the absence of effusion is difficult and measurement of cardiac pressures via catheterisation is usually required.
Pericardectomy (including removal of the epicardium if affected) is required for resolution of signs.
Pericardial Diseases of Dogs and Cats
Causes of Pericardial Effusion in Cats (n = 83)5
Congenital disorders
Peritoneopericardial diaphragmatic hernia
Pericardial cyst
Pericardial defects
Congestive heart failure (45%)
Neoplasia (19%)
Feline Infectious Peritonitis (10%)
Systemic infection (8%)
Pericarditis (4%)
Disseminated intravascular coagulation (4%)
Trauma (4%)
Peritoneopericardial diaphragmatic hernia (2%)
Chronic renal failure (2%)
Hypoalbuminaemia (1%)
Myocardial necrosis (1%)
Acquired disorders
Pericardial effusion
Hydropericardium (transudate)
Congestive heart failure
Hypoalbuminaemia
Pericarditis (exudate)
Infectious (bacterial, fungal)
Sterile (idiopathic, metabolic, viral)
Haemopericardium (haemorrhage)
Neoplasia
Idiopathic
Trauma
Cardiac rupture
Coagulopathy
Pericardial mass lesions (+ effusion)
Pericardial cyst
Neoplastic
Granulomatous (fungal)
Abscess
Constrictive pericardial disease
Idiopathic
Infectious
Pericardial foreign body
Neoplastic
References: 1) Kittleson et al. Small Animal Cardiovascular Medicine 1998:5, 413. 2) Schwarz et al. J Am Vet Med Assoc 2005; 226(9): 1512. 3)
Stafford Johnson et al. J Sm An Prac 2004; 45: 546. 4) Macdonald et al. J Am Vet Med Assoc 2009; 235(12): 1456. 5) Davidson et al. J Am An
Hosp Assoc 2008; 48: 5. 6) Hall et al. J Vet Intern Med 2007; 21: 1002. 7) Thomas et al. J Am Vet Med Assoc 1984; 184(5): 546. 8) Myers et al.
Am Heart J 1999; 138(2): 219. 9) Reineke et al. Int Vet Emerg Crit Care Symp 2005. 10) Buchanan et al. J Am Vet Rad Soc 1964; 5: 28-39.
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BRONCHOSCOPY – WHAT’S IT GOOD FOR?
Mike Coleman BVSc FANZCVS
Veterinary Specialist Group, Auckland, New Zealand
INDICATIONS
Bronchoscopy is a valuable tool for investigating cats and dogs with both acute and chronic coughing, stridor,
dyspnoea, haemoptysis, abnormal respiration and exercise intolerance. Bronchoscopy is used for visualising airway
collapse, neoplastic and non-neoplastic masses of the larger bronchi and trachea and foreign bodies. Targeted
biopsies and lavage can then be done. A bronchoalveolar lavage (BAL) using a bronchoscope results in a better cell
yield than when done ‘blindly’. Therapeutically bronchoscopy can be used to remove foreign bodies and mucus
plugs. It may be used to guide the placement of tracheal stents for collapsing airway, although fluoroscopic guidance
for this is most common. A recent case series described bronchoscopic debulking of tracheal carcinomas in three
cats. As well as being able to examine the trachea and larger bronchi, examination of the nasophyarynx and larynx
can be easily performed during the same procedure.
EQUIPMENT
For cats and small dogs a small diameter (e.g. 5-6 mm) flexible scope is required. These have a ‘multi-use’ biopsy
channel –oxygen administration, passing biopsy forceps and saline for BALs. Tip motion is in one plane only e.g. up
or down. A gastroduodenoscope can be used in larger dogs. While rigid scopes can be used complete examination
and obtaining good BAL samples will be much more difficult. Other equipment includes biopsy forceps, cytology
brushes, foreign body retrieval forceps and tubing.
ANAESTHESIA
Often animals that are candidates for bronchoscopy have compromised respiratory function. A ‘risk-assessment’
needs to be made – do the benefits of a diagnosis outweigh the risk of the procedure. I do not have a set anaesthetic
protocol, each case is treated individually. Having said that some general guidelines are:
• Preoxygenation for 10-15 min before induction is important. This allows for a longer induction
period before the animal becomes hypoxic. I use a facemask in dogs, and an oxygen tent in
smaller dogs and cats.
• If laryngeal paralysis is suspected then a light plane of anaesthesia is required to examine the
larynx. Careful titration of propofol is my choice in this situation. The dog needs to be taking
reasonably deep breaths to evaluate laryngeal function accurately. The injectable respiratory
stimulant doxopram can be given to aid the diagnosis.
• Laryngeal obstruction or collapse can make intubation very difficult. It is good to be prepared
beforehand with a laryngoscope, various ET tube sizes and even equipment for an emergency
tracheotomy if required.
• Remember cats can laryngospasm very easily, application of topical lidocaine is important.
Topical lidocaine can also be sprayed into the trachea to reduce the cough reflex in both dogs and
cats.
• In smaller dogs and cats it is not possible to pass the bronchoscope through the ET tube. Repeated
extubation and intubation is required. Be as gentle as possible as inflammation and swelling of the
laryngeal region will make both intubation and recovery more difficult.
• I always intubate the animal first and use isoflurane to reach a good, relatively deep plane of
anaesthesia before starting the procedure.
• Oxygen can be administered through the biopsy channel of the bronchoscope while the animal is
not connected to the anaesthetic machine.
• Often repeated doses of injectable anaesthetic are required during the procedure.
TECHNIQUE
It is important to be both quick and thorough with the examination, particularly in small animals when the scope
may be occluding most of the airway. I have two people assisting me, one constantly monitoring the patient and the
other to assist with sample collection. Sternal or lateral recumbency can be used. Once the scope is through the
arytenoids I orientate the scope so the dorsal tracheal membrane is at the top of the screen. This means the right
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main stem bronchus will be on the left of the screen and the left main stem bronchus on the right. The bronchial tree
can be examined in a systematic manner – see Figure 1 for the anatomy.
Figure 1. Endobronchial anatomy during bronchoscopy in the dog (From Amis TC, McKiernan BC Am J Vet Res 47:2649, 1986)
A systematic approach makes returning to an abnormal area for sample collection much easier. Once you meet
resistance, stop advancing the scope, remember the view is smaller than the diameter of the scope. Make a note of
mucous membrane appearance, presence of mucus, airway collapse, masses or foreign bodies.
BRONCHOALVEOLAR LAVAGE (BAL)
The tip of the bronchoscope is ‘wedged’ in a bronchus. Warmed sterile saline is flushed through the biopsy port of
the scope, or through a sterile tube placed through the port. I use 5 mL aliquots in cats and small dogs and 10-20 mL
in larger dogs. The lavage is repeated several times. A cloudy, frothy appearing fluid is ideal. Hypoxia following
BAL can occur and ongoing oxygen support may be required.
The retrieved saline is submitted for both cytology and culture for aerobes, anaerobes and Mycoplasma. Normal cell
counts in the dog and cat are approximately 200 to 400 cells/mL. Cellular make up is typically: 65% macrophages
in the cat and 83% macrophages in the dog; neutrophils are around 5% of the cells in dogs and cats; lymphocytes
4% to 6%; mast cells 1% to 2 %; and eosinophils up to 25% in the cat and 4% in the dog. Healthy animals can have
positive cultures, so interpretation of results in conjunction with radiographic and cytologic findings is important.
BIOPSY
Biopsy is most useful when there is a focal mass and differentiating neoplastic disease from a non-neoplastic polyp
is important. I have not had a lot of success with biopsies of an inflamed looking bronchial mucosa. The samples are
very small and often have crush artefact.
References: 1) Johnson, et al. J Vet Intern Med 2007; 21(2):219. 2) Queen EV et al. J Vet Intern Med 2010; 24(4): 990. 3) Tenwolde AC et al. J
Vet Intern Med 2010; 24(5):1063. 4) Mercier E et al. Vet J 2011; 187(2):225. 5) Johnson LR et al. J Vet Intern Med 2011; 25(2): 236. 6) Heikkila
HP et al. J Vet Intern Med 2011; 25(3): 433. 7) Ettinger and Feldman (Eds) Veterinary Internal Medicine. Seventh Ed: 408, 1063. 8) Tams (Ed)
Small Animal Endoscopy Second Ed: 377 8) Amis et al. Am J Vet Res 1986: 47:2649
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COMPUTED TOMOGRAPHY USE IN RESPIRATORY MEDICINE
Marjorie Milne, BVSc FANZCVS (Radiology)
University of Melbourne Veterinary Hospital, Werribee, VIC
INTRODUCTION
Computed Tomography (CT) is a cross-sectional imaging modality based on x-ray attenuation. Images are acquired
in a transverse plane through the animal, and are displayed as slices through the patient. The images can be
reconstructed in any plane using a technique called multi-planar reformatting (MPR). Three-dimensional models can
also be rendered. Images may be optimised to show soft tissue, lung parenchyma, or bone. The increasing
availability of CT in veterinary medicine requires a greater understanding of how CT can be applied.
TECHNICAL PRINCIPLES - THE BASICS OF CT
Images are created by rotating a thinly collimated, fan-shaped x-ray beam around the patient. The amount of xradiation is detected by an array of detectors, and attenuation of the x-ray beam along a projection line is calculated.
X-ray attenuation information is collected from many angles and computer algorithms calculate x-ray attenuation
within many individual volume elements or ‘voxels’ of the patient, by solving multiple simultaneous equations
using a mathematical method called filtered back projection, or by 2-D Fourier Analysis. The attenuation
information is called the ‘raw data’. Attenuation is represented by the CT number, with units of Hounsfield Units
(HU). CT numbers range from approximately -1000 to +3000 HU, and are characteristic for tissues of varying
densities.
Substance
CT Number (HU)
Air
Fat
Water
Muscle
Grey Matter
White Matter
Bone
-1000
-100 to -80
0
+35 to +50
+35 to +40
+20 to +35
+1000 to +3000
The attenuation information is displayed as a gray-scale 2-D cross-sectional image, representing a 3-D ‘slab’ of
tissue within the patient. Each pixel of the image represents a voxel within the patient.
The brightness of the pixel represents the amount of x-ray attenuation. Bone appears white, tissues are gray, and gas
is black. Unfortunately, the human eye can only distinguish about 32 to 64 shades of gray - this falls far short of the
4000 different attenuation values that represent the range of a CT image. Computer monitors can only display 256
shades of gray. Because of these limitations, we alter the way the CT image is displayed by ‘windowing’ - adjusting
the centre point about which a range of grays is displayed. In order to best see soft tissues, we select a narrow range
of grays - a narrow ‘window’ of 350 HU, and centre this window at the average soft tissue attenuation of
approximately 40 HU. We refer to this as a window width of 350 and a window level of 40. All CT values below the
lower window limit will be displayed as black, and all of those above the upper window limit will be displayed as
white.
Tissue type
soft tissue
lung
bone
Window Width (HU)
350
1700
1500
Window Level (HU)
+40
-500
+300
Simply windowing a CT image is not enough: we need to ensure the reconstruction algorithm is appropriate to best
represent the type of anatomy of interest. Algorithms may improve the detection of the edges of structures - called
‘sharpening’ filters or bone algorithms, used to evaluate the lung parenchyma or bone structures. To evaluate soft
tissue structures we apply a smoothing filter or ‘soft tissue’ algorithm, which improves contrast resolution and
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makes image ‘noise’ much less apparent. Images should be reviewed with both the appropriate filter and
windowing. For thoracic imaging, we use a smoothing filter and soft tissue window for mediastinal structures, and a
sharpening filter and lung window for pulmonary parenchyma.
Spatial resolution is the ability to distinguish two small adjacent structures of differing attenuation. The size of the
pixel/voxel relates to the spatial resolution of the image. Voxel size is determined by slice thickness, matrix size, and
displayed field or view - all parameters that can be controlled by the operator. For example, thoracic scans often use
a matrix of 512 x 512, which is 512 pixels high and 512 pixels wide. The image acquisition field should include all
patient anatomy to avoid streaking artefact, but the reconstruction field of view should be of a size appropriate for
showing the area of interest only.
“Generation” of CT scanner
There are different types of CT machines, often referred to as different ‘generations’. This reflects the design and
motion of the x-ray tube and detector array. Third and fourth generation scanners are most common and use a thinly
collimated ‘fan’ shaped x-ray beam. Third generation scanners have detectors arranged in an arc, which rotate
opposing the x-ray tube. Fourth generation scanners have a fixed ring of detectors encircling the patient. The
detectors remain stationary and the x-ray tube rotates 360º around the patient. Image quality and scan times are
generally comparable between both ‘generations’ of scanners.
Axial vs. helical CT scanning modes
CT scanning may be performed in axial or helical modes. Early CT machines operated in axial mode only, while
newer machines can operate in either axial or helical mode.
An axial CT scan creates the image by rotating the x-ray tube in a complete circle around the patient; slices are
acquired one at a time, the table then moves a small increment, and the next slice is acquired. This produces ‘discs’
of x-ray attenuation information through the patient. This type of scan is relatively slow to acquire but results in an
image that has high quality compared to helical modes of scanning.
A helical CT scan operates by continually rotating the x-ray tube around the patient as the patient table continually
moves through the CT gantry; this produces a ‘spiral’ or ‘helix’ shape around the patient. Image acquisition is much
faster than for axial scans - often the entire thorax can be scanned during a single breath hold. The computer
reconstruction algorithms use interpolation to produce individual ‘slice’ images: so attenuation information is
calculated rather than measured and image quality may be less than for axial modes of scanning. However in most
cases, the benefits from fast acquisition time outweigh this small loss in image quality. Beam pitch is the distance
(mm) the table travels during one rotation of the x-ray tube, divided by the slice thickness/beam width (mm). A pitch
of 1 will produce contiguous spiral slices. Increasing pitch by increasing table speed will reduce the scan time, but
because slices are now no longer contiguous, more interpolation is required, resulting in decreased image resolution.
Maximum pitch of 1.5 is recommended before unacceptable degree of image quality loss.
Single vs. multi-slice CT scanners
The ‘number of slices’ of a CT scanner is determined by the number of detector arrays in the z-axis direction (along
the long axis of the patient bed). For a single slice CT scanner slice thickness is determined by the collimation width
of the x-ray beam and is limited by the length of the detector element. Scans take longer to acquire compared to
multi-slice scanners, and because single slice scanners required more rotations of the x-ray tube, tube heat-loading
can be a problem. A larger volume of anatomy can be scanned with thick slices or the pitch may be increased. Multislice CT scanners use multiple detector arrays, so can image more patient anatomy for every rotation of the x-ray
tube. Imaging times are very fast. Detector elements are much smaller than for a single-slice machine e.g.16 slice
scanners have detector elements 0.625 mm in length, allowing sub-millimetre slice thickness, and ‘isotropic
resolution’.
PATIENT PREPARATION AND POSITIONING
General anaesthesia or sedation, and controlling patient respiration
Most patients require general anaesthesia for thoracic CT so that movement is eliminated and respiration can be
controlled. Following anaesthetic induction, the patient should be immediately placed in sternal recumbency with
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positive pressure ventilation to reduce dependent atelectasis. Controlling the patient’s respiration is an important
consideration. How this is achieved will depend on the set up of your CT room, but radiation safety should be
considered at all times. Long anaesthetic tubing to the rebreathing bag may allow the anaesthetist to stand outside
the room and manually breath hold. An alternative is to hyperventilate the patient; there may be enough time for the
anaesthetist to induce apnoea and leave the room before the scan commences.
Pneumothorax or pleural effusion
Patients with pleural effusion or pneumothorax should have as much effusion or free air drained as is practical, to
allow the lung to aerate.
Positioning the patient
Patients should be positioned in sternal recumbency to reduce patient motion due to respiration, with forelimbs
drawn forward. Symmetric positioning helps - use radiolucent foam wedges and ties. Take care with the height of
the patient table, to ensure the centre of the patient will be at the centre of the laser light guide.
ACQUISITION PARAMETERS
Most CT scanners will have protocols set up for different anatomic areas, but occasionally protocols may need to be
‘tweaked’ for optimal imaging. Each machine will be slightly different in required settings, so the information below
is to be used as a guide only for scanning the respiratory system.
Scans should be performed pre-contrast, and following the administration of intravenous contrast (see below).
Most thoracic CT scans are acquired in helical mode. The scan field should extend from thoracic inlet to L2-3.
Images are first reconstructed using a soft tissue algorithm, with subsequent reconstructions using a sharpening
algorithm and windowed for lung. Increasing pitch and reducing slice thickness, and overlapping reconstruction
slices will increase the sensitivity of a study for detecting small lesions.
For general thoracic scanning, suggested slice thicknesses range from 3 to 10 mm.
High resolution computed tomography - HRCT
High resolution CT techniques were developed to specifically evaluate the pulmonary parenchyma. This method
uses an axial mode of scanning, a tightly collimated x-ray beam, high kVp and high mA technique, decreased field
of view and high sharpening filters, to produce images with very high spatial resolution1. This technique may be
particularly useful to characterise diffuse lung disease, interstitial infiltrates, or perform a metastases check. It is
useful if you have an axial CT scanner, or single slice CT scanner that can operate in axial mode. With multi-slice
CT scanners the image may be reconstructed using sub-millimetre thick slices and are very high in spatial
resolution, so HRCT may not offer additional benefits.
INTRAVENOUS CONTRAST IN COMPUTED TOMOGRAPHY
Contrast between tissues and identification of lesions is improved by the use of intravenous contrast media.
Iodinated contrast agents such as iohexol (Omnipaque) are used. Arterial and venous phases identify vascular
anatomy and vascularisation of mass lesions. The delayed parenchymal phase will delineate lesion boundaries and
reveal the pattern of enhancement. The ideal timing for arterial, venous and parenchymal phases depends on the rate
and volume of contrast injected2. Vascular phases are best imaged with rapid bolus injections: these phases may
only last seconds and can be imaged with helical CT scanners. The most effective separation of arterial and venous
phases is achieved with multi-slice CT scanners, ideally using a power injector.
For identification of parenchymal lesions a dose of 660 mgI/kg is recommended3. The rate of injection is not as
crucial as for CTPA, and hand injection through a large bore catheter is often sufficient to achieve parenchymal
opacification, with the scan acquired 1 to 3 minutes after injection.
For CT pulmonary angiography a dose of 400 mgI/kg at a rate of 5 mL/second is recommended4. Alternatively, a
lower constant rate of injection over the duration of image acquisition has been described2. Bolus tracking software
helps time acquisition with peak arterial enhancement, but peak enhancement of the right MPA is approximately 8
seconds4. Opacification of pulmonary vessels is dependent on body weight of the patient, injection volume and rate,
viscosity of contrast medium, site of injection, and cardiac output. For CTPA, evaluation of MPRs and 3D
reconstructions will aid interpretation.
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CT GUIDED BIOPSY
CT guided biopsy was first described in veterinary patients by Tidwell and Johnson in 19945. This free-hand
technique is useful for sampling lesions deep within the lung, covered by aerated pulmonary parenchyma and thus
not visible with ultrasound. CT guided biopsy is also useful to target sampling of viable, contrast enhancing tissue.
Potential complications of CT guided lung biopsy include haemorrhage and pneumothorax, and are reported to
occur in 32 - 43% of patients, however these are usually self-limiting complications and do not show clinical signs
nor require treatment. Tissue core biopsy provides a clinical diagnosis in 83 - 83% of patients6,7.
TIPS & TRICKS FOR PERFORMING THORACIC CT
1. Review images in different windows with the appropriate reconstruction filter, to adequately evaluate all
tissues.
2. Acquire both pre- and post-contrast scans, or you won’t know what you’re missing!
3. Minimise anaesthesia-induced atelectasis by placing the patient in sternal recumbency IMMEDIATELY
after induction, and using positive pressure ventilation.
4. If atelectasis is a problem or if pleural effusion is present, scan the patient in both sternal recumbency and
dorsal recumbency
5. Consider where ECG leads are positioned: they may cause significant streaking artefact
6. Use an ET tube without a metallic marker, to avoid streaking artefact
7. Place an oesophageal stethoscope so you can readily identify the oesophagus
References: 1) Johnson VS et al. J Small Anim Pract. 2004. 45:134-143 2) Makara M et al. Vet Radiol Ultrasound 2011. 52(6): 605-610 3)
Wright M & Wallack S Animalinsides.com 2007 4) Habing A et al. Vet Radiol Ultrasound 2011 52(2): 173-178 5) Tidwell AS & Johnson KL
Vet Radiol and Ultrasound 1994. 35(6):445-456. 6) Vignoli M et al. Euro J Companion Anim Pract. 2008. 17(1):23-28 7) Zekas LJ et al. Vet
Radiol Ultrasound 2005. 46(3):200-204
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CT USE IN RESPIRATORY MEDICINE
Some principles of interpretation
Cathy Beck BVSc Dip Vet Clin Stud MVS FANZCVS (Radiology)
University of Melbourne Veterinary Hospital, Werribee, VIC
Thoracic radiographs remain the standard tool for screening of the pulmonary parenchyma due to the availability,
low cost and ability to perform the study on conscious patients. However it well recognised that thoracic radiographs
have limited diagnostic accuracy1. Computed tomography (CT) is a superior imaging modality for the evaluation of
the respiratory tract. CT is a form of cross sectional imaging, thus superimposition of anatomy is eliminated. In
addition once the data has been obtained reformatting may be performed to reconstruct the images in different
planes and with differing windows and levels (see previous talk “Computed tomography use in respiratory
medicine” by Dr Marjorie Milne).
As for radiology when interpreting a CT study of the thorax knowledge of the normal findings and normal anatomy
is vital. The normal lung consists of the pulmonary vascular structures, bronchi, bronchioles, alveolar airspace,
lymphatics and supporting interstitium. As for radiology do not forget to evaluate the entire study. These notes focus
on terms used for describing alterations to the pulmonary parenchyma. Do not forget to evaluate the thoracic wall,
pleura, mediastinum, trachea and heart.
The normal bronchial wall thickness can be assessed by measuring the internal and external cross sectional areas
(CSA) of the bronchus. The internal CSA is subtracted from the external CSA to obtain the bronchial wall CSA. A
bronchial wall ratio can be obtained by dividing the bronchial wall CSA by the external bronchial CSA. This ratio
should not exceed 0.5. A bronchoarterial diameter ratio can be used to assess overall bronchial size for
bronchiectasis with a normal range of 0.8 to 2. A bronchial diameter that exceeds twice the diameter of the adjacent
pulmonary artery indicates bronchiectasis2.
The pulmonary vascular structures can be followed to the fourth-degree branch as tubular soft tissue structures.
Arteries and veins can be distinguished by their relationship to the bronchus. The pulmonary arteries are directly
adjacent to the bronchi. The veins travel in a distance from the bronchi. This distance increases towards the
periphery. The pleural lining of the lung is usually a faint hyperattenuating line. It may not be seen on transverse
images, thus the exact lung lobe borders may be difficult to define. Orthogonal reconstructions and narrower and
lower window settings may help identify the lung lobe borders3.
PRINCIPLES OF INTERPRETATION OF THE PULMONARY PARENCHYMA
When evaluating a thoracic CT for abnormalities of the pulmonary parenchyma, first define the zone or region
affected, then the pattern of change.
Johnson et al1 described a novel classification system for high-resolution CT in the dog. The lung is divided into
three specific zones, which should be evaluated individually for abnormalities:
• Zone 1- the pleural region. Defined as a 1 mm zone at the periphery of each lung lobe.
• Zone 2- the subpleural zone. Defined as a band of parenchyma parallel with and adjacent to the
pleural surface and measuring in diameter 5% of the maximum lobar width.
• Zone 3- the peribronchovascular region. Defined as the remainder of the lung parenchyma not
within Zones 1 and 2.
•
Descriptive terms for alteration to pulmonary opacification have been described for dogs1 and humans4. A recent
paper described the relationships among subgross anatomy, CT and histologic findings in dogs with disease
localised to the pulmonary acini5. This paper makes an assumption that the dog has a secondary pulmonary lobule.
In man the interlobular septae demarcate the secondary pulmonary lobular (type III lung). The dog has a type II lung
that lacks interlobular septae6 thus terminology relating the secondary pulmonary lobule such as centrilobular,
panlobular and perilobular may not be appropriate.
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DESCRIPTIVE TERMS
Some descriptive terms that may be used for describing abnormalities of the lungs as seen on CT:1,4
Abnormalities of the pulmonary parenchyma identified on CT may be divided into one of four categories1.
• Linear and reticular opacities
• Nodules and nodular opacities
• Increased lung opacity
• Decreased lung opacity
LINEAR AND RETICULAR OPACITIES
A reticular pattern is a collection of innumerable small linear opacities that, by summation produce an appearance
resembling a net. This finding usually represents interstitial lung disease4. The reticular pattern can be further
classifed1, 4:
• Interface sign
• Presence of irregular interfaces at the edges of pulmonary parenchymal structures
• Peribronchovascular interstitial thickening
• Abnormal thickening of the peribronchovascular interstitium, maybe smooth, nodular or irregular.
The peribronchovascular interstitium is a connective tissue sheath that enclosed the bronchi,
pulmonary arteries and lymphatic vessels. It extends from the hila to the lung periphery.
• Parenchymal bands
• Non tapering reticular opacity, usually several mm thick and several cm long, often peripheral,
extending to the visceral pleura. Parenchymal bands reflect pleuroparenchymal fibrosis.
• Subpleural interstitial thickening
• Abnormal thickening of the subpleural interstitium- most easily seen adjacent to fissures
• Subpleural lines
• Curvilinear lines, a few mm thick, parallel and close to the pleural surface. This may be seen in
atelectasis of the dependent lung and as such will disappear with changes in patient position. It
may also be seen in pulmonary oedema or fibrosis.
NODULES AND NODULAR OPACITIES
Nodules may be a soft tissue or ground glass attenuation. Margins may be well or poorly defined.
Small nodules:
Large nodules:
Masses:
Focal rounded opacity
Rounded opacity
Rounded opacity
< 1 cm in diameter
> 1 cm in diameter
> 3 cm in diameter
INCREASED LUNG OPACITY
Increased lung attenuation may be due to disease that produces
1) partial or complete filling of the alveolar airspaces with fluid or cells
2) Increased alveolar wall thickness due to proliferation of pneumocytes, neoplastic infiltration or expanded
inters,titium
3) increased capillary blood volume due to increased flow or reduced drainage or
4) a combination5.
Ground glass opacity
Hazy increase in pulmonary opacity without obscuration of the underlying vessels is known as a ground glass
opacity. Ground glass opacity is caused by partial or complete filling of the airspaces with products of disease,
interstitial thickening (due to fluid, cells and or fibrosis), partial or complete collapse of alveoli, increased capillary
blood volume or a combination of these. The common factor is the displacement of air. Ground glass opacity is less
opaque than consolidation in which bronchovascular margins are obscured.
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Crazy paving
Crazy paving describes images as for ground glass opacity but with the superimposition of a reticular pattern. This is
seen in diffuse lung diseases that affect both the interstitial and air space compartments.
Calcification
High attenuation deposits, usually interstitial but can involve septae, bronchioles and arteries.
Consolidation
Homogeneous increase in pulmonary attenuation with obscuration of underlying pulmonary vessels; air
bronchograms may be present
Atelectasis
Atelectasis is reduced inflation of all or part of the lung. It is seen as reduced volume accompanied by increased
attenuation of the affected part of the lung. The distribution may be lobar, segmental or subsegmental.
Note: Increased blood flow to the lungs due to inflammation, overcirculation, obstructed venous drainage or other
causes might be an under recognised cause of increased lung opacity in dogs. It also might explain why sampling of
the lung is non diagnostic in some circumstances, or why rapid changes in lung attenuation may be observed5.
DECREASED LUNG OPACITY
Honeycombing
Air-filled cystic spaces several mm to several cm in diameter. Honeycombing is usually subpleural and
characterised by well defined walls. It seen in pulmonary fibrosis and in people secondary to interstitial pneumonia.
Honeycombing represents destroyed and fibrotic lung tissue containing cystic airspaces with thick fibrous walls.
Lung cysts
Thin-walled wall (l < 2 mm) well-defined rounded and circumscribed lesion with uniform thickness wall, usually
containing air or fluid. Included bullae, pneumatoceles and lung cysts.
Emphysema
Permanent abnormal enlargement of airspaces distal to the terminal bronchiole and accompanied by destruction of
their walls. Seen as low attenuation regions without visible walls.
Bronchiectasis
Localised or diffuse irreversible bronchial dilation. Traction bronchiectasis is bronchiectasis with and irregular
contour.
Mosaic attenuation pattern
Regional attenuation differences giving rise to a patch work pattern. Regions of differing attenuation may be due to
patchy interstitial disease, obliterative small airways disease or occlusive vascular disease. Vessels in the lucent
regions are smaller than those in the dense regions
A little note on the use of the term “infiltrate”.
Infiltrate was formerly used as a term to describe a region of pulmonary opacification caused by airspace or
interstitial disease seen on radiographs and CT. Infiltrate remains controversial because it means different things to
different people. The term is not longer recommended and has been replaced by other descriptors such as opacity.
References: 1) Johnson VS et al JSAP 2004; 45,134 2) Cannon MS et al Vet Radiol Ultrasound 2009; 50: 622 3) Tobias S, Johnson V in Lungs
and Bronchi in Veterinary Computed Tomography Wiley-Blackwell 2011 4) Hansell DM et al Radiology 2008 246:697 5) Scrivani PV et al Vet
Radiol Ultrasound 2012; 53:1 6) McLaughlin RF et al Am J Anatomy1961:108; 149
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CT use in respiratory medicine – case discussions
Steven Holloway, Margorie Milne, and Cathy Beck
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THE APPROACH TO THE PATIENT IN RESPIRATORY DISTRESS
Dez Hughes BVSc MRCVS Dip ACVECC
Section of Emergency and Critical Care, University of Melbourne, Werribee, VIC
Successfully managing an animal with severe respiratory distress is one of the greatest challenges we face as
emergency clinicians. But the magnitude of the challenge means that it is also one of our most rewarding
experiences. Successful management demands that we remain acutely aware of the fragility of the dyspnoeic patient.
The stress of life-threatening disease coupled with transport and the unfamiliar surroundings of a noisy emergency
clinic should never be underestimated. Even a brief evaluation of the patient may prove fatal, especially in cats, so
the initial major body system assessment may have to be performed in stages. All dyspnoeic animals should
immediately be given supplemental oxygen using the least stressful method available. Furthermore, prior to
performing any diagnostic tests on the animal, the risks of any procedure should always be carefully weighed
against the potential benefits. To appreciate the significance of this, ask yourself the following question: In your
experience, what the most common cause of death in dyspnoeic cats? Do they die spontaneously? Or do they die
when something is being done to them? Unfortunately it is usually the latter which tells us that we all need to be
very, very careful with this patient group. Many cases will stabilise to some degree with oxygen and stress reduction
alone. So our greatest challenge with these patients is to have the confidence to do nothing other than give oxygen
for a time while the animal stabilises even though our impulses are screaming for us to do something!
INITIAL EVALUATION AND PHYSICAL EXAMINATION
As previously mentioned, the dyspnoeic animal is an extremely delicate creature, many of them teetering on the line
between life and death and they must be handled with great care. It is imperative that they are not stressed
excessively; oxygen should be supplied immediately and examination in the first instance should be limited and
directed at identification of the cause of dyspnoea.
On arrival at the practice it is likely that the animal will have suffered a car journey and be stressed at the
unfamiliarity of the situation. If possible the patient should be provided with oxygen supplementation and a very
brief examination of the respiratory tract should be carried out and then the patient left to relax (as much as
possible). Remember that muscle activity greatly increases the oxygen consumption of skeletal muscles. And when
that essential oxygen goes to the skeletal muscles instead of the heart and brain that is when you get a respiratory
and then cardiac arrest. Do not make them do anything that makes their skeletal muscles work. You can very easily
restrain them to death if you are not careful; or radiograph them to death; or blood sample them to death; or IV
catheter them to death. You guys with me on this one? If they are really, really bad then you may have to be brave
and sedate/anaesthetise/intubate them. Actively taking control of the airway (which often only requires very small
doses of sedative) is vastly superior to tubing them following a respiratory arrest!
While they are getting some oxygen have someone get a capsule history with particular reference to pre-existing
clinical signs or previous diagnoses, concurrent medication, history of trauma and the onset and progression of the
condition. Does their signalment correspond to any breed predisposition? Giant breeds and DCM, old small breed
dogs may have tracheal collapse or mitral valve disease especially if they are Cavaliers; older middle size dogs like
Labs might have laryngeal paralysis. Recently kennelled is a no brainer for possible kennel cough. Very old animal
makes neoplasia ascend your differential list. Most dogs with heart failure have premonitory signs like exercise
intolerance, coughing, orthopnoea or overt dyspnoea but most new cases of heart failure in cats do not. Asthmatic
cats almost always cough (if the owners can recognise it) but cats with heart disease do not. Many cats with heart
disease are young whereas many dogs are old. If they’ve been vomiting then aspiration pneumonia is higher on your
list. If they’ve been regurgitating it is higher still. Bangs on the head, pulls on the choke chain, other head or neck
trauma and, of course, electric cord bite may result in neurogenic pulmonary oedema. If there’s anticoagulant
rodenticide anywhere in the animal’s vicinity them pulmonary haemorrhage and haemothorax may be your cause of
dyspnoea. If they’ve licked some paraquat, you know why they are dyspnoeic.
Anyway, now for a quick segue into anatomy before we continue our patient assessment:
Remember that the respiratory tract is split into five main regions for the purposes of localisation of the disease
process: upper airways, lower airways, parenchyma, pleural space, chest wall and diaphragm. Your aim is to
establish where the problem is as quickly as possible. The methods of stabilisation, diagnostic tests required,
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underlying conditions, treatments and prognosis are all different for each area so localisation is of paramount
importance.
Back to the animal: the first part of the evaluation of the respiratory tract should be to watch and listen without a
stethoscope. The patient should be evaluated for: respiratory rate, respiratory effort, respiratory noise, respiratory
pattern, abdominal movement
Normal animals have respiratory rates of 15-30 breaths a minute and the majority of inspiration is due to
diaphragmatic contraction, so you see little chest wall movement. As the diaphragm contracts the abdominal
contents are pushed caudally and the abdominal wall moves out (passively). That means that in a normal animal the
chest and abdomen both move out on inspiration. In cats and small dogs a very slight inward movement of the
cranioventral thorax can be a normal finding.
Rate is self evident but don’t forget it. For effort, try to rate their respiratory effort as mild, moderate, severe or
imminently life threatening. The postural manifestations of dyspnoea include an extended neck, abducted elbows,
open mouth breathing, an anxious facial expression, a glazed-eyed stare, increased abdominal movement and
paradoxical abdominal movement. Paradoxical abdominal movement is when the abdomen moves in, instead or out,
on inspiration. It means that there is something preventing adequate lung inflation despite the outward movement of
the chest. There are only a few possibilities: upper respiratory tract obstruction, diaphragmatic rupture or paralysis,
decreased lung compliance and severe pleural effusions. Straightening of the neck and open mouth breathing occur
in both dogs and cats, however, some other postural manifestations of more severe dyspnoea vary between species.
Dogs prefer to stand with abducted elbows, while cats tend to sit in sternal recumbency. Constantly changing body
position in cats implies a much worse degree of dyspnoea than it does in dogs. Lateral recumbency due to dyspnoea
is a serious sign in a dog, however, it often means impending respiratory arrest in a cat. If you see a dyspnoeic cat’s
pupils dilate significantly then it is respiratory arresting NOW! Also be aware that puppies can lie to you!
Sometimes they do not show the same degree of difficulty breathing as an adult dog despite severe lung problems.
To evaluate the respiratory pattern watch the timing of inspiration and expiration (and a pause in between if they are
breathing normally). Count: in, in, in, in to yourself (or out loud) as the animal inspires. Continue until you are
confident that you have correctly identified when the animal is breathing in and when it is breathing out. Next,
compare the time spent on each phase compared to normal. If one particular phase is longer than normal then this is
the one that is causing the animal the most difficulty and we can then characterise the dyspnoea as inspiratory,
expiratory, or both.
Inspiratory dyspnoea (more difficulty breathing in) with a short expiratory phase and with stridor or stertor is
associated with a dynamic upper airway obstruction (most commonly in dogs and usually due to laryngeal
paralysis). Some cats with severe, chronic, pleural effusions may have an inspiratory dyspnoea but without stertor.
An expiratory dyspnoea (an expiratory push) may be seen in some cats with feline allergic airway disease. An
increase in both inspiratory and expiratory effort can be seem with a fixed (i.e. not dynamic) upper airway
obstruction e.g. granulomatous laryngitis in cats or laryngeal neoplasia in either species or a ball occluding the
pharynx. A fixed upper airway obstruction is rare but it is vital that you recognise this pattern because these animals
with go from alive to dead very rapidly if you mess with them without sorting out the obstruction first. Most other
causes of dyspnoea will be associated with tachypnoea and a mixed respiratory pattern. Short shallow respiration
may be seen in some animals with pleural space disease but this finding is obviously not specific for pleural space
disease. Be careful because some animals with severe pleural space disease may only show tachypnoea and shallow
respiratory movements.
PULMONARY AUSCULTATION
Auscultation is one of the true arts of veterinary medicine but it can be learnt and perfected with some diligence and
perseverance. It requires a methodical approach and a decent stethoscope. You have to make a serious effort:
lackadaisical auscultations are tantamount to useless. But with dedication, many respiratory abnormalities can be
differentiated on physical examination alone, especially in cats.
The easiest way to ensure a relatively complete auscultation is to divide the chest into a noughts and crosses board
i.e. 9 smaller fields, and then to auscult each square. This enables comparison of dorsal, middle and ventral aspects
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of the cranial, middle and caudal lung fields. For a complete auscultation each individual stethoscope field should be
examined (if the patient is sufficiently stable). Lung sounds should be compared between different areas on the same
side of the chest and to the same area on the opposite side. Lung sounds are normally slightly louder and coarser in
the cranioventral lung fields compared to the dorsocaudal fields. In some large breed dogs and in dogs or cats taking
very shallow breaths, it can be difficult to hear lung sounds in the caudodorsal chest. Normal lung sounds are always
symmetrical when the same area is compared on both sides of the chest except for the area of cardiac dullness in the
cranial portion of the left ventral chest. This means that, regardless of whether one can determine which is the louder
or quieter side, any asymmetry is abnormal. You should also cross reference at all stages with respect to what you
would expect to hear given the tidal volume of the animal. An increased tidal volume per se will cause louder lung
sounds. So an animal that is breathing faster and deeper due to stress for example should have louder lung sounds.
Take a dog that has been hit by a car. If it is just tachypnoeic from pain then it will have increased lung sounds that
are symmetrical and have the normal difference between the dorsocaudal and cranioventral lung fields. If the
dorsocaudal fields are quieter than they should be then there may be a pneumothorax. Contusions make the lung
sounds coarser than normal or cause crackles or both. If you hear coarse lung sounds, are they coarser and louder
than they should be for the dog’s respiratory rate and tidal volume?
In human medicine, adventitious lung sounds are classified as either rales (crackles) or rhonchi (wheezes) and then
subdivided on their acoustic nature and the various subgroups have diagnostic relevance. In small animals, we are
not so lucky. I personally think that the term “wheeze” is rather vague and confusing so I don’t use it. One person’s
wheeze is another person’s whistle! Occasionally, asthmatic cats and animals with other processes which narrow the
conducting airways generate true wheezes but many have only harsh lung sounds. I attempt to classify abnormal
lung sounds into two groups: Harsh lung sounds i.e. louder and coarser than normal and Crackles- which can be
either fine or coarse.
Harsh lung sounds can be caused by parenchymal or airway disease. Somewhat surprisingly, many dogs with
pneumonia or pulmonary contusions exhibit harsh lung sounds but not crackles. Pulmonary crackles: To hear
crackles, the animal must be taking sufficiently deep breaths to inflate the lung. Consequently, they are usually
loudest at the end of inspiration. Fine crackles are usually only heard at the very end of inspiration and are probably
generated by the opening of collapsed small airways. These are the ones you hear in sixteen year old Poodles with
no parenchymal disease! In contrast coarse crackles are usually associated with parenchymal disease but
occasionally can be due to airway disease. In my experience the most severe airway crackles occur with eosinophilic
bronchitis in dogs. Nevertheless, if you hear coarse crackles, it is most likely that the animal has a fluid build up of
some sort in its lungs. By auscultation you cannot tell whether that fluid is blood, exudate from pneumonia,
hydrostatic oedema from left heart failure or fluid overload, neoplasia related fluid, or neurogenic pulmonary
oedema.
The distribution of the abnormal (adventitious) lung sounds can provide supportive evidence as to the cause of the
disease. A cranioventral distribution of crackles or harshness in dogs can be appreciated in many dogs with
aspiration pneumonia. Cardiogenic oedema may sometimes be associated with sounds loudest over the heart base.
Neurogenic oedema (which is seen most commonly after head or cervical trauma, seizures, upper respiratory tract
obstruction and electric cord bite) results in either a caudodorsal or a generalised distribution of harshness/crackles.
Pleural space disease is associated with an absence of lung sounds in the affected area. The pattern of dullness
provides information as to the possible cause:
•
•
•
•
Ventral dullness- fluid or soft tissue
Dorsal dullness- pneumothorax
Gut sounds may be heard with diaphragmatic rupture
Decreased thoracic compliance may be apparent with intrathoracic masses and sometimes pleural effusion.
Pleural effusion allows the lungs to float into the dorsal aspect of the chest cavity so there is an absence of ventral
lung sounds and the dorsal sounds are often harsh. Don’t be fooled by the heart sounds in cats with pleural effusion:
they may not be muffled and occasionally can radiate over a larger area of the chest than normal. In contrast to
pleural effusion, pneumothorax results in muffling of the lung sounds in the dorsal pleural space as air accumulates
in this area. Most people find pleural effusion easier to detect by auscultation than pneumothorax because the
distribution of lung sounds (quiet ventrally and harsh dorsally) is the opposite of normal. Many dogs with
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pneumothorax after being hit by a car also have pulmonary contusions that can seriously complicate the
auscultation. The pneumothorax dampens lung sounds, whereas the pulmonary contusions make them louder and
coarser. This can sometimes result in an absolute volume close to normal. With practice, one can appreciate that the
lung sounds are both harsh and muffled; however, the severe dyspnoea in such a patient with normal volume lung
sounds should point towards concurrent pulmonary contusions and pneumothorax.
PUTTING IT ALL TOGETHER
The ability to establish a working diagnosis and treat on the basis of history and physical examination without
additional diagnostics, such as chest radiographs, can mean the difference between life and death in some dyspnoeic
animals. As we said earlier, an immense amount of information can be obtained by simply watching the animal
breathe in the oxygen cage. Look at the animal’s body condition (for a clue on chronicity) in conjunction with the
history. Also watch the degree of distress the animal is experiencing relative to the degree of chest movement. Large
chest excursions but a relatively undistressed patient speaks for chronic rather than acute disease. For example, a
young cat in good body condition with a history of coughing and a mixed dyspnoea with increased effort on
expiration is more likely to have feline asthma. Although chest radiographs would be necessary to be sure, harsh
lung sounds in all fields and the absence of a heart murmur or gallop would just about clinch the diagnosis of asthma
in most situations. An underweight, old cat with lots of chest movement, an inspiratory dyspnoea without upper
airway noise and dull ventral lung sounds has a pleural effusion until proven otherwise.
A WORD ON EMPIRICAL TREATMENT
Some purists may sneer but they will likely be purists with a lower overall survival rate! When empirical treatment
must be instituted prior to a definitive diagnosis, good clinical reasoning and maintaining perspective as to the likely
differential diagnoses is tantamount. The vast majority of cats that present for dyspnoea have a pleural effusion,
heart disease, or asthma. The clinical findings in each of these conditions are often distinct. A severely dyspnoeic cat
with a heart murmur or gallop rhythm and diffuse bilateral crackles will usually have cardiomyopathy and the
benefits of intravenous or intramuscular furosemide almost always outweigh the potential risks. As previously
mentioned, pleural effusion results in quiet ventral lung sounds and harsh dorsal sounds whereas most asthmatic cats
have lung sounds which are harsh in all fields and a concurrent history of coughing (and hopefully not an incidental
heart murmur!). Some cats may be so dyspnoeic that virtually any handling outside of 100% oxygen proves fatal. In
these cases it is not unreasonable to treat for potential pulmonary oedema and asthma with furosemide and an
injectable, fast acting corticosteroid such as dexamethasone prior to establishing a definitive diagnosis. Another
example of maintaining perspective as to the most likely diagnoses is in the puppy with dyspnoea. Many 2-6 month
old puppies have neurogenic oedema, rodenticide intoxication, or occasionally pneumonia following kennel cough
or distemper virus infection. Although there is no replacement for following the problem-oriented approach with a
complete problem list and all diagnostic differentials, the emergency clinical must always maintain perspective as to
what are the most likely probable diagnoses.
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THE DIAGNOSTIC APPROACH TO THE DOG OR CAT WITH CYANOSIS
Niek J. Beijerink DVM PhD Dipl. ECVIM-CA (Cardiology)
University Veterinary Teaching Hospital, Faculty of Veterinary Science, University of Sydney, NSW
Cyanosis is blue to red-purple discolouration of tissue; it is the visible consequence of increased amounts of
deoxygenated haemoglobin (Hb) in the blood. Cyanosis is generally observed when deoxygenated Hb levels exceed
3-5 g per 100 mL blood within capillaries. In animals with normal Hb levels, oxygen saturation must decrease to
levels below 73-78% (PaO2 of 39-44 mm Hg) to produce visible cyanosis. As a result, and although cyanosis is a
valuable and recognisable clinical sign, it is a very insensitive indicator of blood oxygen content. In addition, the
ability to observe cyanosis is dependent on red blood cell count. Polycythaemic animals, for example, have higher
absolute Hb levels, making it easier for deoxygenated Hb to exceed the threshold. Conversely, in anaemic animals,
cyanosis is rarely present; a reduction in Hb severe enough to produce cyanosis means that SaO2 must decrease to
levels incompatible with life.
Cyanosis is a clinical sign observed in many different disease processes, and is typically categorised as central or
peripheral (Table 1).
Table 1. Various causes of cyanosis
Possible cause
Peripheral cyanosis
Arterial thromboembolism
Peripheral vasoconstriction (hypothermia, shock)
Obstruction of venous drainage (constricting band, venous thrombosis)
Central cyanosis
Low inspired oxygen concentration: e.g. high-altitude, anaesthetic
complication
Hypoventilation in room air:
Non-obstructive: e.g. pleural space disease, respiratory muscle fatigue
Obstructive: e.g. laryngeal paralysis, tracheal foreign body
Venous admixture:
Low V/Q regions:
Small airway and alveolar collapse
Diffusion impairment
No V/Q: atelectasis
R-L shunting cardiovascular shunts
Non-oxygen carrying haemoglobin (methaemoglobinaemia)
Peripheral cyanosis occurs when local blood flow to tissue is significantly reduced. Peripheral cyanosis can occur in
the terminal stages of acute hypovolaemic shock, and during hypothermia. Peripheral cyanosis most commonly
occurs when blood flow to a region is obstructed, e.g. by arterial thromboembolus or a constricting band. The classic
case would be a cat with nonpigmented pads that has a thromboembolus in the terminal aorta. In most situations the
cause is obvious, and treatment is directed at the underlying cause.
Central cyanosis is caused by either severe hypoxaemia or methaemoglobinaemia. Methaemoglobin (metHb) is a
normal product of haemoglobin oxidation, which is maintained at low levels by the red blood cell enzyme metHb
reductase. When this enzyme is overwhelmed, or congenitally absent, metHb levels can rise to clinical significant
levels. As metHb is incapable of carrying oxygen, desaturation will occur. Congenital methaemoglobinaemia is rare
in dogs and cats. Methaemoglobinaemia more commonly results from toxicity, following ingestion of
acetaminophen (Panadol; paracetamol). Toxicity can also result in acute haemolytic anaemia, and hepatic damage.
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Animals with severe toxicity are presented with respiratory distress and mucous membranes that are blue or
brownish. The blood can have a characteristic chocolate brown colour. In the case of methaemoglobinaemia the
arterial oxygen tension (amount of oxygen dissolved in the plasma) would still be normal. The blood metHb
concentration will however be increased, and the blood metHb reductase concentration reduced. Treatment consists
of attempts to removal of toxin from the GI tract, N-acetylcysteine, cimetidine, hepatic protectants, and supportive
care.
Most dogs or cats with central cyanosis have severe hypoxaemia as the underlying abnormality. Hypoxaemia may
be caused by a low inspired oxygen concentration, hypoventilation, or venous admixture.
A low inspired oxygen concentration must be considered any time an animal is attached to a mechanical apparatus
such as a face mask, anaesthesia machine, or in an enclosed environment such as an oxygen cage. Hypoventilation is
defined by an elevated PaCO2, and can be obstructive or non-obstructive. In most situations the recognition of low
inspired oxygen concentration or hypoventilation is relatively straightforward (e.g. airway obstruction is often
obvious because of the marked stridor).
Venous admixture represents a reduced efficiency of lung oxygenating ability. Venous admixture is all of the ways
in which venous blood can get from the right side of the circulation to the left side of the circulation without being
properly oxygenated; this less-than-optimal oxygenated blood then admixes with optimally arterialised blood
flowing from the more normal lung units and dilutes its oxygen content. There are four causes of venous admixture:
low ventilation/perfusion regions; small airway and alveolar collapse; diffusion defects; and anatomic right-to left
shunts. Low ventilation/perfusion regions occurs secondary to airway narrowing from bronchospasm (reflex or
disease induced), fluid accumulation along the walls of the lower airways, or epithelial oedema. The effect is
hypoventilation of the involved lung units relative to their blood flow and suboptimal oxygenation of the blood
flowing through the area. This is a common mechanism of hypoxaemia in mild to moderate pulmonary disease, and
this mechanism of hypoxaemia is very responsive to oxygen therapy. A low V/Q disturbance could also be
attributed to an increase in blood flow to the area. This may be part of the explanation for hypoxaemia in pulmonary
thrombo-embolism. Small airway and alveolar collapse (a no ventilation but still-perfusion scenario) is caused by
spontaneous collapse of small airways and alveoli caused by either positional stasis or by an increase in airway
fluids, which increases surface tension and collapsing tendency. The effect is that the blood flowing through the area
will not be oxygenated at all. This is a common mechanism of hypoxaemia in moderate to severe pulmonary
disease. This mechanism is not very responsive to oxygen therapy. These small airways and alveoli must be opened
by positive pressure ventilation if they are to become functional gas exchange units. Diffusion impairment, due to a
thickened respiratory membrane, is an uncommon cause of hypoxaemia. This mechanism of hypoxaemia is partially
responsive to oxygen therapy.
Patients with cyanosis secondary to right-to-left cardiovascular shunts may have generalised cyanosis or cyanosis
confined to the caudal half of the body. Tetralogy of Fallot and Eisenmenger's complex is rare but is the most
common causes of a right-to-left shunt and generalised cyanosis. A right-to-left shunting patent ductus arteriosus
most commonly causes caudal cyanosis. However, it can also cause generalised cyanosis.
Cyanotic patients are frequently presented in a critical condition. In these cases, most diagnostics should be delayed
until the animal is more stable. A working diagnosis can usually be obtained from signalment, history, and physical
examination. Patients with right-to-left shunts may be tachypnoeic and hyperpnoeic but usually are not dyspnoeic.
Most dogs or cats with tetralogy of Fallot will have a murmur. Blood work (haematocrit, PaO2, PaCO2) and pulse
oximetry can be very helpful. Most patients with a right-to-left shunt severe enough to cause cyanosis will also have
polycythaemia, whereas many patients with respiratory disease severe enough to cause cyanosis have not had the
disease long enough to develop polycythaemia. Most patients with respiratory disease severe enough to cause
extreme hypoxaemia will have evidence of a severe abnormality on a thoracic radiograph. Some patients do not
have radiographic evidence of disease (e.g. pulmonary thromboembolism). Although pulmonary thromboembolism
can produce radiographic abnormalities, in many cases it does not. Pulmonary thromboembolism should be the
primary consideration in a patient that is tachypnoeic and dyspnoeic but without radiographic evidence of
pulmonary disease and without stridor. Echocardiography can be extremely helpful to identify cardiac disease.
Another method touted for differentiating a right-to-left shunt from other causes of venous admixture is to
administer 100% oxygen and repeat the blood gas. With a right-to-left shunt, the arterial oxygen tension should not
increase or should increase slightly. With most respiratory abnormalities, the oxygen tension should increase.
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Thoracic angio-CT and bronchoscopy with bronchoalveolar lavage can be recommended to further elucidate the
cause of challenging cases with a pulmonary cause of cyanosis.
Using case examples the above information will be implemented during the lecture.
References: 1) Allen J. Cyanosis. In: Ettinger SJ, Feldman EC, eds. Textbook of veterinary internal medicine. 7th ed. Philadelphia: WB Saunders
Co, 2010; 283-285. 2) Lee JA, Drobatz KJ. Respiratory distress and cyanosis in dogs. In: King LG, ed. Textbook of respiratory disease in dogs
and cats. 1st ed. St Louis, MO: Saunders; 2004; 1-12. 3) Kittleson MD, Kienle RD. Small Animal Cardiovascular Medicine. St Louis, MO:
Mosby Inc; 1998.
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PYOTHORAX
Trudi McAlees BSc BVSc MANZCVS FANZCVS (E&CC)
Animal Accident & Emergency, Essendon Fields & Point Cook, Melbourne, VIC
Pyothorax is the accumulation of purulent material in the pleural space. Infection may be initiated by
haematogenous or lymphatic spread, a penetrating wound, inhalation of infective material or extension from an
adjacent structure (1-3). The majority of infections are polymicrobial with mixed aerobic and anaerobic isolates (1,4).
Isolates in cats are consistent with normal oropharyngeal flora (1,5) whereas isolates in dogs tend to be both
oropharyngeal and environmental (4,5) suggesting differing aetiologies for pyothorax in these species. Diagnosis of
pyothorax is not difficult. Animals are usually dull, febrile and often dyspnoeic on presentation. Clinical
examination reveals decreased chest sounds and a diagnostic thoracocentesis can be performed as part of your initial
examination. Thoracic ultrasound or radiography will confirm a diagnosis of pleural effusion if needed. Treatments
vary greatly and at this time no one treatment has been identified that consistently results in a better outcome. This
talk will focus on the evidence available to support the recommended treatments for pyothorax in cats and dogs.
Most animals presenting with pyothorax will be clinically unstable, with many meeting SIRS criteria (2).
Stabilisation of these patients prior to invasive treatments including thoracocentesis, sedation or anaesthesia,
thoracic drain placement and surgery is mandatory. Several papers report deaths during thoracocentesis and thoracic
drain placement in the first day of hospitalisation (1,4,6). This is likely to reflect the degree of systemic illness in these
patients, but may also be the result of inadequate resuscitation prior to treatment. All animals with a septic
respiratory disease will benefit from supplemental oxygenation, decreased stress through analgesia or anxiolytic use
and improvement of perfusion via intravenous fluid therapy if haemodynamically unstable.
ANTIBIOTIC TREATMENT
All animals with pyothorax require antibiotics. Initially, a broad-spectrum antibiotic will usually be chosen while
waiting for results of aerobic and anaerobic culture and sensitivity testing, or as a minimum, cytology to guide
further treatment decisions. One study reported that the results of culture and sensitivity prompted a change to the
initially selected antibiotic therapy in 35% of cases (4).
Cats generally have a mixed growth of obligate and facultative anaerobes in their pleural fluid. The vast majority of
non-ß-lactamase producing anaerobes are susceptible to amoxicillin-clavulanate, ticarcillin-clavulanate and
metronidazole. In poly-microbial infections, facultative bacteria use oxygen making the environment more suitable
for anaerobes. For this reason, a combination of drainage and an antibiotic effective against non-ß-lactamase
anaerobes will be adequate for control of infection (1,7). Combination empirical antibiotic therapy with a penicillin
derivative and a fluoroquinolone or an aminoglycoside is therefore not necessary in cats.
In canine pyothorax, it is more common to isolate enterobacteriaceae such as E coli and/or environmental organisms
in addition to oropharyngeal organisms. In dogs, initial empirical therapy will often include penicillin derivative and
a fluoroquinolone or aminoglycoside.
The optimal duration of antibiotic treatment has not been established. Published treatment times range from 1 – 16
weeks (1,6,8). One study simply describes antibiotic treatment as prolonged, but also reports recurrence 40 days after
the start of treatment in one dog (3). Interestingly most studies, even those comparing treatment outcomes, do not
record antibiotic duration. The use of serial radiography to monitor response to treatment and duration of antibiotic
therapy was successful in a small case series of 15 dogs treated medically (8).
MEDICAL OR SURGICAL TREATMENT?
Medical treatment is divided into less-invasive treatment with one or a small number of thoracocentesis or more
invasive treatment where an indwelling thoracostomy tube is placed in one or both hemithoraces. Good outcomes
are achieved with medical treatment, with survival to discharge reported between 63 and 100% (1,2,4,6,8) in treated
animals. Placement of an indwelling thoracic drain appears to improve outcome, though in cases where a drain
cannot be placed (usually for financial reasons) one thoracocentesis and long-term antibiotic therapy can still yield
good outcomes in both cats and dogs (1,8).
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Surgical treatment is usually via a median sternotomy to expose and allow exploration of both sides of the chest. It is
indicated in cats and dogs that have evidence of mediastinal or pulmonary masses, compartmentalised fluid, when
complications requiring surgical treatment such as refractory pneumothorax or ruptured oesophagus exist and in
animals that have failed to respond to medical treatment. (2-4,6,8). The time given for response to medical treatment
varies greatly with one study reporting up to 21 days drainage and no cases requiring surgery for medical failure (6).
Dogs with granular or filamentous organisms such as Nocardia and Actinomyces may have a better outcome if
treated surgically (3) though this is not a universal recommendation as other papers report successful outcomes in
dogs with Nocardia treated medically (6,8).
Overall, success rates for medical and surgical treatments are similar. One publication that concluded that surgical
treatment is associated with a better outcome analysed disease free interval rather than survival (3). Deaths during
treatment including in the perioperative period were not taken into account. Reading this paper failed to convince
me that surgery really was the better option for treatment of pyothorax in dogs.
TO LAVAGE OR NOT?
Thoracic lavage is advocated to aid drainage of particulate or viscous fluid, break down adhesions and
compartmentalised pockets and decrease the pH of the effusion. Thoracic lavage may be performed once, at drain
insertion or at set intervals varying from every other day to four times a day. Serum electrolytes must be monitored
to ensure lavage does not result in electrolyte depletion, particularly potassium.
In the treatment of human empyema, thrombolytics such as streptokinase are sometimes added to lavage solutions to
decrease adhesion formation. These drugs are expensive and their efficacy and potential side effects have not been
evaluated in small animals. Heparin is added to lavage solution at concentrations of 10 – 100 IU/ml. Heparin
decreases adhesion formation in experimentally induced pleuritis in rabbits and peritonitis in dogs. One paper
reported shorter drainage times in dogs that had thoracic lavage compared to those that did not, and shorter drainage
times in dogs that had heparin 10 IU/ml in the lavage fluid compared to no heparin (4).
WHEN TO REMOVE THE DRAIN?
The papers reviewed reported indwelling thoracic drains for 0.5 – 21 days with a mean of 5 – 8 days (1,2,4,6). Removal
of the drain is dictated by retrieved fluid volume, radiographic and ultrasonographic monitoring for resolution of the
pleural effusion, the absence of bacteria in the pleural fluid (daily Gram stain, culture) and any mechanical
complications. Remember that up to 2 ml/kg/day fluid production may be secondary to the presence of the drain in
the thoracic cavity, so fluid production will never decrease to zero.
SUPPORTIVE CARE
When treating animals with a serious systemic illness, it is important to remember that no one treatment is going to
be the magic bullet. These patients will require supportive care tailored to the specific manifestations of their illness
for a good outcome.
Analgesia: the pleura is an exquisitely sensitive tissue. Any disease resulting in pleural inflammation is painful,
with every breath resulting in a pleural “rub”. Thoracic drains are also painful. Most animals with a pyothorax and a
thoracic drain will require mu agonist opioid analgesia with or without further adjunctive analgesia such as a
lignocaine and/or ketamine CRI. Once they are more stable, a NSAID may be a suitable addition to the analgesic
regimen.
Nutrition: animals with septic processes are cachexic. Many will present after a period of days or even weeks of
decreased caloric intake. Early, preferably enteral feeding will improve immune function and hasten healing.
IV fluid therapy: decreased oral intake coupled with a large volume pleural effusion rapidly results in
hypovolaemia. Septic animals may also have temporary ADH resistance resulting in polyuria. It is very important
that oral and intravenous fluids supplied, the “ins” are matched with obligate losses plus volumes drained from the
chest, the “outs”.
TREATMENT RECOMMENDATIONS
•
Stabilisation with fluid therapy, oxygen and analgesia on presentation. Perform a needle/catheter
pleurocentesis in large volume effusions then wait an hour or two for ventilation to improve prior
to sedation or anaesthesia for further diagnostics and treatment.
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•
•
•
•
•
•
In-house Gram stain and submission of a sample for culture and sensitivity to guide antibiotic
selection.
Empirical treatment with amoxicillin-clavulanate or ticarcillin-clavulanate alone in cats;
amoxicillin-clavulanate or ticarcillin-clavulanate and fluoroquinolone or aminoglycoside in dogs.
A thorough assessment with of the thoracic cavity with ultrasound (or CT) and, in dogs, cytology
of effusion to rule out granular or filamentous organisms such as Nocardia and Actinomyces to
guide case selection for early surgical intervention.
Lavage of the thoracic cavity with a sterile isotonic crystalloid solution (0.9% NaCl or Lactated
ringers solution) if a thick, flocculent effusion is present, or there is evidence of adhesions and
compartmentalisation of the pleural space. The addition of heparin 10 IU/ml does not appear to
cause any adverse effects and may shorted drainage time.
Long-term antibiotic use: a minimum of 6 weeks would seem to be indicated.
Monitoring resolution of the effusion with imaging: serial radiography and ultrasound or CT to
assess any areas of increased pulmonary parenchymal density. Use this information to guide
duration of thoracic drainage and antibiotic therapy
References:
1) Barrs VR, et al. J Feline Med Surg 2005; 7: 211. 2) Waddell LS, et al. J Am Vet Med Assoc 2002; 221(6):819. 3) Rooney MB, et al. J Am Vet
Med Assoc 2002; 221(1):86. 4) Boothe HW, et al. J Am Vet Med Assoc 2010; 236 (6):657. 5) Macphail C. Vet Clin Small Anim 2007; 37:975.
6) Demetriou JL et al. J Small Anim Pract 2002; 43:388. 7) Greene. Infectious diseases of the dog and cat, Sanders Elsevier. 2006; 3rd ed. 8)
Johnson MS et al. J Small Anim Pract 2007; 48:12.
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ADVANCED CARDIOPULMONARY MONITORING
Lisa Smart BVSc DipACVECC
Murdoch University, Murdoch, WA
The purpose of the cardiopulmonary system is to deliver oxygen and nutrients to the tissues and remove metabolic
waste. Without adequate blood flow at the level of the capillary beds, life cannot be sustained. In order to achieve
blood flow, the system must have a pump as well as a circulatory system that can maintain a pressure gradient down
to the level of the tissues. Cardiac output (CO) is a measure of the performance of the pump: the volume of blood
that leaves the heart over one minute.
CO = stroke volume x heart rate
In order for cardiac output to be adequate, there must be adequate filling of the heart during diastole, which is
affected by preload, space available within the ventricles and time over which diastole occurs. Preload is the wall
stress of the ventricles at the end of diastole and, therefore, is related to the volume delivered to the ventricle during
diastole. Central venous pressure (CVP) is equivalent to right atrial pressure and is used as a guide to preload, as is
pulmonary artery wedge pressure (PAWP), which is equivalent to left atrial pressure.
The other important factors that affect cardiac output are myocardial contractility and afterload. Afterload is the
ventricular wall stress at the end of systole so anything that impedes ejection during systole will increase afterload.
Examples include high mean arterial blood pressure (MAP) and aortic stenosis.
Adequate cardiac output must be paired with a sufficient pressure gradient down the arterial system in order for flow
to be adequate at the tissue level. The arteries and arterioles provide some degree of resistance, through smooth
muscle tone, in order to preserve the pressure gradient. This is called systemic vascular resistance (SVR). The
pulmonary arterial system is a lower pressure system compared to the systemic circulation but the same principle
applies. The relationship between flow, pressure and resistance is demonstrated by the following equation:
Flow (CO) = Change in Pressure (MAP-CVP) / Resistance (SVR)
Oxygen delivery is a measure of how much oxygen is being delivered to the arterial system and is calculated by the
following equation:
Oxygen delivery (DO2) = CO x Oxygen Content
Oxygen Content (CaO2) = (Hb x SaO2 x 1.34) + (PaO2 x 0.003)
Where Hb is the haemoglobin concentration, SaO2 is the arterial oxygen saturation and Pa02 is the partial pressure
(or dissolved) oxygen. The DO2 far exceeds the needs of the cells [Oxygen Consumption (VO2)], under normal
circumstances.
VO2 = CO x (CaO2 – CvO2)
In this equation, venous oxygen content is calculated in the same way as arterial oxygen content. The Oxygen
Extraction Ratio illustrates the relationship between what is delivered and what is consumed.
O2ER = VO2 / DO2
In states of decreased perfusion, the O2ER will increase as DO2 gets progressively smaller in order to still meet the
needs of VO2. This is one way the body compensates in states of decreased perfusion. There will come a point,
however, when DO2 can no longer meet the needs of VO2 and both progressively decline. This stage is called ‘flow
dependency’ and is an indicator of anaerobic metabolism. This is around the same time that lactate levels will start
to increase. A decrease in mixed venous haemoglobin saturation, which can be continuously monitored, can be a
good indicator of increasing O2ER.
All the parameters in bold above can be measured in a clinical setting. These parameters, however, do not tell us
directly about adequate tissue blood flow. Many pieces of information are needed to make this decision, starting
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with the physical examination. The goal of advanced cardiovascular monitoring is to help determine the root of the
cause when perfusion appears abnormal. The advanced techniques are useful in the critical care patient that shows
conflicting information on physical examination or when there is no response to fluid loading during shock, or when
standard monitoring of vital parameters, arterial blood pressure and urine output fail to give us the information we
need to make a treatment decision.
This talk will focus mainly on the usefulness of the pulmonary artery catheter to measure the above variables. Case
examples will also be provided. Invasive arterial blood pressure monitoring and central venous monitoring will not
be included in the talk specifically.
PULMONARY ARTERY CATHETER (SWANN-GANZ CATHETER)(PAC)
The PAC is commonly used in human critical care settings for monitoring and diagnostic purposes, however, in
recent years its utility has been called into question due to the risk of complications and time it takes to gain reliable
data1, 2. The catheter is inserted into the jugular vein and fed into the pulmonary artery through the right side of the
heart, guided by waveform analysis. It measures cardiac output using thermodilution; a given volume of cool saline
is injected into the vena cava and the temperature change is detected in the pulmonary artery, which allows the
computer to calculate CO.
Less invasive technology for measuring CO, such as pulse contour analysis and partial CO2 re-breathing, are on the
rise in human critical care medicine but these methods have yet to prove themselves in the veterinary clinical setting.
Pulse contour analysis currently relies on human based algorithms and either shows too much error3 or requires
femoral artery catheterisation4. The NICO system estimates cardiac output using the Fick method and end tidal
carbon dioxide after a period of re-breathing, therefore, requiring intubation of the patient5. The lithium dilution
method only requires arterial catheterisation and has been shown to be reliable in measuring cardiac output,
however, it becomes costly when multiple measurements are required.
Although it is promising that new non-invasive CO monitoring technologies are emerging, these techniques do not
measure pulmonary arterial pressure or PAWP, and do not provide ongoing oxygenation parameters, such as mixed
venous haemoglobin saturation. Therefore, the PAC still holds a place for patients that have questionable left sided
cardiac function and require continuous oximetry monitoring in conjunction with cardiac output monitoring. It can
be useful for guiding inotropic, vasopressor and vasodilator therapy. The utility of the PAC lies in the technique of
placement, accuracy of the measurements and correct interpretation of the data: none of which are reliably
straightforward. Suffice to say, it can be a tricky business. Despite this, the data gained from this technique can be
valuable and the thermodilution method using the PAC remains one of the gold standards for measuring CO.
Understanding the PAC and the thermodilution method is important when comparing other methods of CO
measurement.
Very little has been published on the clinical use of PACs in the veterinary setting although results from laboratory
studies on dogs (euvolaemic and hypovolaemic) have been reported5,6. Peyton et al presented an abstract at IVECCS
2007 on a case series of 40 dogs with cardiac disease, sepsis or MODS, which had a PAC placed mostly by
waveform guidance. The study reported few complications but is yet to be published.
FURTHER READING
If you are interested in learning more about pulmonary artery catheterisation, the following textbooks are useful:
Tobin MJ, ed. Principles and Practice of Intensive Care Monitoring (1997), McGraw-Hill, USA. Chapters 41-46.
An excellent reference for all theory and technical information related to the PAC. The text is now out of print but
second hand copies can still be found.
Silverstein DC and Hopper K, eds. Small Animal Critical Care Medicine, (2009), Saunders. Chapter 50.
A good introduction to the PAC, including indications, placement and complications.
References 1) Vincent JL et al. Critical Care Medicine 2008; 36(11): 3093-6. 2) Richard C et al. Current Opinion in Critical Care 2011; 17(3):
296-302. 3) Valverde A et al. JVECCS 2011; 21(4): 328-334. 4) Shih et al. JVECCS 2011; 21(4): 321-327. 5) Haskins SC et al. Comparative
Medicine 2005; 55(2): 158-63. 6) Haskins SC et al. JVECCS 2005; 15(2): 100-9. 7) Peyton JL et al. JVECCS 2007; 17(3)(S1): S7.
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THE AIRWAYS IN CRISIS
Bruce Mackay BVSc FANZCVS
Veterinary Specialist Services, Brisbane, QLD
There are many causes of patients in small animal practice presenting dyspnoeic or tachypnoeic. Upper airway
obstruction may be due to a structural or functional obstruction of the large airways (neoplasia, polyps, abscess,
foreign bodies, laryngeal collapse, elongated soft palate, everted saccules, tracheal collapse or stenosis or tracheal
stricture). Lower airway obstruction occurs due to narrowing of the bronchial lumen due to bronchospasm or the
accumulation of mucus, exudate or oedema. Pulmonary parenchymal diseases may be associated with infectious
microorganisms, inflammatory or neoplastic cells (e.g. infectious pneumonia, aspiration pneumonitis, interstitial
lung diseases, cardiogenic or non-cardiogenic pulmonary oedema, haemorrhage, neoplasia or ARDS). Pleural cavity
disease may be associated with the accumulation of fluid ( transudate, pus, haemorrhage, chyle….) or air.
Pulmonary thromboembolism refers to the obstruction of blood flow in the pulmonary vasculature by a thrombus or
embolus formed either in the systemic circulation or the right heart.
Some cases of respiratory crisis represent a “chronic” disease finally getting to the stage where the patient can no
longer manage: e.g. a West Highland white terrier with pulmonary fibrosis - the dog may have been “coping” albeit
hypoxaemic for many months before finally decompensating or developing pulmonary hypertension; or a cat with
laryngeal lymphoma that has had noisy breathing for a couple of weeks before presenting cyanotic with upper
airway obstruction; the small breed dog that has had a subclinical murmur for two years before rupturing a chorda
tendona and presenting with fulminant pulmonary oedema. Other patients present with acute onset of dyspnoea
related to another systemic disease – e.g. the patient with pulmonary thrombo-embolism (PTE) secondary to a
protein losing enteropathy or nephropathy, cancer, pancreatitis or IMHA.
Other patients present with pneumonia, immune mediated pulmonary disease or toxicities or airway foreign bodies
either with an acute onset or a “perceived” acute onset.
Evaluation of the patient presenting with severe respiratory distress must be multifactorial, considered, timely and
precise to maximise the patient’s chances of recovery. History taking is always paramount in evaluating any medical
problem. It is also possibly the component of evaluation that suffers the most in the haste to “sort out” a patient
presenting cyanotic. In our practice, we have seen airway foreign bodies ranging from dental calculi, tennis balls,
palm seeds, bones, barley awns, dog biscuits and ball bearings. Dogs with rodenticide toxicity may present
dyspnoeic with a pleural effusion or with severe bruising within the trachea causing airway obstruction.
Signalment is also important. Cats with heart disease usually do not present with a cough but with respiratory
distress. Similarly if a small breed dog presenting with marked dyspnoea does not have a murmur, it probably is not
heart disease causing the clinical picture.
Causes of non-cardiogenic pulmonary oedema are often easily diagnosed based on history taking – i.e. near
drowning, choking, seizures etc. The distribution of pulmonary oedema in these patients is usually dorso-caudal
compared to ventral in patients with pneumonia.
A careful physical examination should give the veterinarian some pretty sound “clues” as to the localisation of the
problem as well as the cause. Restrictive breathing may be seen in patients with a pleural effusion and stridor with
upper airway obstruction. Thoracic auscultation may reveal absent or quiet lung sounds supportive of pleural
disease, crackles supporting parenchymal disease or a murmur or arrhythmia, supporting cardiac disease.
Radiography is probably the single most important diagnostic tool in evaluating patients with respiratory disease. A
critical part of the examination is the decision making as to when to perform further diagnostics. In many patients,
further diagnostic tests must await appropriate stabilisation. Depending on the patient, this will frequently involve
supplemental oxygen ± tranquilisation. Chest radiography, ultrasound, a CBC or biochemistry, blood gases and
cytology by transthoracic aspirate, tracheal wash, transtracheal wash or an endoscopic bronchoalveolar lavage
(BAL) may all be indicated but should be carefully considered as these patients can decompensate if stressed.
Particular care should be taken with chest radiography where stressful positioning a patient for radiography could
cause the death of the patient. Sometimes it is easier, quicker and safer to perform a “FAST” ultrasound, which can
be performed without stressing the patient. Similarly, a general anaesthetic to perform a tracheal wash may
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decompensate an already critical patient, either causing the death of the patient or the deterioration of the patient
such that it requires mechanical ventilation. A CBC with blood smear evaluation may indicate an eosinophilia,
which is an important “marker” and leads the veterinarian down a particular diagnostic track.
Pulmonary eosinophilic diseases. There is little agreement in the veterinary literature on the classification of
eosinophilic diseases. In human medicine, eosinophilic diseases are divided into diseases of determined or
undetermined origin, e.g. eosinophilic diseases associated with heartworm or cryptococcosis would be of determined
origin, whereas immune mediated diseases would be of undetermined origin. Eosinophilic pneumonia most
commonly occurs in young adult dogs with Rottweilers and huskies overrepresented, however any breed or age may
be affected. The clinical course of the disease may be acute or chronic, with coughing being the predominant clinical
sign: however, some dogs are dyspnoeic, systemically affected and losing weight. Chest radiographs usually reveal a
diffuse broncho-interstitial lung pattern, however, an alveolar pattern may also be recognised. A peripheral
eosinophilia is present in ~ 50% of cases. Cytology collected by BAL or tracheal wash reveals an eosinophilic
infiltrate. The fluid should always be cultured and in endemic areas, heartworm testing and faecal testing for
parasites should also be carried out.
Once other infectious or neoplastic causes have been ruled out, treatment with tapering immunosuppressive doses
should be carried out. The prognosis is usually good.
Pulmonary thromboembolism (PTE) is a complication of many systemic diseases that predispose to a
hypercoagulable state. These diseases may include cancer, hyperadrenocorticism, protein losing nephropathies and
protein losing enteropathies, IMHA, heart disease, pancreatitis and sepsis. Any acute, unexplained dyspnoea with
variable abnormalities on thoracic radiographs, and in a patient with a predisposing cause of hypercoagulability,
should prompt consideration of this diagnosis.
The antemortem diagnosis of PTE is difficult. Thoracic radiographs may be normal, show an abrupt loss of
pulmonary vasculature, blunting of a pulmonary artery, variable pleural effusion or lobar pulmonary infiltrates
associated with oedema or haemorrhage. Arterial blood gases are sensitive but nonspecific – i.e. it is not surprising
that a profoundly dyspnoeic patient is hypoxaemic. Echocardiography may identify a large thromboembolism in the
proximal pulmonary artery. Pulmonary hypertension may be identified by Doppler examination if there is tricuspid
or pulmonary artery regurgitation, however pulmonary hypertension is not always present in patients with PTE.
Changes on 2D echocardiography such as a flattened septum, paradoxical septal motion and an enlarged right
ventricle and pulmonary artery branches are frequently seen with severe pulmonary hypertension. Definitive
diagnosis of PTE requires pulmonary angiography, ventilation perfusion scans or post mortem.
In one series of cases of confirmed or suspected PTE, out of 47 cases, 16 had no clinical signs referable to PTE and
were only diagnosed at postmortem examination. Twenty-two of these cases were suspected of having PTE, but the
diagnosis could not be confirmed.
Common causes of oedema (pulmonary / pleural) in small animal medicine*
Surface area &
permeability
Colloidal osmotic
pressure
Lymphatic
drainage
Mixed
Venous hydrostatic
pressure
Sepsis
ARDS
Hypoproteinaemia
Hepatic
Glomerular
Gastrointestinal
Neoplasia
Noncardiogenic
pulmonary oedema
Pericardial disease
Lymphangectasia
Malnutrition
Post op.
Radiation therapy
Infection
Pancreatitis
(Head trauma, seizures,
airway obstruction,
electrocution)
Anaphylaxis
Organ torsion
CHF
Thrombosis
Iatrogenic fluid
overload
*Modified from Ettinger: Textbook of Internal Medicine
Further Reading: Clercx C, Peeters D, Snaps F, et al: Eosinophilic bronchopneumopathy in dogs. J Vet Intern Med 2000; 14:282.
Clercx C, Peeters D: Canine eosinophilic bronchopneumoopathy. Vet Clin Small Anim 2007; 37:917. Conn AW, Miyasaka K, Katayama M, et
al: A canine study of cold water drowning in fresh versus salt water. Crit Care Med 1995; 23:2029. Corcoran BM, Cobb M, Martin MWS, et
al: Chronic pulmonary disease in West Highland white terriers. Vet Rec 1999; 144:611. d’Anjou M-A, Tidwell AS, Hecht S: Radiographic
diagnosis of lung lobe torsion. Vet Radiol Ultrasound 2005; 46:478. Goldkamp CE, Schaer M: Canine drowning. Comp Cont Educ Vet
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2008; 30:340. Kellum HB, Stepien RL: Sildenafil citrate therapy in 22 dogs with pulmonary hypertension. J Vet Intern Med 2007; 21:1258.
LaRue MJ, Murtaugh RJ: Pulmonary thromboembolism in dogs: 47 cases (1986-1987). J Am Vet Med Assoc 1990; 197:1368-1372.
Murphy KA, Brisson BA: Evaluation of lung lobe torsion in Pugs: 7 cases (1991-2004). J Am Vet Med Assoc 2006; 228:86.
Neath PJ, Brockman DJ, King LG: Lung lobe torsion in dogs: 22 cases (1981-1999). J Am Vet Med Assoc 2000; 217:1041.
Reinero CR, Cohn LA: Interstitial lung diseases. Vet Clin North Am Small Anim Pract 2007; 37:937. Serres F, Chetboul V, Gouni V, et
al: Diagnostic value of echo-Doppler and tissue Doppler imaging in dogs with pulmonary arterial hypertension. J Vet Intern Med 2007; 21:1280.
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CANINE NASAL DISEASE
Lynelle Johnson DVM MS PhD Dipl.ACVIM
School of Veterinary Medicine, University of California, Davis, USA
Chronic nasal discharge and sneezing are common clinical complaints in dogs. The most common causes of chronic
nasal discharge include neoplasia, aspergillosis, nasal foreign body, rhinitis secondary to dental disease, and
idiopathic or inflammatory rhinitis. An accurate history, physical examination, and a complete diagnostic work-up
are helpful in determining the aetiology of disease, however these disorders are challenging to control and are often
refractory to therapy.
Nasal tumours represent a small percentage of neoplasms in animals; however the majority of cases exhibit
malignant behaviour through local invasion of facial bones or the central nervous system and via extension to
regional lymph nodes. Tumour types include lymphosarcoma, adenocarcinoma, squamous cell carcinoma,
undifferentiated carcinoma, and fibrosarcoma.
Nasal aspergillosis is most commonly seen in young to middle aged dolicocephalic dogs. German shepherd dogs
and Rottweilers seem to be predisposed. In some cases, aspergillosis occurs because of previous trauma to the nose
or in association with a nasal foreign body.
Idiopathic lymphoplasmacytic rhinitis (LPR) has been referred to as immune-mediated or allergic rhinitis because
initial reports of this disorder suggested that steroid therapy was curative, however more recent evidence suggests
these dogs often fail to respond to steroid therapy. Dogs with idiopathic LPR generally are young to middle-aged,
large breed dogs. Males and females are equally affected. German shepherd dogs and shepherd mixes, Labrador
retriever mixes, and collies are affected commonly.
CLINICAL SIGNS
Dogs with nasal neoplasia develop typical clinical signs of nasal discharge (unilateral or bilateral), epistaxis,
sneezing, and pawing at the face. Neurologic signs such as seizures, behavioural changes, or cerebral dysfunction
may be seen alone or in conjunction with upper respiratory signs. The presence of these signs is highly suggestive of
tumour invasion into the central nervous system and warrants a guarded prognosis. Dogs with nasal aspergillosis
usually present with copious nasal discharge that can be unilateral or bilateral, and depigmentation of the nasal
planum may be noted by the owner. Chronic unilateral or bilateral nasal discharge is the most common clinical
complaint in dogs with LPR. Discharge is typically mucoid or mucopurulent in most dogs, but can be serous.
Haemorrhagic or blood tinged discharge are also not uncommon. Some dogs may present with true epistaxis rather
than nasal discharge.
Physical exam
Physical examination should include an assessment of nasal air flow (decreased or normal, unilateral or bilateral
change) and palpation of the palate and facial bones for pain, swelling, or evidence of bony lysis. Loss of nasal
airflow is a prominent finding in neoplastic processes. Dental examination and palpation of the gingival margins will
help rule out periodontal disease as cause for epistaxis or nasal discharge, however occult dental disease or oronasal
fistulae can be easily missed on physical exam. Neurologic exam should focus on detecting signs of cerebral
dysfunction such as weakness and visual deficits. These may signify either neoplastic invasion of the cranium or
extension of a fungal infection through the cribriform plate. In aspergillosis, nasal airflow is usually present,
depigmentation may be noted, and some dogs exhibit facial pain. In dogs with LPR, physical examination is
generally unremarkable. Any cause of nasal discharge may result in regional lymphadenopathy.
Diagnostic testing
A minimum database is required for animals with nasal discharge since further diagnostics will require general
anaesthesia. A platelet count and coagulation profile should be obtained when haemorrhagic nasal discharge is
present, and blood pressure evaluation should be performed when epistaxis is the primary complaint. Whenever
possible, regional lymph nodes should be aspirated. When suspicious of aspergillosis, fungal serology (agar gel
immunodiffusion) should be considered since a positive result is likely to indicate disease (although a negative test
does not rule it out).
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The second wave of diagnostics includes skull radiographs or CT under general anaesthesia followed by rhinoscopy
with biopsy. A full skull series would include lateral views, an open mouth or intra-oral view, and the frog-eye view
that highlights the frontal sinuses. Visualisation of nasal structures is limited on the lateral view because of
superimposition of densities in the region of the nasal cavity, but it may show loss of the air column within the
nasopharynx, suggesting the presence of a mass lesion. The most useful view is the open mouth view since it allows
characterisation of bony destruction, a mass lesion, or turbinate lysis within each side of the nasal cavity.
Radiographic changes seen in nasal neoplasia include increased soft tissue density in the nasal cavity, lysis of the
nasal turbinates, and lysis or deviation of the vomer bone, however many of the radiographic changes of neoplasia
overlap with those of chronic rhinitis.
Computed tomography provides more complete information on the extent of disease within the nasal cavity.
Tumours lead to turbinate destruction that can involve one or both nasal cavities, soft tissue masses that are either
unilateral or bilateral, and sinus disease due to mass effect or obstruction of fluid drainage. Importantly, CT allows
evaluation of the cribriform plate. Tumour-related destruction of this bony barrier to the central nervous system
warrants a guarded prognosis. CT scans are recommended in staging of nasal tumours in order to define tumour
boundaries and to plan radiation therapy.
Biopsies of masses should be obtained with direct visualisation during rhinoscopy whenever possible; however, a
blind approach may be required when blood or mucus obscures the view. The biopsy instrument should not be
extended beyond the medial canthus of the eye in order to avoid penetrating the central nervous system. Collection
of multiple biopsy samples is recommended to increase the likelihood of obtaining a diagnosis, however bleeding
can be significant. Cytologic impression smears of mass lesions or nasal cytology can be used to document
lymphoma; however other tumours usually require architectural histology.
Diagnosis of aspergillosis is made by a combination of characteristic findings on CT and rhinoscopy as well as
detection of fungal hyphae in biopsy samples of plaques from the nasal cavity. Radiographs and CT are usually
remarkable for dramatic turbinate loss in the nasal cavity, with variable sinus involvement. In some cases, only the
sinuses are involved and fungal granulomas can be visualised in this region with various imaging modalities. CT is
preferred for evaluation of dogs with Aspergillus because it provides the opportunity to evaluate the integrity of the
cribriform plate prior to local anti-fungal therapy. Rhinoscopy is an important part of both diagnosis and therapy for
aspergillosis. Visualisation of fungal plaques with biopsy of these lesions provides the diagnosis. It is important to
biopsy the plaque itself, since surrounding nasal tissue may be characterised by lymphoplasmacytic or neutrophilic
rhinitis. The fungi are observed as long, septate hyphae.
The diagnostic work-up for LPR serves to rule out aggressive causes of nasal discharge such as neoplasia or
aspergillosis that require specific treatment. Nasal radiography has low sensitivity in differentiating inflammatory
rhinitis from neoplasia or mycotic rhinitis, since soft tissue opacification, turbinate destruction, and frontal sinus
disease can be seen with all three conditions. Computed tomography provides improved definition of the extent and
severity of abnormalities of the nasal cavity, although LPR can cause aggressive CT lesions that mimic those found
with these other conditions. Turbinate destruction is found commonly, although it is generally mild or moderate in
most cases. Fluid accumulation, soft tissue opacification, gas pocketing, and frontal sinus involvement are also
common CT findings, and abnormalities can be unilateral or bilateral. Rhinoscopy typically reveals hyperaemic,
friable, inflamed epithelium, and mucus accumulation. Mild turbinate destruction is sometimes seen. Biopsies reveal
variable severity of lymphoplasmacytic infiltrates, mucosal oedema, and bony remodelling of turbinates. Culture of
nasal swabs usually results in minimal growth of bacterial flora. Molecular studies suggest an increase in fungal
DNA in the nasal cavity of dogs with LPR, as well as a partial type two hypersensitivity response however it is
unclear what role these findings might play in disease or therapy.
TREATMENT
Nasal lymphoma typically responds to radiation therapy or chemotherapy. Other tumours respond variably to
radiation therapy, with predicted disease-free intervals ranging from 6-16 months depending on the size of the
tumour and local spread. Predictable early side effects of radiation therapy include mucositis and skin irritation.
When radiation therapy is not an option, chemotherapy might be considered. Some success has been reported using
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combination therapies. Finally, piroxicam (0.3 mg/kg PO once daily) is recommended for palliative therapy of
epithelial or mesenchymal nasal neoplasia until epistaxis or neurologic signs worsen quality of life.
Nasal infection with Aspergillus is best treated with topical infusion of an anti-fungal agent (clotrimazole or
enilconazole) since oral agents have relatively poor efficacy against infection. Prior to infusion of antifungal
medication, meticulous debridement of fungal plaques must be performed. Clotrimazole has been reported to be
effective as a single, one-hour instillation, with 39 of 60 dogs cured in one study. A second treatment cured an
additional 11 of 60 dogs. Clotrimazole is available over the counter as a 1% solution in 10 mL bottles. One hour
infusion of enilconazole given for two - three treatments through endoscopically placed tubes has also been effective
in the cases reported. Enilconazole is supplied as a concentrated, commercial-grade solution that must be diluted to a
1, 2, or 5% solution prior to instillation in the nasal cavity.
If local therapy for Aspergillus is not possible because the cribriform plate is breached or neurologic signs are
evident, the best option for therapy would likely be voriconazole, a new generation azole used in human medicine.
However this medication is very expensive and has not been evaluated in veterinary medicine. Itraconazole therapy
is preferred over ketoconazole because of greater efficacy and fewer side effects. Itraconazole, administered at 5
mg/kg BID for 2-6 months may cure up to 60% of dogs with aspergillosis, although some studies have shown no
effect of itraconazole on nasal aspergillosis. Fluconazole is ineffective against Aspergillus.
Treatment of dogs with idiopathic LPR is frustrating. Systemic and topical corticosteroids do not appear to be
effective in controlling signs in most dogs, and attempts at allergen avoidance may or may not be helpful.
Modulatory anti-microbial therapy with long-term doxycycline or azithromycin and anti-inflammatory treatment
with piroxicam can be helpful in some dogs, although a guarded prognosis for cure must be given. Further
investigations into the potential aetiology of lymphoplasmacytic infiltration of the nasal cavity are required for
improved treatment recommendations.
References: JS Pomrantz et al. J Am Vet Med Assoc, 2010; 236(7): 757. JS Pomrantz, et al J Am Vet Med Assoc, 2007; 230 (9): 1319. LR
Johnson et al. J Am Vet Med Assoc, 2006; 228(5): 738. RC Windsor et al, J Vet Int Med 2006; 20: 250. RC Windsor et al, J Am Vet Med Assoc
2004; 224(12): 1952. Peeters D, et al. Vet Immunol Immunopathol. 2007; 117(1-2): 95. Peeters D, et al. J Comp Pathol 2005; 132(4): 283.
Ashbaugh EA, et al. J Am Anim Hosp Assoc. 2011; 47(5): 312. Belshaw Z, et al. Vet Comp Oncol. 2011; 9(2): 141.
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CANINE BRONCHIAL DISEASE
Lynelle Johnson DVM MS PhD Dipl.ACVIM
School of Veterinary Medicine, University of California, Davis, USA
Canine chronic bronchitis is described by the presence of a daily cough for greater than two months of the year.
Inflammatory damage to the airway results in epithelial cell hypertrophy and squamous metaplasia, goblet cell
hypertrophy, submucosal gland hyperplasia, and mucosal/submucosal inflammation, oedema, and fibrosis. These
result in an increase in the amount and viscosity of airway mucus, narrowing of the airway lumen, and chronic
irritation within the airway. Clinically, these changes are manifest by chronic cough.
Chronic bronchitis most commonly affects middle-aged to older dogs (> 8 years of age). Classically, small breed
dogs such as poodles and terriers have been considered to have a higher incidence of chronic bronchitis: however,
clinical studies and experience have shown that large breed dogs are equally affected. Cough, exercise intolerance,
and/or wheezing are variably present in individual cases. Wheezing on expiration is considered a classic finding
although many dogs have only a diffuse increase in adventitious lung sounds. Most dogs exhibit tracheal sensitivity
on palpation. With worsening disease, increased respiratory effort with an abdominal push may be noted, with or
without cyanosis. Obesity is a common finding. Dogs that have concurrent airway collapse often have a honking
cough and an end-expiratory snap can be heard over the thorax. Small breed dogs are often affected by myxomatous
valvular disease and a murmur of mitral insufficiency may be an incidental finding. Some dogs will develop a right
sided heart murmur associated with pulmonary hypertension as a consequence of long standing airway disease.
The diagnosis of chronic bronchitis requires exclusion of other causes of cough. Tracheal/airway collapse,
bordetellosis, Mycoplasma infection, heartworm disease and neoplasia should be ruled out, although these disorders
can also be found concurrently with bronchitis. A minimum database (CBC, chemistry, urinalysis) evaluates the
dog’s general health, but it does not specifically address the diagnosis of chronic bronchitis. Thoracic radiographs
are an important part of the work-up since they aid in the diagnosis of chronic bronchitis and help rule out other
causes of cough. Classically, radiographs show a bronchial pattern or increased number and thickness of airway
walls; however radiographs can also be relatively unremarkable. Even in these dogs with chronic cough but normal
radiographs, airway sample collection or bronchoscopy will show obvious airway inflammation.
Airway sampling is used to define the disease process in dogs with cough. A transoral or transtracheal wash can be
useful for obtaining bronchial cytology and ruling out infection. This is a straightforward procedure that can be
performed using items commonly found in most veterinary practices. For small dogs, a transoral wash is most
appropriate. A sterile endotracheal tube and a sterile polypropylene or red rubber catheter are needed. Do not put
lubricant on the endotracheal tube as it can interfere with cytology. The animal is anaesthetised with a short-acting
anaesthetic agent. Prior to intubation, the function of the larynx is assessed: abduction of the corniculate processes of
the arytenoids should be visualised on inspiration. The endotracheal tube is passed into the trachea, taking care to
avoid touching the oral mucosa or larynx with the end of the tube. This will help limit contamination of the tube by
oropharyngeal bacteria. The cuff of the endotracheal tube does not need to be inflated during the procedure, but an
assistant should hold the tube in place to prevent the animal from aspirating it into the lower airway.
With the endotracheal tube held in place and using sterile technique, the urinary catheter is passed through the tube
to the level of the carina (pre-measure the catheter to the fourth intercostal space). The three-way stop-cock with
syringe is attached to the catheter. An aliquot of saline (4-10 mL) is instilled into the airway followed by ~2 mL of
air to clear the catheter, and suction is used to retrieve the fluid and cells from the lower airway (hand suction or
wall suction). Removal of fluid can be enhanced by having the assistant coupage the chest or by stimulating a cough
during aspiration. Instillation and aspiration of fluid can be repeated several times until an adequate sample has been
retrieved (~1.0 mL is usually sufficient for culture and cytology). The presence of mucus or debris usually indicates
that an adequate airway sample has been obtained. Fluid is submitted for bacterial and Mycoplasma culture and
susceptibility testing (culture tube or red top tube) and for cytologic examination (EDTA or red top tube).
Bronchoscopy is also a highly useful technique in evaluating dogs with chronic cough. Changes are commonly seen
on visual inspection of the airway and include mucosal hyperaemia, increased mucus secretions, and irregular
mucosal borders. Bronchitic nodules can be seen protruding into the airway lumen in chronic cases. Cytologic
specimens in chronic bronchitis usually show neutrophilic inflammation or occasionally, eosinophilic inflammation.
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Bacterial and mycoplasmal cultures are warranted in all animals with suspected bronchitis to rule out a significant
bacterial infection.
Anti-inflammatory therapy with corticosteroids is used to break the cycle of mucosal damage and to reduce
excessive production of secretions in dogs with chronic bronchitis. Prednisone or prednisolone can be used at
relatively high doses initially (0.5 - 1.0 mg/kg BID for 5-7 days) and then tapered to daily therapy for approximately
twice as long as BID therapy was used. The dosage is further tapered as rapidly as possible while maintaining
control of cough. Some dogs require alternate day therapy for prolonged periods of time, and exacerbation of disease
is treated with an increase in prednisone to the dose that effectively controlled clinical signs. Animals that cannot be
controlled on glucocorticoids or those that suffer excessively from side effects associated with steroid use can be
treated with inhaled steroids. Oral steroids are generally continued during the first several weeks of inhaled therapy
because of a delay in the onset of efficacy for inhaled medications. Oral steroids will help reduce mucus in the
airways and allow penetration of the topical drug. As a clinical response is noted, the oral dose can be tapered
downward to the least possible dose and then discontinued.
Because animals will not inhale on command, a facemask and spacing chamber are needed for delivery of
medication from a metered dose inhaler (MDI). Aerodawg® (Trudell medical) has a round facemask suitable for use
in most dogs, and the spacing chamber has a FlowVu indicator that allows owners to monitor respirations easily.
Administration of drugs via the inhalational route is valuable because it delivers a potent amount of drug at the site
of disease. The respiratory tract has a large surface area for topical delivery, and drugs that can be administered
locally to reduce inflammation or control infection are efficacious and avoid potentially harmful systemic side
effects.
The most commonly recommended steroid for use in controlling signs of chronic bronchitis is Flovent®
(Fluticasone propionate inhalation powder), which is available in a MDI containing 120 doses to deliver 44, 110, or
220 µg/puff (US). Initial therapy with the 110 mcg/puff MDI with BID dosing appears to be used most commonly.
If steroid side effects are noted, a lower concentration can be employed. The MDI must be shaken well prior to
actuation and should be attached to the spacer before the dose is ejected. If the MDI is not used for a week or more,
the unit must be primed prior to use, meaning that 1-4 doses of drug must be ejected from the canister prior to
application to the spacing chamber.
Some dogs that fail to respond to anti-inflammatory therapy may benefit from the addition of a bronchodilator to
improve expiratory airflow or to support a reduction in the dose of steroid required. Bronchodilators commonly used
include the methylxanthines (extended release theophylline at 10 mg/kg BID) or beta agonists such as terbutaline
(0.625 - 5 mg/dog BID) and albuterol (50 µg/kg TID). Theophylline has variable metabolism among individuals,
and side effects include vomiting, diarrhoea and agitation. Often these can be avoided by starting initially at a dose
of 5 mg/kg PO BID for a few days then increasing the dose to 10 mg/kg PO BID if the dog tolerates it. Extendedrelease properties of theophylline are maintained when the drug is split in half, but the pill cannot be quartered and
remain effective.
When inflammation has been controlled but cough persists, narcotic cough suppressant may be required. This occurs
most often in dogs with concurrent airway collapse. Success can generally be obtained with hydrocodone (0.22
mg/kg PO BID-QID) or butorphanol (0.55 - 1.1 mg/kg PO PRN). I start with frequent administration and increase
the dosing interval as the dog responds.
For dogs with excessive mucus production, nebulisation can be helpful. Nebulisation can be achieved using an
ultrasonic nebuliser, vibrating mesh nebuliser, or compressed air nebuliser. These machines are designed to convert
liquid (sterile water or saline) into droplets sufficiently small (< 5 microns) to deposit in the lower airways. To
ensure that the appropriate machine is being used, the specifications for each type of nebuliser or humidifier should
be evaluated for particle size.
Nebulisers are available in a variety of conformations. Mesh nebulisers are the smallest machines but tend to be the
most expensive (~US$200). Ultrasonic nebulisers are often the most quiet and range in price from US$50-150.
Nebulisers are usually sold in a package containing a power source, nebuliser cup, extension hoses and/or mask, and
a measuring device for adding medication to the cup. To administer drugs, a facemask is essential, however for
purposes of hydration of secretions, an aquarium, sealed cage, or plastic carrier covered in plastic can be used as a
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holding chamber to trap the mist. For the latter application, it is helpful to have additional extension hoses for
connecting the nebuliser to the patient’s holding chamber. In large dogs, the nebuliser hose can be inserted into an
Elizabethan collar covered in plastic.
Finally, weight loss should be recommended for obese animals because this can result in improvement in gas
exchange and reduction in cough. This is best achieved by obtaining a careful diet history and calculating current
caloric intake, paying particular attention to the type and number of treats that the dog is provided. The owner can
start feeding 80% of the current dietary intake and monitoring for a 1-2% weight loss per week. Often it is helpful to
meal feed the majority of calories but to hold 10% of the dog’s calories for use as treats. This can improve owner
compliance. If current caloric intake cannot be determined, the resting energy requirement can be calculated using
the formula: RER = 70 (body weight in kg)0.75. Prescription diets may be required when major weight loss is needed
to ensure that adequate nutrition is provided during the weight loss program. Gentle exercise can be encouraged
(using a harness or gentle leader) but many dogs have limited capacity due to induction of cough.
Owners should be aware that the prognosis for bronchitis is guarded regarding abolition of cough. Bronchitis is a
chronic disease, and the therapeutic goal is to control clinical signs. Worsening of disease might lead to
bronchiectasis or cor pulmonale. Visualisation of bronchitic nodules or irregular epithelium during bronchoscopy
indicates the irreversibility of the process. Cough may never be abolished in these dogs, and owners must understand
the need for continuous therapy.
References: Hawkins EC, et al. J Vet Intern Med. 2010; 24(4): 825. Hawkins EC, et al. Am J Vet Res. 2007; 68(4): 435. Bexfield NH, et al. J
Small Anim Pract. 2006; 47(7): 377. McKiernan BC. Vet Clin North Am Small Anim Pract. 2000; 30(6): 1267. Singh MK, et al. J Vet Intern Med.
2012; 26(2): 312. Adamama-Moraitou KK, et al. Vet J. 2012; 191(2): 261.
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MEDIASTINAL MASSES IN CATS
Sue Bennett BSc BVMS MANZCVS FANZCVS
Murdoch University Veterinary Hospital, Perth, WA
The mediastinum is a connective tissue that runs, somewhat obliquely, through the thoracic midline and is
continuous with the connective tissue of the neck and retroperitoneum. It is bordered by pleural membrane, divides
the thorax into left and right hemithoraces and is supplied by the systemic circulation. Anatomically, it is described
as having cranial (to heart), middle (containing the heart), caudal (to heart), dorsal (to tracheal bifurcation) and
ventral (to tracheal bifurcation) parts. In cats and dogs, it rarely forms a barrier between left and right hemithoraces
as both are think pleura species. It contains non-lung thoracic structures (Thrall):
structure
Cranial vena cava
thymus
Sterna lymph nodes
Aortic arch
Brachiocephalic artery
Left subclavian artery
Mediastinal lymph nodes
Trachea
Vasosympathetic trunk L and R
Dorsal intercostal artery and vein
Internal thoracic artery and vein
Oesophagus
Thoracic duct
Phrenic nerve
Sympathetic trunks L and R
Descending aorta
Broncho-oesophageal artery and vein
Azygous vein
Heart
Tracheobronchial lymph nodes
Main pulmonary arteries and veins
Principal bronchi
Caudal vena cava
Vagus nerve L and R
Cranial
middle
caudal
Diagnostic imaging
Structures contained in the mediastinum that are routinely visible on thoracic radiographs of normal animals are the
heart, trachea, caudal vena cava, thymus (<5-6 months of age) and some of the oesophagus. A vague radio-opacity
ventral to the trachea on a lateral radiograph represents vestigial thymus, cranial vena cava, brachicephalic trunk,
mediastinal lymph nodes and the left subclavian artery within the cranial mediastinum and without sufficient
contrast to distinguish individual structures.
There are 3 deviations of the mediastinum off the midline that may be seen radiographically in the adult cat. The
cranioventral reflection is visible on the vd/dv projection as a curvilinear radio-opacity in the left cranial thorax and
respresents vestigial thymus situated where the cranial border of the right cranial lobe crosses the midline. On a
lateral projection, it abuts the heart and lacks sufficient radiographic contrast with the heart to be identified
separately. The caudoventral reflection is visible on the vd/dv projection where the accessory lobe of the right lung
crosses the midline and may be widened in fat animals. The caudal venacaval reflection (plica vena cava) is not seen
in health.
Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
The main radiographic abnormalities associated with mediastinal diseases are mediastinal shift, seen on a vd//dv
projection as altered position of the visible reflections and associated with asymmetrical change in lung volume, and
mediastinal masses that widen the medistinum and/or displace or compress normal mediastinal structures. Enlarged
sternal, cranial mediastinal and tracheobronchial lymph nodes appear as opacities in the parasternal, cranial
mediastinal and hilar locations respectively. Mediastinal fluid is rarely recognised and is confused with a mass
without horizontal beam radiography to locate a fluid line. Mediastinal air does not expand the mediastinum
significantly but it does contrast against normal mediastinal structures making them more obvious.
Non-cardiac thoracic ultrasound has been reported for 26 cats plus 49 dogs (Reichle et al). Masses were considered
mediastinal if located on the cranioventral midline. Cysts, thymoma and lymphoma were the most common diseases.
Use of CT of the feline thorax is reported (Henninger). Regarding the mediastinum, the trachea, oesophagus and
mediastinal vessels were consistently identified. Lymph nodes were not identified except when enlarged in which
case there was a soft opacity at their normal position and mass effect on local normal structures. The pericardium
was not visible. Overall, CT is considered sensitive but not specific. Calculation of hounsfield units was used to
select solid tissue for biopsy. Differential diagnoses for masses can be considered based on location rather than by
specific qualities of the mass.
Infrequently reported masses of the feline mediastinum
There is one report each of lymphangiosarcoma (Hinrichs et al), caudal mediastinal grass seed abscess (Koutinas et
al), fibrosarcoma (Carpenter), thymolipoma (Vilafranca et al) and lipoma (Nickel and Mison) in the published
literature from 1975 and with histological diagnoses. As ectopic thyroid and parathyroid masses mostly present as
endocrine problems they will not be discussed here. Thymic hyperplasia and mast cell tumour are vaguely
described.
Commonly reported masses of the feline mediastinum
Thymoma, cranial mediastinal/thymic lymphoma and cranial mediastinal cysts dominate the literature from 1975.
The thymus is the site of central selection of T cells. Migration of pre-T cells to the thymic cortex and development
to mature CD 4 or 8 T cells (and a few other subtypes) is facilitated by orderly migration towards the medulla
through multiple specialised sub-locations directed by chemokines (Murphy, Conrad et al, Annunziato et al). The
major interactions are: SDF-1 with CXCR4 attracting pre (double negative)-T cells to the thymic cortex; TECK with
CCR7 holding double positive T cells in the cortex; MDC with CCR4 attracting T cells to the outer medulla where
CD4 positive selection occurs; IP-10 and CXCR3 to the medulla where CD8 selection occurs.
The thymus is formed from the 3rd branchial/pharyngeal pouches of the embryonic pharyngeal endoderm and
migrates down the neck to the developing thorax with the adjacent 3rd and 4th aortic arches (Noden and De Lahunta).
Presenting problems of thymic disease as reported in cats.
Four papers quantify presenting problems associated with thymic masses in cats (Zitz et al, Carpenter and
Holzworth, Day, Patnaik et al, Gruffydd-Jones and Gaskell) and various case reports report uncommon problems
(Fidel et al, Sottiaux and Franck, Thilsted and Bolton, Rottenberg et al). Results have been combined in the
following table:
Lymphoma
Thymoma
problem
(n = 40)
(n=55)
dyspnoea
33
26
cough
2
8
Lethargy/anorexia/malaise/weight loss/illthrift
2
2
Vomiting
2
Regurgitation
20
2
Myasthenia gravis
3
Chest wall stiffness
6
Granulocytopenia (Fidel et al)
1
pyrexia
1
polymyositis
1
Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
Lymphoma
(n = 40)
problem
Polymyocytis plus myocarditis
Precaval syndrome (Sottiaux and Franck)
Mineral radiographic opacity due to bony metaplasia of mass
(Thilsted and Bolton)
Exfoliative dermatitis (Rottenberg et al)
Thymoma
(n=55)
2
1
1
1
5
Horner’s syndrome is described in textbooks but is not reported in the papers I sourced. Branchial cysts may cause
clinical signs or be identified incidentally. Small thymomas may be found in patients undergoing post-mortem due
to dermatopathy, myopathy or MG. Hypertrophic osteopathy has not been reported in association with mediastinal
masses in cats. Any thymic disease increases the risk of concurrent (even future) immune mediated MG,
polymyositis and/or dermatopathy. The mechanism of immunoreactivity remains unclear. The associated
dermatopathy presents as pruritus and alopecic crusting lesions mostly of the head and ears but generalised.
Histopathological assessment reveals an interface dermatitis that is mostly cell-poor with cell-rich pockets where
CD3 lymphocytes predominate (Rottenburg et al).
Cranial mediastinal cysts are mostly diagnosed incidentally in geriatric cats presented due to other lesions. They
are formed during embryogenesis from various vestigial structures that develop from the pharyngeal/branchial
pouch endoderm. In addition to 8 single case reports, a series of 9 is reported (Zekas et al). Of these, only one had
clinical signs relating to the cyst (dyspnoea and precaval syndrome that resolved with cyst drainage). The diagnostic
criteria are not clarified in most of the case reports and many may actually be reports of cystic thymoma.
Diagnosis is achieved by identification of cranial mediastinal cyst(s) and aspiration of fluid. The main differential
diagnoses for cranial mediastinal cysts are cystic thymoma, pleural cyst (low protein, fluid), thymic branchial cyst
(mucinous fluid), parathyroid cyst (high protein fluid) and thryoglossal cyst (colloid). The fluid from all is clear,
colourless and poorly cellular. Should histopathology be deemed appropriate in order to differentiate cysts from
cystic thymoma, an epithelial lining, which may be ciliated, columnar, cuboidal, squamous or pseudostratified, is
seen. Unlike thymic branchial cysts of dogs which may become inflamed and clinically significant, feline
mediastinal cysts, including thymic branchial cysts, tend to remain incidental subclinical problems and no therapy is
required.
Mediastinal/thymic lymphomas may occur in many feline cohorts however young adult cats, Siamese cats and
FeLV positive cats seem to be relatively predisposed. FeLV was present in about 50% of young cat thymic
lymphomas from Bristol 1983 – 1996 (Day). In Eastern Australia, where FeLV infection is rare, young and Siamese
cats still comprise most cases (Court et al). Approximately 20% of all lymphomas were thymic in Sydney 1984approximately 1997 (Gabor et al). In comparison, 48% of all lymphomas were thymic in a British study published in
1979 (Gruffydd-Jones and Gaskell) and 25% in USA in 1972. The geographical and temporal differences may
reflect relative prevalence of FeLV in these populations. There is one study of thymic lymphoma in 19 cats where
Siamese cats are not over-represented (Day).
The mechanism of induction of thymic lymphoma by FeLV is insertional mutagenesis, specifically, at the flit-1 site
of LTR U3, leading to an increase the expression of ACVRL1 which codes for a protein in the TGF-β family of
cytokines (Fugino et al).
Thymomas tend to occur in middle aged and (mostly) geriatric cats. They tend to progress slowly, expanding from
the cranial mediastinum to the dorsal and caudal mediastinum and, sometimes, into the cervical region. There is one
report of primary cervical thymoma arising from ectopic thymus in a cat (Lara-Garcia et al). Secondary pleural
effusion may occur. The majority are encapsulated but some are invasive. Distant metastasis occurs very rarely.
There are 3 histological types: lymphocyte predominant; epithelial predominant; mixed (Jacobs et al). Mostly, the
epithelial cells are spindle shaped and pancytokeratin positive. Mostly lymphocytes are small but about 1/3 have
large lymphocytes within them. The tumours are heterogenous with regions of haemorrhage, necrosis, lymphocytes
and epithelia (Jacobs et al). Cystic thymoma is reported in a series of 14 cats (Patnaik). These were not true cysts as
they lacked an epithelial lining and were probably caused by distension and fusion of perivascular spaces as
proposed in the similar human variant of cystic thymoma. Thymoma with multilocular cysts is reported in humans
Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
and these fit the criteria for true cysts. It is not reported in cats. Some reports of thymic branchial cysts may actually
represent either of these variants.
Thymoma holds a good prognosis, responding well to surgical excision alone with an 89% 1 year survival and 48%
3 year survival reported (Zitz et al). This is excellent considering the corhort. Recurrences were slow and none of the
four histologically invasive tumours recurred. Prognosis is better for lymphocyte predominant tumours.
Radiation therapy has been reported in 3 cats (Kaser-Hotz et al). These tumours were very radiation sensitive,
responding well to a palliative style protocol. Tumours reduced slowly as expected given the relatively low mitotic
rate of thymomas.
Thymomas are variably chemosensitive and this feature may be exploited to improve anaesthetic risk in preparation
for surgical excision. Prednisolone is generally effective.
Differentiation of thymoma and cranial medistinal lymphoma in cats:
parameter
signalment
Clinical progression
FNA
histopathology
u/s
CT
IHC
PARR
thymoma
older
slow
misleading
Inconclusive alone in the case of
lymphocyte predominant type
Solid or cystic
Narrows down to ddx for location
only
Labels with anti-pancytokeritin
(AE1/AE3). Lymphocytes are CD3
(mostly) and CD79a labelled.
Lymphocyte population polyclonal
Cranial mediastinal lymphoma
Young, +/- Siamese +/- FeLV
rapid
Neoplastic lymphoblasts
Mostly diagnostic
solid
Narrows down to ddx for location
only
Neoplastic lymphocytes label with
CD3
Lymphocyte population
monoclonal
Signalment is a cheap, safe, readily available and reliable parameter to use in the differentiation between these
diseases. The only parameter of comparable or better utility is PARR.
References
Thrall D. 2007. Chapter 31: The Mediastinum. In Thrall Textbook of Veterinary Diagnostic Radiology 5th ed. Editor Wilkel A. pp
541-554.
Reichle J et al. Veterinary Radiology and Ultrasound. 41:2. 2000. 154-162.
Henninger W. Journal of Small Animal Practice. 44. 2003. 56-64.
Hinrichs U et al. Veterinary Pathology. 36. 1999. 164-167.
Koutinas C et al. Journal of Feline Medicine and Surgery. 5. 2003. 43-46.
Carpenter et al. 1987. Chapter 11: Tumours and Tumour-like Lesions. In Holsworth Diseases of the Cat. pp406-596.
Vilafranca M. Journal of Feline Medicine and Surgery. 7. 2005. 125-127.
Nickel J and Mison M. Journal of the American Animal Hospital Association. 47. 2011. e127-e130.
Murphy K. 2012. Chapter 8: The development and survival of lymphocytes. In Janeway’s Immunobiology 8th ed. pp275-333.
Conrad C et al. European Journal of Immunology. 30. 2000. 3371-3379.
Annunziato F et al. Trends in Imunology. 22 (5). 2001. 227-281.
Noden and De Lahunta. 1985. Chapter 14: Pharynx and pharyngeal pouches. In The embryology of domestic animals. pp270-278.
Zitz J et al. Journal of the American Veterinary Medical Association. 232. 2008. 1186-1192.
Carpenter J and Holzworth J. Journal of the American Veterinary Medical Association. 181(3). 1982. 249-251.
Day M. Journal of Small Animal Practice. 38. 1997. 393-403.
Patnaik A et al. Journal of Feline Medicine and Surgery. 5. 2003. 27-35.
Gruffydd-Jones T and Gaskell C. The Veterinary Record. 104. 1979. 304-307.
Fidel J et al. Journal of the American Animal Hospital Association. 44. 2008. 210-217.
Sottiaux J and Franck M. Journal of Small Animal Practice. 39. 1998. 352-355.
Thilsted J and Bolton R. Veterinary Pathology. 22. 1985. 424-425.
Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
Rottenburg S et al. Veterinary Pathology. 41. 2004. 429-433.
Zekas L et al. Veterinary Radiology and Ultrasound. 43(5). 2002. 413-418.
Court et al. Australian Veterinary Journal. 75(6). 1997. 424-427.
Gabor L et al. Australian Veterinary Journal. 77(7). 1999. 436-441.
Gabor L et al. Australian Veterinary Journal. 76(11). 1998. 725-732.
Jacobs R et al. 2000. Thymoma. In: Tumours of Domestic Animals 4th ed. Editor: Menten D. pp 165-166.
Fugino Y et al. Virology. 386. 2009. 16-22.
Lara-Garcia A et al. Veterinary Clinical Pathology. 37(4). 2008. 397-402.
Kaser-Hotz B et al. Journal of the American Animal Hospital Association. 37. 2001. 483-488.
Small Animal Medicine and Feline Chapters
2012 ANZCVS Science Week
IDENTIFICATION OF CATS WITH CARDIAC DISEASE I: SOUND ADVICE
BEFORE THE ECHO
Richard Woolley BVetMed DipECVIM-CA (Cardiology) MRCVS
Pet Emergency & Specialist Centre, Melbourne, VIC
In this presentation I will predominantly discuss the identification of cardiac disease in cats with acquired
cardiomyopathies prior to echocardiographic examination.
CLINICAL SIGNS
Feline cardiomyopathies are a highly heterogeneous group of diseases and therefore, the associated clinical signs are
highly variable. Since many cats with even severe cardiac changes are asymptomatic, apparent unexpected sudden
death may occur. In others, stress may induce dyspnoea, with acute pulmonary oedema or pleural effusion being
seen. Other reported clinical signs include tachypnoea, anorexia, vomiting, syncope or paresis, which is typically
posterior paresis due to an aortic thromboembolism of the terminal aorta, lethargy or cachexia and occasionally
ascites. Cough is an inconsistent sign.
Sleeping respiratory rate may be useful in the early identification of congestive heart failure. Currently a sleeping
respiratory rate of consistently over 30 breaths/min is thought to be suggestive of congestive heart failure and
thoracic radiographs are recommended to confirm.
PHYSICAL EXAMINATION
Physical examination may reveal a normal or hyperdynamic cardiac apical pulse. Cardiac auscultation may reveal a
murmur, predominantly a systolic murmur, or an audible S3 or S4 heart sound, known as a ‘gallop’ sound.
When present, murmurs are usually the result of dynamic outflow tract obstruction or atrioventricular valve
regurgitation. In some instances (particularly in cardiomyopathies in which hypertrophy is a feature) these may
occur concurrently; turbulence within the left ventricular outflow tract causing systolic displacement of the septal
leaflet of the mitral valve and with this mitral valve insufficiency. This phenomenon is known as systolic anterior
motion or SAM. Specific mechanics of this displacement are not completely understood, but appear to involve
situations where the papillary muscles are able to encroach on the left ventricular outflow tract (LVOT) in systole,
such as when they are enlarged with hypertrophic cardiomyopathy (HCM) when the left ventricle (LV) is
hyperdynamic and with hypovolaemia. The papillary muscles then drag a portion of the septal leaflet of the mitral
valve into the blood flow stream in the LVOT, which catches the leaflet and slams it up against the interventricular
septum. Other factors may also contribute to SAM at times. Dynamic SAS and SAM are most commonly associated
with HCM (where it is sometimes referred to as hypertrophic obstructive cardiomyopathy or HOCM), although it
can be rarely observed in cats without evidence of HCM. Additionally, dynamic LV obstruction may be present at
all heart rates and dynamic states in cats with cardiac disease (HCM) resulting in a constant (rather than dynamic)
heart murmur. A fixed LV obstruction usually due to hypertrophy of the base of the intraventricular may also be
responsible for a murmur, usually in older cats.
Murmurs in cats may also be due to non-pathologic causes including dynamic obstruction of the right ventricular
outflow tract obstruction (DRVOTO). It appears to be unique to this species. The exact cause of DRVOTO is not
known but a retrospective study of this condition suggested that it was associated with volume depletion (e.g.
secondary to renal failure) or hyperdynamic states (e.g. hyperthyroidism or anaemia) in older cats and with left
ventricular disease (e.g. HCM) in younger cats. The heart murmur is created by apposition of the RV free wall
against the septum in mid-to-late systole at the start of the RV outflow tract near the infundibulum. The heart
murmur itself is a benign finding but is often associated with either cardiac or non-cardiac diseases. In both
situations, the dynamic nature of the heart murmur can often be appreciated by careful auscultation as the patient
relaxes resulting in a diminution or even elimination of the heart murmur. Conversely, in a relaxed patient where the
heart murmur has disappeared, mild agitation (such as a tail pinch or turning on water in a sink) can often allow the
heart murmur to appear or get louder.
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Postitional and iatrogenic are murmurs are not uncommon in cats as they have very compliant thoracic cages.
Therefore, it is possible to induce a soft murmur in a cat by pressing too hard with a stethoscope while ausculting effectively the clinician "squashes" the heart, most likely the compliant right ventricle, producing DRVO. Thus, it is
important to auscult cats in a standing or sitting position and to only gently apply the stethoscope to the chest.
The presence of a gallop rhythm is indicative of diastolic dysfunction with poor ventricular distensibility. Due to the
common presence of non-pathologic causes of cardiac murmurs in cats the presence of a gallop rhythm is more
sensitive for the identification of pathologic cardiac disease although specificity is poor. A gallop rhythm must be
differentiated from a systolic ‘click’.
Arrhythmias, typically tachyarrhythmias, are not uncommon.
If congestive heart failure is present there may be moist pulmonary rales and/or a decrease in thoracic resonance. In
such cases, heart and lung sounds may be muffled.
Pulse quality may be reduced, or pulses may be absent if there is thromboembolic disease.
If there is severe right heart disease, there may be abnormal jugular pulses and distended jugular veins. Occasionally
cachexia and/or ascites may be seen.
Arterial blood pressure is usually normal unless the cause of disease is systemic hypertension. Cats with profound
CHF are occasionally hypotensive with associated hypothermia and bradycardia.
PRIMARY (SPECIFIC) CAUSES OF FELINE CARDIOMYOPATHY
Nonsuppurative myocarditis occurs sporadically in cats. The cause is unknown and definitive diagnosis requires
microscopic examination. Plasma troponin-I elevations are nonspecific for inflammation, and the diagnosis is
usually tentative or reserved for the necropsy table. Some cats with myocarditis are presented for ventricular
arrhythmias, while others develop fulminant heart failure, restrictive cardiomyopathy (RCM) or thromboembolism.
The clinical diagnosis is based on suspicion and exclusion of other diseases.
Thyrotoxicosis causes cardiac hypertrophy related to a hypermetabolic state, peripheral vasodilation, and increased
demands for cardiac output. In addition, increased sympathetic activity and thyroid hormone levels may stimulate
myocardial hypertrophy. In chronic cases of hyperthyroidism, the LV becomes hypertrophied. Concurrent systemic
hypertension may contribute to this. Hypertension in these cats can be multifactorial: from high cardiac output;
aortic stiffness in cats with aortoannular ectasia; or related to concurrent renal disease. In advanced hyperthyroidism,
there will be sufficient cardiac dysfunction and fluid retention to cause more generalised cardiomegaly or even CHF.
Systemic hypertension in cats is defined as elevation of arterial blood pressure, particularly values exceeding 170
mm Hg in the presence of target organ injury. While systemic hypertension does stimulate myocardial
hypertrophy, neither heart failure nor thromboembolism is a common complication of this disease. The cardiac
condition most often resembles mild HCM, with a gallop or murmur with mild cardiac enlargement evident by
radiography. LV hypertrophy may regress following successful control of blood pressure. Hypertension can cause
cardiac disease; cardiac disease cannot cause hypertension.
Primary (specific) causes of feline cardiomyopathy that should be considered in differential diagnosis1
Cause
Myocardial lesion(s) commonly observed
Hyperthyroidism
Modest septal hypertrophy and a reduction in
fractional shortening
Concentric left ventricular hypertrophy
Concentric left/right ventricular hypertrophy
Concentric left ventricular hypertrophy
Concentric left ventricular hypertrophy and
hypokinesis
Concentric left ventricular hypertrophy and
hypokinesis, hyperechoic endocardium and
hyperechoic and slightly enlarged papillary muscles
Depressed and hypokinetic myocardial area,
ventricular chamber dilation
Hypersomatotropism
Left/right outflow tract obstruction
Systemic hypertension
Myocardial tumours (e.g. lymphomas)
Dystrophin-deficient hypertrophic feline muscular
dystrophy
Myocardial infarction
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Tricuspid dysplasia
Right ventricular and right atrial chamber dilation
resembling ARVC
Concentric left/right ventricular hypertrophy
Myocarditis
ARVC = Arrhythmogenic Right Ventricular Cardiomyopathy
RADIOGRAPHS
Although radiographs can be normal in mild disease, cardiomegaly, apex shifting, and atrial enlargement are often
observed. With congestive heart failure (CHF), the cardiac silhouette may be further enlarged by a small to moderate
pericardial effusion related to untreated CHF. Prominent pulmonary vascular patterns are common. Increased lung
densities compatible with pulmonary oedema and may be focal, patchy, or diffuse. Pleural effusion is common in
acute CHF and in chronic, longstanding cases of heart failure. Unlike dogs, cats may develop pleural effusion with
left or right sided congestive heart failure. With generalised or right-sided heart failure, hepatosplenomegaly and/or
ascites may also be present. If the cardiac silhouette can be imaged adequately, enlargement of one or more
chambers may be observed. This is frequently the left atrium, or left auricular appendage. Although biatrial
enlargement, with right ventricular enlargement and shifting of the apex toward the midline of a dorsoventral
projection, (the ‘valentine shaped’ heart) has been described as a classical finding in HCM, this is non-specific and
can be seen in other forms of cardiomyopathy.
ECG
A diverse spectrum of electrocardiographic changes has been reported in cats with cardiomyopathies. All of these
are non-specific. Amongst the most common findings are the presence of a left anterior fascicular block, which has
been reported to occur in between 11%2 and 33%3 of cats with HCM. Reported abnormal rhythms include sinus
tachycardia, atrial fibrillation, supraventricular tachycardias and ventricular premature complexes. Increased
amplitude and/or duration of individual electrocardiographic (ECG) waveforms are commonly reported. These are
thought to represent enlargement of one or more chambers.
BLOOD CARDIAC BIOMARKERS
Biomarkers are rapidly becoming useful diagnostic techniques in diagnosing heart disease. N-terminal pro-brain
natriuretic peptide (NT-proBNP) and N-terminal proatrial natriuretic peptide (NT-proANP) have been evaluated for
their usefulness in distinguishing heart disease from primary respiratory disease as the cause for respiratory
difficulty in cats. A cutoff value of 265 pmol/L for NT-proBNP resulted in 90.2% sensitivity, 87.9% specificity,
92% positive predictive value, and 85.3% negative predictive value (area under ROC curve, 0.94) in distinguishing
cats with cardiac disease compared to a primary respiratory cause of respiratory difficulty. A cutoff of 517 fmol/mL
for NT-proANP concentration had a sensitivity of 90% and specificity of 82% for detecting cardiomyopathy in
cats.4,5 Troponin I has also been investigated as a diagnostic tool for CHF as a cause for respiratory distress in cats.
A cut-off of 0.81 ng/mL identified cardiac disease as the cause for respiratory distress with a sensitivity and
specificity of 65.2% and 90.0% respectively. However, the authors noted that there was considerable overlap in
troponin concentrations between the 2 groups and therefore this modality should be used in conjunction with other
evidence in evaluating for heart failure.6 The usefulness of biomarkers will continue to be investigated.
GENETIC MARKERS (HCM)
A molecular definition of HCM poses problems, as hundreds of different mutations can result in a human HCM
phenotype. The majority of HCM mutations affect one of 10 genes encoding sarcomeric proteins, including myosin
binding protein C (MyBPC). Of the two mutations identified so far in feline HCM, both affect the MyBPC gene.7, 8
Interpretation of genetic testing is fraught with difficulties. In Maine coon cats, the penetrance of the identified
MyBPC mutation is incomplete, so that echocardiographic testing is still necessary to identify phenotype in
individual cats.9, 10 In addition; wild-type mutations may exist alongside the previously documented HCM
mutations.
References: Ferasin L, J Feline Med Surg. 2009 Mar; 11(3):183; Fox PR, Textbook of canine and feline cardiology 1999, 621; Bright JM et al
Journal of Small Animal Practice 1992, 33, 266; Fox, et al. J of Vet Card, (2009)11, S51; Zimmering, et al. JAVMA 2010; 237:665; Connolly, et
al. J of Vet Card (2009)11, p 71; Meurs KM, et al. Human Molecular Genetics 2005; 14:3587; Meurs KM, et al. Genomics 2007; 90:261; Wess
G, et al. J Vet Intern Med 2010; 24:527; Mary J, et al. J Vet Cardiol 2010; 12:155
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AIRWAY OBSTRUCTION IN CATS
Lynelle Johnson DVM MS PhD Dipl. ACVIM
School of Veterinary Medicine, University of California, Davis, USA
Successful management of an animal in respiratory distress depends upon accurate anatomic localisation of disease
and efficient diagnostic planning. Assessment of the pattern of breathing, careful examination and auscultation of
the respiratory tract, and swift determination of the history of the complaint will assist in determining the site
responsible for generation of respiratory distress.
Associated signs include sneezing and nasal discharge in animals with nasal diseases. Cats with nasal disease
causing obstruction and respiratory distress generally have decreased nasal airflow on physical examination. Cats
with nasopharyngeal disease can breathe well through the mouth but exhibit distress when one nostril is occluded or
when the mouth is held closed. Whenever possible, the caudal aspect of the soft palate should be palpated for
abnormalities. Generally, the soft palate is easily depressed into the roof of the nasopharynx with digital palpation.
A nasopharyngeal mass or polyp can be felt as a space-occupying lesion dorsal to the soft palate.
Cats with laryngeal disease may present for inspiratory difficulty, abnormal purr or loss of meow. They may exhibit
repeated attempts to swallow. Auscultation over the larynx or trachea will reveal harsh or stridorous sounds.
NASOPHARYNGEAL STENOSIS
The opening to the caudal nasopharynx can be reduced to less than one mm by a web of scar tissue spanning the
opening from the nasal cavity into the pharynx. This tissue may be a congenital malformation or can develop as a
response to inflammation associated with chronic upper respiratory disease or regurgitation into the nasopharynx.
The condition is characterised by formation of a tough fibrous membrane that obstructs the caudal opening of the
nares. It is usually found relatively close to the end of the soft palate.
Signs associated with nasopharyngeal stenosis may be classic for upper respiratory infection, with sneezing, stertor,
and mucopurulent nasal discharge. However, signs due to nasal obstruction usually predominate in this condition,
and most cases lack nasal discharge. Respiratory distress can be induced in these cats when nasal breathing is
required. Signs that can be alleviated by open mouth breathing localise the abnormality to bilateral nasal passages or
the nasopharynx.
Radiographs are insensitive in detecting nasopharyngeal stenosis. Occasionally, a malformation may be visualised
on CT, particularly with sagittal reconstruction of the image. Nasopharyngeal stenosis is most easily diagnosed
using a flexible endoscope to obtain a view of the nasopharynx. A 180° flexion is required to visualise the region.
The investigator must have an appreciation of the normal anatomy of the caudal nasopharynx to recognise this
syndrome. Therefore, it is worthwhile to include a view of the caudal nasopharynx in the work-up of any cat with
upper respiratory disease. The nasopharynx in normal animals is continuous with the oropharynx, and the region can
be indirectly evaluated by passing a 3 - 5 French catheter caudally through the ventral meatus. In the normal cat, this
should pass easily into the pharynx; however a stenosed region will block passage of the catheter in affected cats.
Treatment of this obstructive breathing disorder is best achieved through balloon dilation. Various manipulations
may be required to traverse the stenotic region with wires, cutting balloons, and dilator balloons, but a good outcome
is usually achieved. For recurrent stenosis, placement of a balloon expandable stent across the region may be
required.
NASAL NEOPLASIA
Nasal tumours represent a small percentage of neoplasms; however the majority of cases exhibit malignant
behaviour through local invasion and extension. Tumour types encountered include lymphosarcoma,
adenocarcinoma, squamous cell carcinoma, undifferentiated carcinoma, and fibrosarcoma.
Cats with nasal neoplasia present with clinical signs similar to those seen with other nasal disorders. Epistaxis or
nasal discharge (unilateral or bilateral) is commonly seen along with sneezing or pawing at the face. On physical
examination, loss of nasal airflow is a common finding. Facial deformity or a mass protruding from the nostrils is
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reported in 70% of cats with nasal tumours, and epiphora is also common. Neurologic signs such as seizures,
behavioural changes, or cerebral dysfunction may be seen alone or in conjunction with respiratory signs. The
presence of these signs is highly suggestive of tumour invasion into the central nervous system and warrants a
guarded prognosis. Although the biologic behaviour of most nasal tumours is characterised by local extension,
metastasis to regional lymph nodes or to the lungs can occur and worsens prognosis.
The diagnostic work-up for nasal neoplasia included testing for feline viruses, CT, and rhinoscopy. Nasopharyngeal
examination and biopsy of mass lesions are critical since some neoplasms affect only the caudal nasopharynx.
Obtaining histopathologic samples with visualisation is the best means for obtaining a definitive diagnosis. After
examination of the choana, rostral rhinoscopy with biopsy is performed. Tumours generally appear as a mass lesion
protruding from between the turbinates.
The most commonly employed treatment of nasal tumours is radiation therapy and median survival times are 9 - 23
months. Surgery alone does not palliate signs or result in increased survival. Side effects of radiation therapy are
predictable and expected. If no early side effects are seen in normal tissue, it is unlikely that the dose administered
was high enough to palliate the tumour. Early side effects of radiation therapy include mucositis, conjunctivitis, and
moist desquamation of skin. Artificial tears are employed to lubricate the eye, but specific treatment of the skin is
not recommended. If mucositis causes anorexia, cold tea mouth rinses may make the animal more comfortable. Late
effects of radiation therapy are generally irreversible. Radiation treatment plans are designed to reduce the incidence
of delayed side effects such as bone necrosis, cataracts, and keratoconjunctivitis sicca. For nasal lymphoma,
chemotherapy may be used in addition to radiation therapy or it may be employed as a single therapeutic modality.
LARYNGEAL DISEASE
Animals with laryngeal disease present with variable degrees of respiratory distress, exercise intolerance,
tachypnoea, and cough. Gagging may also be seen, or dysphagia. Careful questioning of the owner may reveal a
voice change or a reduction in vocalisation in the recent history. The aetiology may be a laryngeal mass (due to
inflammatory laryngitis or laryngeal neoplasia) or laryngeal paralysis.
There have been a few small case series in the literature describing inflammatory laryngitis in cats that is presumed
to be primary in origin. Secondary laryngitis is likely far more common. Most cats with primary inflammatory
laryngitis are middle-aged to older at presentation, and neoplasia is the primary differential diagnosis. Cats are
presented with chronic, progressive signs of inspiratory respiratory distress and coughing or acute onset of severe
signs. Increased inspiratory effort is virtually always observed and stridor may be ausculted in some cats. Laryngeal
palpation is generally normal however radiographs of the cervical region can reveal a soft tissue density in the
region of the larynx. Careful positioning is required to evaluate neck radiographs because slight deviations in
positioning can result in artefacts. Mass lesions obstructing the rima glottidis caused by inflammation are typically
visible on laryngoscopy in affected cats, and these resemble neoplastic masses. The key to differentiating these
masses is histopathology, which reveals granulomatous, lymphocytic inflammation.
Some cats may be successfully managed with aggressive steroid therapy. Surgical excision or debulking may be
helpful in some cases, however permanent tracheostomy may be required. Caution is warranted in performing this
procedure in the cat because some tend to obstruct the tracheostomy site with excessive mucus production.
Unfortunately, laryngeal neoplasia is encountered more commonly than inflammatory laryngitis. The most common
neoplasms to affect the larynx are lymphosarcoma and squamous cell carcinoma. While chemotherapy (with or
without radiation therapy) may be helpful in reducing airway obstruction associated with lymphoma, some cats may
require tracheotomy during anaesthetic recovery or while waiting for a clinical response to therapy. Squamous cell
carcinoma is poorly responsive to most therapies. A couple of studies in oral squamous cell carcinoma in the cat
have demonstrated variable staining for COX-2 (positive staining in 1-18% of masses) which suggests that COX-2
inhibition might possibly be beneficial in an individual cat. Piroxicam is often used as a trial therapy at 0.3
mg/kg/day. Surgical debulking and tracheostomy must be considered for some cats. Tracheostomy in the cat is
challenging because of the small size of the airway relative to the dog. Cats seem to develop the complication of
tracheostomy site occlusion more commonly than dogs.
Laryngeal paralysis is also a disease primarily of older cats, although because it can be encountered as a congenital
syndrome, it may occasionally be seen in young cats. The acquired syndrome may be associated with trauma to the
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recurrent nerve anywhere along its pathway, a mass lesion impinging on the nerve, or a neuromuscular disease.
Paralysis can be unilateral or bilateral.
History, presenting complaints, and physical examination are similar to those found with other laryngeal diseases.
Cervical radiographs can reveal caudal retraction of the larynx associated with increased inspiratory effort. Thoracic
radiographs may reveal hyperinflation or an air-filled oesophagus, which must be differentiated from
megaoesophagus. Diagnosis is based on visualisation of decreased or absent laryngeal abduction on inspiration
while the animal is under a light plane of anaesthesia. Prior to anaesthetising the patient, a radiograph or ultrasound
of the larynx should be considered. Radiographs may reveal a soft tissue density in the larynx suggestive of a mass
lesion. In dogs, ultrasound can provide an indication of laryngeal paralysis prior to direct examination under
anaesthesia. This will allow preparation of the owner, patient, and surgeon for immediate intervention. An
accomplished ultrasonographer may identify either a failure of laryngeal cartilages to abduct on inspiration or can
identify a mass lesion. The use of ultrasound in feline laryngeal disease has not been fully explored.
Laryngoscopy is best performed under light anaesthesia while avoiding laryngospasm. It is important that an
assistant identifies inspiratory motions to the examiner during the procedure in order to correlate laryngeal abduction
with inspiration. Motion can be slightly asymmetric and still be within normal limits, and complete closure of the
laryngeal cartilages may or may not be observed on expiration. In dogs, when a definitive diagnosis of laryngeal
paralysis cannot be made based on visual examination, respirations are stimulated using doxapram (1.0 mg/kg IV).
This drug has not been assessed for clinical use in cats with laryngeal dysfunction.
Cats that display marked clinical signs associated with bilateral laryngeal paralysis require surgical treatment via
unilateral arytenoid lateralisation. Aspiration pneumonia does not appear to occur post-operatively as often as it is
reported in the dog. Less severely affected animals can be managed with weight loss and avoidance of heat,
humidity, and over-exertion.
TRACHEAL DISEASE
Cats are rarely affected by tracheal collapse although tracheal or bronchial collapse can be seen occasionally in cats
with chronic lower airway disease. Extraluminal compression of the trachea due to an oesophageal or thyroid mass
occurs more commonly. Intraluminal obstruction can result from neoplasia or granuloma. The most common
neoplasms are lymphoma, adenocarcinoma, and squamous cell carcinoma. Others such as plasmacytoma,
chondrosarcoma, or fibrosarcoma can also be seen. Granuloma associated with fly larvae (Cuterebra) has also been
reported as a cause of large airway obstruction.
Clinical signs are generally related to obstruction of respiration and include stridor, loud breathing, cyanosis, and
coughing. Neck or chest radiographs may show an intraluminal mass outlined by air however mural masses are
sometimes relatively large before they become visible. Anaesthesia is a great concern in cats with large airway
obstruction that cannot be bypassed by tracheotomy.
Diagnosis required visualisation of the lesion and collection of samples for histopathology. Tracheal masses can be
difficult to sample because they are parallel to the endoscope and biopsy instruments are hard to manipulate in this
plane. Use of biopsy forceps with an internal spike might facilitate purchase within the tissue. In some
circumstances, a loop snare can be used to withdraw tissue samples. This is particularly useful if the mass originates
from a pedunculated stalk.
Some tracheal tumours may be amenable to chemotherapy while others require resection and anastomosis. Placing
an intraluminal stent to expand neoplasm away from the airway can provide palliative therapy.
References: EV Queen, et al. J Vet Int Med 2010; 24(4): 990. Thunberg B, et al. J Am Anim Hosp Assoc. 2010; 46(6): 418. Hardie RJ, et al. Vet
Surg. 2009; 38(4): 445. Tasker S, et al. J Feline Med Surg. 1999; 1(1): 53. Berent AC, et al. J Am Vet Med Assoc. 2008; 233(9): 1432. Schachter
S et al. J Am Vet Med Assoc. 2000; 216(7): 1100. Stepnik MW, et al. Vet Surg. 2009; 38(4): 445. Guenther-Yenke CL, et al. J Feline Med Surg.
2007; 9(6): 451. Jakubiak MJ, et al. J Am Anim Hosp Assoc. 2005; 41(5): 310.
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IDENTIFICATION OF CATS WITH CARDIAC DISEASE II –
ECHOING WHAT HAS GONE BEFORE
Fiona Campbell MANZCVS PhD DipACVIM(Cardiology)
Veterinary Specialist Services, Gold Coast, QLD
INDICATIONS FOR ECHOCARDIOGRAPHY
Echocardiography is indicated for all cats with an abnormal cardiac auscultation and for all cats with clinical signs
or physical exam findings that are potentially referable to heart disease. Echocardiography, by an experienced
echocardiographer, is also necessary to accurately screen cats for hypertrophic cardiomyopathy (HCM). While
identification of cardiac disease sufficiently advanced to produce clinical signs may be straightforward, achieving an
accurate definitive diagnosis of specific cardiac disease and identifying the subtleties of mild disease, requires
advanced training and extensive echocardiographic experience.
RESTRAINT/ SEDATION FOR ECHOCARDIOGRAPHY
While competent restraint will suffice for many cats, sedation is sometimes necessary to facilitate a comprehensive
echocardiographic examination. ACP 0.1 mg/kg and hydromorphone 0.1 mg/kg SC is a published protocol that does
not alter the 2D and m-mode dimensional measurements of the left heart. The theoretical risk of afterload reduction
exacerbating dynamic outflow tract obstruction in cats with systolic anterior motion of the mitral valve does not
appear clinically relevant for the majority of cats.
DIAGNOSTIC CRITERIA FOR HYPERTROPHIC CARDIOMYOPATHY (HCM)
The American College of Veterinary Internal Medicine subspecialty of Cardiology has established criteria by which
hypertrophic cardiomyopathy (HCM) is defined. The key morphologic feature of HCM is a concentrically
hypertrophied non-dilated left ventricle (LV) where diastolic interventricular septal or free wall thickness is 6 mm or
greater. Hypertrophy may homogenously involve the entire LV or may be focal. When possible systemic
hypertension, hyperthyroidism, pseudohypertrophy secondary to volume depletion, diffusely infiltrative neoplasms,
acromegaly and fixed outflow obstruction (aortic stenosis, aortic coartation) need to be excluded as differential
diagnoses for HCM.
Echocardiographic examinations that are equivocal for HCM are those which identify: diffuse or segmental LV enddiastolic wall thickness between 5.5-5.9 mm, hypertrophied LV papillary muscles without septal or free wall
thickening, and/ or systolic anterior motion of the mitral valve. Systolic anterior motion of the mitral valve is
commonly identified in cats with HCM but this is not specific for HCM and it can be identified in cats with other
cardiac pathology that alters LV outflow haemodynamics (e.g. septal hypertrophy with pulmonic stenosis, mitral
valve dysplasia).
The left atrium may be normal or enlarged and there is no correlation between left atrial size and degree of LV
hypertrophy. Spontaneous contrast, indicative of sluggish blood flow (< 0.2 m/s) and rarely, thrombi, may be seen in
a dilated left atrium/ auricle.
ECHOCARDIOGRAPHIC TECHNIQUE
Echocardiographic examination should include a full 2D evaluation for assessment of structural integrity of the
valves, atrial and ventricular septa, left and right ventricular free walls, left and right atria/ auricles. Measurement of
the LV septum and free wall can be performed from m-mode or 2D images but care must be taken not to overlook
focal regions of hypertrophy that may not be included in a standard m-mode plane. Colour-flow Doppler assessment
of all valves and outflow tracts at an appropriate Nyquist limit (usually around 100 cm/sec) is necessary to identify
regions of “turbulence”, the colour mosaic produced by the addition of yellow and pale blue hues to the classic
BART colour map. Spectral Doppler assessment of both outflow tracts is routinely indicated, but especially when
the colour-flow signal suggests turbulence, in order to quantify obstructive gradient. Furthermore, the high
proportion of dynamic outflow murmurs in cats that may disappear when heart rate slows validates provocation
during echocardiographic examination to document spectral dispersion and increased peak velocity of pulsed-wave
flow in dynamically obstructed outflow tracts. Spectral Doppler assessment of mitral inflow (and pulmonary venous
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flow) can provide supportive evidence of ventricular diastolic dysfunction. Newer imaging modalities such as tissue
Doppler imaging and speckle-tracking echocardiography for myocardial systolic and diastolic velocities as well as
strain and strain-rate assessment are proving to have superior sensitivity for identification of diastolic dysfunction
prior to morphological LV changes with HCM but the application of these techniques in HCM screening is
precluded until diagnostic guidelines are established.
ECHOCARDIOGRAPHIC PITFALLS
A high-frequency probe (12 mHz) is preferable when measuring LV wall thickness to facilitate accurate
identification of tissue boundaries. A high frame rate should also be selected, particularly when measuring wall
thickness from 2D images at fast heart rates to ensure that a frame is acquired that reflects true end-diastole and not
early systole where wall thickness will be increased. Measuring diastolic wall thickness from m-mode images (at the
onset of the QRS complex on a simultaneously recorded ECG) overcomes the problem of suboptimal sampling rate
by allowing accurate identification of end-diastole, however this modality also has limitations. M-mode
measurements may fail to identify focal hypertrophy, non-perpendicular alignment of the cursor with the LV wall or
transection of a papillary muscle may result in exaggerated LV wall measurements, and tissue boundaries can be
difficult to identify with m-mode, particularly if papillary muscle hypertrophy precludes cursor bisection of the 2D
guided short-axis image.
DISEASES THAT MIMIC HCM
There are several conditions that need to be considered in a patient with increased diastolic LV wall thickness before
a diagnosis of HCM can be made. These include:
• pseudohypertrophy of the LV myocardium due to volume depletion
• systemic hypertension
• hyperthyroidism
• fixed left ventricular outflow obstruction e.g. aortic stenosis, subaortic stenosis
• others e.g. infiltrative cardiac neoplasm, aortic coarctation, acromegaly.
Pseudohypertrophy with volume depletion, systemic hypertension, hyperthyroidism and acromegaly produce only
mild LV hypertrophy. Fixed aortic stenosis will produce hypertrophy in proportion to the severity of the obstruction.
Infiltrative neoplasms can increase wall thickness but also compromise systolic function producing either regional or
global LV hypokinesis.
It should be noted that HCM is a very common disease; affecting up to 20% of overtly healthy cats. Cats with
congenital or other acquired cardiac diseases, are likely to have a similar frequency of HCM and as such,
echocardiographic identification of HCM should not abbreviate the echocardiogram or preclude comprehensive
assessment for concurrent cardiac disease that may be more clinically relevant to that individual and that may alter
treatment/ prognosis.
DYNAMIC RIGHT VENTRICULAR OUTFLOW TRACT OBSTRUCTION
This is a common cause of heart murmurs in cats. It results from the systolic apposition of the right ventricular free
wall and interventricular septum and produces low velocity (> 1.7 ms) turbulence in the right ventricular outflow
tract. Because the obstruction is low-grade, there are no adverse haemodynamic consequences and the associated
murmur is termed “innocent”. It can be found in cats with and without concurrent cardiac disease and its
identification, as causative of an auscultated murmur should not preclude thorough echocardiographic examination
for other concurrent disease.
References: 1. Campbell FE, et al. J Vet Intern Med 2007;21:1008. 2. Snyder PS, et al. J Vet Intern Med 2001;15:52. 3. Rishniw M, et al. J Vet
Intern Med 2002;16:547. 4. Cote E, et al. J Am Vet Med Assoc 2004;225:384. 5. Paige CF, et al.. J Am Vet Med Assoc 2009;234:1398. 6. Riesen
SC, et al.. Schweiz Arch Tierheilkd 2007;149:73. 7. Schober KE, et al. J Vet Intern Med 2006;20:120. 8. Moise NS, et al. Am J Vet Res
1986;47:1476.
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EXUDATIVE PLEURAL DISEASE
Lynelle Johnson DVM MS PhD Dipl. ACVIM
School of Veterinary Medicine, University of California, Davis, USA
Cats develop pleural effusion in conjunction with infectious diseases, traumatic incidents, cardiac diseases, or
congenital conditions. Presenting signs might include an acute onset of tachypnoea and respiratory distress in
conjunction with a long-standing history of anorexia and debility, or respiratory signs may be the only abnormality
detected. Pleural effusive disorders can be divided into chylothorax, hydrothorax, haemothorax, and pyothorax
depending upon fluid characteristics. Diagnosis of the type of pleural fluid present and detection of underlying
abnormalities is essential for appropriate treatment of disease.
The pleural lining of the respiratory system keeps the lung parenchyma dry and coordinates respiratory movement
by tethering lung expansion to enlargement of the thorax during inspiration. The parietal pleura lines the inner
surface of the chest wall, diaphragm, and mediastinum. The visceral pleura lines each lung lobe and is responsible
for the interlobar fissure lines seen on radiographs. A space exists between the two layers of pleura normally
contains 2-3 mL of fluid produced by transudation from blood vessels in the parietal and visceral pleura. Lymphatic
openings in the parietal pleura drain fluid from the pleural cavity. Disruption of the pleural space by entrance of
fluid, air, or organ herniation results in disturbance of the forces that typically coordinate breathing.
The primary clinical sign associated with pleural disease is tachypnoea, with either a rapid, shallow breathing
pattern or hyperpnoea, with paradoxic abdominal excursions. Elbows are abducted and the neck is extended in order
to facilitate movement of air into the alveoli. Usually, the degree of respiratory distress is associated with the
rapidity of fluid or air accumulation rather than with the specific volume present. Cats seem to be particularly
sensitive to addition of a critical volume of fluid that overcomes their ability to compensate for filling of the pleural
space.
Auscultation and percussion of the chest wall aids in the diagnosis of a pleural disorder, although percussion in a cat
is limited because of the small size of the thoracic cavity. With pleural effusion, lung sounds are ausculted in the
dorsal fields only and muffled sounds are heard ventrally. Heart sounds are also muffled. Percussion of an area filled
with fluid reveals a dull sound, and a fluid line may be noted. Pneumothorax leads to an absence of lung sounds
dorsally due to the presence of air, and this area may be hyper-resonant on percussion. Lung sounds are present in
the ventral fields only. Pleural effusion can lead to decreased thoracic compressibility, while pneumothorax may be
associated with a barrel shaped appearance to the chest. Lateralising differences in auscultation can be found with
unilateral pneumothorax or pleural effusion, typically caused by chylothorax or pyothorax.
Other aspects of the general physical exam, especially cardiac evaluation, abdominal palpation, and fundic
examination assist in identifying the aetiology of pleural disease, although further diagnostics will be required. For
example, the cat in right-sided heart failure should have distension of the jugular veins and a heart murmur or gallop
sound on physical exam. These findings would suggest the need for echocardiography to define the type of cardiac
disease. Elevated central venous pressure measured with a jugular catheter supports the diagnosis of cardiac disease,
however pleural fluid in excess of 17 mL/kg can increase CVP in the absence of right heart failure. CVP will
increase by 1 cm H2O with each additional of 10 mL/kg of pleural fluid. Therefore, a normal CVP can rule out heart
failure, but CVP should be measured before and after thoracocentesis.
Cats with a pleural disorder often present with acute respiratory embarrassment. An immediate decision must be
made whether to proceed with diagnostic radiographs or ultrasound, or to perform thoracocentesis to alleviate
respiratory distress. Oxygen administration is minimally effective in decreasing respiratory effort, however
reduction in stress is essential, and cautious sedation may be useful in some cats. When taking radiographs, it is
important to place the animal in sternal recumbency rather than performing a ventrodorsal view. Positioning for the
VD view places excessive stress on the respiratory system and increases the likelihood of decompensation. Both left
and right lateral views are beneficial, especially when unilateral effusion is present, and radiographs should be
repeated after thoracocentesis.
Pleural effusion is easily recognised on radiographs by the presence of interlobar fissure lines, rounding of the lung
borders at the costophrenic angles, sternum, and thoracic cage, and blurring of the cardiac silhouette. Pneumothorax
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also causes retraction of the lung margins from the thoracic wall, but lucent areas are seen peripherally that lack
vascular markings. The heart is lifted off the sternum in the lateral views with pneumothorax.
Thoracocentesis is performed as a diagnostic and therapeutic technique, before or after radiographic confirmation of
a pleural disorder. The region of the 7th – 8th intercostal space is clipped and scrubbed ventrally for fluid or in the
dorsal 1/3 of the chest for air. I prefer to use a 19-21 gauge butterfly needle on extension tubing to perform
thoracocentesis in cats. Alternately, a fenestrated 18-20 gauge catheter with extension set can be used when a large
pleural effusion is present. A 3-way stopcock and syringe should be immediately accessible for attachment to the
extension set after the pleural space is entered. Specimen collection should be anticipated: EDTA and clot tubes and
a culturette swab should be available, along with a bowl to collect large volumes of fluid.
In-house pleural fluid analysis should always include a PCV, cell count, protein or specific gravity, and cytology.
Smears may also be prepared for Gram staining. Additional tests include bacterial culture and susceptibility testing
(aerobic and anaerobic cultures), cholesterol:triglyceride ratio for the diagnosis of chylothorax, protein
electrophoresis, or immunocytochemistry.
Appropriate diagnostic tests for systemic disease can be chosen after the character of the pleural fluid is determined
because the list of possible differential diagnoses can be constructed based on fluid characteristics. A complete
database including CBC, chemistry profile, and urinalysis should be obtained in all cases. A transudative fluid is
most likely related to hypoproteinaemia. An albumin level less than 1.5 mg/dl would be consistent with this, and
other parameters on the chemistry profile and urinalysis will indicate whether low albumin is related to decreased
production (due to liver disease) or increased loss (due to gastrointestinal or renal disease). Other tests that might be
required include bile acids to characterise liver disease or a urine protein-to-creatinine ratio to support significant
renal loss of protein.
Chest radiographs obtained after removal of pleural fluid are helpful in assessing cardiac size, detecting the presence
of mass lesions or pneumothorax, and determining the inflation capacity of the lungs. Loss of lung volume or
persistent rounding of lung margins despite removal of fluid is suggestive of pleural fibrosis.
Characteristics of pleural fluid
Characteristics of pleural fluid
Transudate
Modified Transudate
Protein (g/dl)
<< 2.5
< 2.5
Cell Count (/µl)
< 500-1500
500-2500
Aetiology
Hypoproteinaemia
Right heart failure
Pericardial disease
Hypoalbuminaemia
Neoplasia
Hernia
Exudate
> 3.0
> 5000
FIP
Neoplasia
Hernia
Lung lobe torsion
Pyothorax
Chylous
> 2.5
> 500
Idiopathic
Cardiomyopathy
Heartworm disease
Neoplasia
Lung lobe torsion
Haemorrhagic
> 3.0
> 1000
Trauma
Coagulopathy
Neoplasia
Lung lobe torsion
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CHYLOTHORAX
Chylothorax is caused by leakage of lymphatic fluid from the thoracic duct into the pleural cavity. The aetiology is
usually idiopathic, however diseases associated with increased right heart pressure, such as cardiomyopathy and
heartworm disease, have been implicated as causes and should be ruled out as a specific diagnosis. Mediastinal
masses (thymoma, lymphosarcoma) and lung lobe torsion have been associated with chylothorax. Traumatic rupture
of the thoracic duct is thought to be a rare cause of chylothorax. Siamese and Himalayan cats appear to have an
increased incidence of chylothorax.
Cats with chylothorax generally present with clinical signs of respiratory abnormalities consistent with a pleural
disorder. Some cats will exhibit a cough, likely due to airway compression or inflammation. General debility may be
evident in cats with long-standing chylothorax because of leakage of protein and fat-rich lymph into the pleural
space.
Chylothorax is typically suspected when a white, opaque fluid is retrieved on thoracocentesis, however in cats that
are malnourished, the lack of fat within lymph may result in a serosanguinous appearance to the fluid. Chylothorax
is diagnosed by performing cholesterol and triglyceride analysis on pleural fluid and serum. Because chyle is
lymphatic fluid, triglyceride levels in pleural fluid are significantly higher than in serum, and cholesterol levels are
lower than in serum. A cholesterol: triglyceride ratio < 0.2 in pleural fluid is considered diagnostic for chylothorax.
Initial therapy for chylothorax should be directed at the cause, if one can be identified. Frequent thoracocentesis
(every two weeks) may be required whether a primary disease is identified or not. Dietary therapy (reduced fat in the
diet, supplementation with medium chain triglyceride oil) has been the mainstay of therapy for quite some time
because it was thought that these dietary changes would reduce lymph flow. Some animals may benefit from dietary
therapy but this is variable. Few cats will tolerate medium chain triglyceride oil, and use of a low fat diet can lead to
a poor nutritional state. Therefore, adequate intake of protein, minerals, and other nutrients should remain a goal of
therapy for any animal with chronic chylous effusion. Therapy with rutin, a benzopyrone, has been suggested for use
in chylothorax and has demonstrated some clinical efficacy. This agent is believed to stimulate macrophage
activation, resulting in protein digestion and a reduction in the stimulus for lymph production. This agent is available
at health food stores and is administered at a dosage of 50 mg/kg PO TID. Few adverse effects have been reported to
date.
Pleurodesis with tetracycline or sterile talc was not successful in experimental studies in dogs and would seem
unlikely to be successful in cats. Problems are encountered in obtaining a dry pleural space in which to instil the
sclerosing agent. If thoracocentesis is required more often than once per week, surgical options should be
considered. Techniques used include thoracic duct ligation, diaphragmatic mesh implantation, and pleuroperitoneal
shunting. Concurrent pericardectomy is often recommended. Success rates of 50-100% have been reported for cats
in surgical treatment of chylothorax.
PYOTHORAX
Pyothorax can result from bite wounds, migrating foreign bodies, haematogenous infection, or from extension of a
pulmonary infection. For cats in which trauma is suspected, the thoracic cage should be closely evaluated for bite
wounds or sites of traumatic penetration. Clinical signs include respiratory distress and shortness of breath. In many
cats, systemic signs of malaise, depression, anorexia, and weight loss predominate. Physical examination may or
may not reveal fever. Tachypnoea is expected, and cats may have reduced thoracic compliance. Muffling of heart
sounds and absence of lung sounds ventrally would be anticipated in a cat with pyothorax.
Pyothorax results in an exudate, with high cell counts and high protein content. Samples of pleural fluid should be
cultured for both aerobes and anaerobes. In a retrospective study in cats, bacteria were isolated from 45 of 47
samples (96%), and were visible on cytology in 41 of 45 samples (91%). Obligate anaerobes were present in 40 of
45 samples (89%), and a mixture of obligate anaerobes and facultative organisms was found in 20 of 45 (44%) of
culture positive cats. An average of 2.1 species of obligate anaerobic bacteria and 1.2 species of aerobic bacteria
were isolated in cats. Pasteurella species were the most common aerobe isolated, and anaerobes isolated included
Peptostreptococcus, Bacteroides, and Fusobacterium.
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Most Pasteurella species will exhibit susceptibility to ampicillin, amikacin, amoxicillin-clavulanic acid,
ceftizoxime, enrofloxacin, gentamicin, and tetracycline. For initial treatment of polymicrobial infection associated
with pyothorax, antibiotics should be directed against obligate anaerobes (efficacious antibiotics include ampicillin,
amoxicillin-clavulanic acid, clindamycin, or metronidazole) and against Pasteurella species in cats. Appropriate
systemic antibiotics generally must be continued for 2-6 months, and the antibiotics used long-term are best based
on susceptibility testing.
Because pyothorax represents an encapsulated abscess, drainage is crucial for resolution of disease. Unilateral or
bilateral chest tubes are required, and constant or intermittent (every 2-4 hours) suction should be employed.
FIBROSING PLEURITIS
Fibrosing pleuritis is a debilitating disease that can result from long standing pleural effusion, particularly when a
high protein pleural effusion such as chylothorax or pyothorax has been diagnosed. Chronic inflammation of the
pleura results in metaplasia of mesothelial cells with production of collagen. The presence of pleural fluid decreases
fibrinolysis within the pleural space resulting in an expansion of the collagen network along the pleura. Thickened
pleura reduces the ability of the lung to expand, and removal of pleural fluid may not substantially lessen respiratory
distress in affected cats. Fibrosing pleuritis is characterised by persistently unexpanded or compressed, rounded lung
fields on radiographs. The radiographic appearance of fibrosing pleuritis is often bizarre and may be mistaken for
hilar lymphadenopathy, lung lobe torsion, neoplasia, or atelectasis. Therapy for fibrosing pleuritis involves surgical
decortication of the pleura. This procedure has been beneficial in humans if fewer than two lobes are affected,
however most animals have generalised pleuritis, which is not easily treated with surgery. Complications of the
procedure include pneumothorax and haemorrhage. If surgery is performed, steroids should be considered for 2-3
weeks post-operatively. Lung function may improve over 2-3 months.
References: Fossum TW, et al. J Vet Intern Med. 2004; 18(3): 307. Barrs VR et al. Vet J. 2009; 179(2): 163. Barrs VR et al. Vet J. 2009; 179(2):
171. Barrs VR, et al. J Feline Med Surg. 2005; 7(4): 211. Waddell LS, et al. J Am Vet Med Assoc. 2002; 221(6): 819. Walker AL, et al. J Am Vet
Med Assoc. 2000; 216(3): 359.
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MEDICAL MANAGEMENT OF FELINE CARDIAC DISEASES
Niek J. Beijerink DVM PhD Dipl. ECVIM-CA (Cardiology)
University Veterinary Teaching Hospital, Faculty of Veterinary Science, University of Sydney, NSW
Evidence-based recommendations on the medical management of feline heart disease are sparse. In contrast to dogs,
where evidence-based practice in cardiology has considerably advanced in recent years due to the results of several
large prospective, randomised, multicentre, controlled clinical trials (e.g. QUEST trial on the treatment of congestive
heart failure (CHF) in dogs using pimobendan1), similar trials in the treatment of feline heart disease are still
missing. With the exception of taurine-supplementation in cats with taurine-deficient cardiomyopathy2, there is
currently no published evidence that any pharmacological treatment may alter the natural history of feline heart
disease. Treatment recommendations are based on assumptions, information from case series and small scale and
often uncontrolled clinical trials, and personal preference. Treatment of feline cardiomyopathies (mainly
hypertrophic cardiomyopathy; HCM) is usually directed at controlling signs of CHF, preventing the recurrence of
systemic or aortic thromboembolism (ATE) or delaying/preventing/reversing progression of subclinical disease.
MEDICAL TREATMENT OF CHF
There is no strong evidence that any drug reduces mortality in cats with CHF. However, clinical benefits are often
very obvious with the use of a combination of sedation, oxygen therapy, drainage of pleural effusion, and drugs
(mainly furosemide, ACE-inhibitors). One not published study (presented as an abstract) suggested no benefit of any
therapy other than furosemide and ACE-inhibition, and potential harm of administering B-blockers in cats with
CHF3. Recent retrospective studies reported on the use of pimobendan in 170 cats with cardiomyopathy and CHF4.
However, due to the study design (open label, retrospective, absence of a placebo group, non-randomisation) results
need to be interpreted with a lot of caution. Most clinicians will use furosemide and ACE inhibitors with evidence of
CHF.
PROPHYLAXIS AND TREATMENT OF ATE
There is no evidence that commonly used oral (aspirin, clopidogrel, and warfarin) and parenteral (low molecular
weight heparins) anticoagulants and platelet inhibitors are effective in cats (prevention of ATE either as a first event
or recurrence). Aspirin has been used at 5 mg/cat/72 h and 40 mg/cat/72 h with no difference in survival. The results
of the currently ongoing prospective, double-blind, active control, multicentre trial (FATCAT study) comparing the
effects of aspirin versus clopidogrel (18.75 mg/cat/24 h) in cats that survived a thromboembolic event are currently
evaluated.
DELAYING/PREVENTING/REVERSING PROGRESSION OF SUBCLINICAL DISEASE
To date, no therapy has been prospectively studied long enough to document effects on clinical outcome such as
sudden death, CHF, or ATE in cats with preclinical cardiomyopathy. Thus, many aspects of chronic therapy of
cardiomyopathy remain controversial with early administration of drugs mandated mainly by personal belief,
opinion, and obvious logic (application of pathophysiological principles). Similarly, no drug has yet been shown to
clearly have a positive impact on circulating biomarkers of cardiac disease or neuroendocrine activation, which may
reflect ongoing myocardial damage or disease severity in cats. Most authors recommend that treatment of occult
cardiomyopathy should be directed toward "key problems" in the development and progression of the disease such
as unwanted tachycardia, diastolic dysfunction, a hyperdynamic left ventricle, increased afterload (obstruction, often
dynamic) and preload (chamber dilatation), arrhythmias, ischaemia, fibrosis, and prevention of thromboembolic
events. Drugs most often used in the clinical management of asymptomatic feline cardiomyopathies include beta
blockers (atenolol), calcium-channel blockers (diltiazem), ACE inhibitors, spironolactone, and anti-platelet drugs
such as aspirin or clopidogrel. There is currently no consensus amongst veterinary cardiologists about the
therapeutic approaches to feline subclinical HCM of varying severity. The following highlights some of the major
studies.
One study, which evaluated Maine Coon cats with a genetic HCM-causing mutation, failed to document reduction
of LV mass, improvement of diastolic function, or reduction of elevated plasma neurohormones after one year of
treatment with the ACE inhibitor ramipril which led to the conclusion that ACE inhibition is not beneficial for cats
with HCM that are not in heart failure5.
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In the same colony of cats, spironolactone, an aldosterone antagonist and supposed antifibrotic drug, did not reduce
LV mass and left atrial size or improve LV diastolic function compared to placebo after four months of
administration. Moreover, about a third of cats developed severe facial ulcerative dermatitis making the use of
spironolactone in cats difficult to justify6.
Diltiazem and atenolol have gained most popularity in the treatment of feline HCM. Studies in cats with HCM and
CHF performed in the early nineties7 revealed that oral administration of diltiazem may have beneficial effects on
LV diastolic function and severity of LV hypertrophy and is clinically well tolerated. Cats previously showing
clinical signs of left-sided CHF stabilised under the influence of diltiazem, heart rate and LA size decreased
significantly, LV hypertrophy regressed in most cats, and survival increased. In studies performed by the same
group, long-term (> 18 months) administration of diltiazem caused reverse remodelling of severe LV hypertrophy to
a normal, non-hypertrophied LV phenotype in the majority (66%) of cats. Unfortunately, due to non-randomisation,
non-blinding, and the absence of matched control groups, results of such studies never gained general acceptance
and could never be reproduced. In contrast, more recent studies in cats with HCM8 indicated that recommended
doses of oral diltiazem frequently cause lethargy, gastrointestinal upset, and weight loss, and that serum diltiazem
concentrations tend to be erratic and unpredictable with the potential of leading to signs of intoxication. Diltiazem is,
in addition, thought to be inferior to atenolol with regard to reduction of murmur frequency, murmur loudness, and
dynamic obstruction of the outflow tract. Therefore, currently most board-certified cardiologists use atenolol (12.5
mg/cat/12 h) over diltiazem, when substantial dynamic left ventricular outflow tract obstruction due to systolic
anterior motion of the mitral valve is present9. Results of prospective long-term studies, focusing on the effects of
atenolol on LV hypertrophy, dynamic outflow obstruction, and survival have not yet been published.
References: 1) Haggstrom J, et al. J Vet Intern Med 2008;22:1124. 2) Pion PD, et al. Science 1987;237:764. 3)Fox PR. Proceedings of the
ACVIM 2003. 4) Macgregor JM et al. J Vet Cardiol 2011;13:251. 5) MacDonald KA et al. J Vet Intern Med 2006;20:1093. 6) MacDonald KA et
al. J Vet Intern Med 2008;22:335. 7) Bright JM et al. J Vet Intern Med 1991;5:272. 8) Wall M et al. J Am Hosp Assoc 2005;41:98. 9) Rishniw M
et al. J Fel Med Surg 2011;13:487.
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FELINE UPPER RESPIRATORY ASPERGILLOSIS: HOW DIFFERENT IS IT
FROM CANINE SINONASAL ASPERGILLOSIS?
Vanessa R. Barrs BVSc MVetClinStud FANZCVS (Feline Medicine) GradCertEd (Higher Ed)
Faculty of Veterinary Science, University of Sydney, NSW
INTRODUCTION
Canine sinonasal aspergillosis (SNA) was first reported in 1897 shortly after the first reports of SNA in humans in
18951. Reports of a similar disease in cats did not appear until the 1980s2-4. Upper respiratory tract aspergillosis
(URTA) is an emerging feline infection with over two-thirds of the approximately 50 reported cases being published
in the last 5 years5-12. Key differences between canine and feline disease include the infecting species, clinical
presentation and response to therapy. In dogs the major form of disease (> 99% of cases) is SNA, a non-invasive
mycosis confined to the sinonasal cavity, while in cats sino-orbital aspergillosis (SOA) is the more common form
(63% of cases)2-3, 5-7, 10-15. SOA is a deeply invasive mycosis that originates in the sino-nasal cavity and extends to
involve orbital and other paranasal tissues.
AETIOLOGY
Controversies in fungal nomenclature and identification (ID)
More than 250 species have been ascribed to the Genus Aspergillus, which is subdivided into 8 subgenera;
Aspergillus, Fumigati, Circumdati, Candidi, Terrei, Nidulantes, Warcupi and Ornati. Each subgenus comprises
from 1 to 4 sections16.
The most common isolates from canine and feline URTA are from the subgenus Fumigati section Fumigati, also
known as the Aspergillus fumigatus complex.12,17-18,28 There are occasional reports of isolates from the subgenus
Circumdati (A. flavus and A. niger)8,19-21 causing SNA in both cats and dogs and from the subgenus Nidulantes (A.
nidulans)21 causing SNA in dogs.
The A. fumigatus complex contains asexual members (anamorphs, mitotic phase), many of which also have sexual
forms (teleomorphs, meiotic phase). There has been controversy around fungal taxonomy because teleomorphs in
this complex have been assigned to a different genus – Neosartorya. Classical nomenclature required that an
organism with alternate names be labeled with that of its sexual phase. This created confusion for organisms such as
A. fumigatus where the teleomorph (Neosartorya fumigata) was only recently discovered.22
Fortunately, in sweeping reforms to the International Code of Nomenclature for algae, fungi and plants a “onefungus, one-name” principle was adopted in 2011.23 The revised nomenclature code will be published in 2013. In
short, it is likely that the oldest generic name (e.g. A. fumigatus), irrespective of whether it is typified by a species
name with a teleomorphic or an anamorphic type, will be used.
It is now well established that members of the Aspergillus fumigatus complex cannot be reliably identified solely on
the basis of phenotypic features. Some, termed A. fumigatus-mimetic species, have very similar anamorph colony
morphology to A. fumigatus. Misidentification of A. fumigatus in human patients with invasive aspergillosis (IA) has
important implications for treatment and prognosis. In a review of 86 isolates from human patients with IA
previously identified as A. fumigatus, 12 isolates were subsequently identified as A. udagawae based on comparative
sequence analyses of beta-tubulin and rodlet A genes.24 In this subset of patients the median duration of illness was
7 times longer and disease was refractory to standard therapy. Similarly, a distinctive form of IA characterised by
chronicity, propensity to spread across anatomical planes and reduced susceptibility to antimycotic drugs was
initially attributed to infection by A. fumigatus. The molecular identity was A. viridinutans.25 A. fumigatus-mimetic
species have higher in vitro minimum inhibitory concentrations for amphotericin-B and triazole antifungal drugs
(e.g. voriconazole) than A. fumigatus.26
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Advances in ID of fungal pathogens in feline and canine URTA
Molecular ID of isolates causing feline and canine URTA has been reported since 2007.5, 27-28 Isolates from 23
Australian cats were identified using PCR and sequencing of the Internal Transcribed Spacer (ITS) region. A.
fumigatus was identified as the cause of SNA in 4 of 6 cats.12 All 17 isolates from cats with SOA were identified as
A. fumigatus-mimetic species from the Aspergillus fumigatus complex. Individual species determination was not
possible using ITS sequence analysis alone. In a subsequent study of these and other isolates at the CBS KNAW
Fungal Biodiversity Centre in Utrecht, sequence comparisons of the beta-tubulin, calmodulin and rodlet A regions
identified A. lentulus, A. thermomutatus (N. pseudofischeri) and a novel species of Aspergillus from cats with SNA.
The majority of isolates from cats with SOA were identified as the same novel species of Aspergillus. A. udagawae/
(Neosartorya udagawae) was identified as a cause of feline SOA in a single case report from Japan on comparative
sequence-based analyses of the ITS and beta-tubulin regions.5 While A. fumigatus was implicated as the aetiological
agent in previous reports of feline SOA, ID was based on morphologic criteria alone.7, 10, 15 Current evidence
suggests that A. fumigatus is the most common cause of SNA in cats and that SOA is only caused by A. fumigatusmimetic species. Analysis of more cases is required to confirm this.
Phenotypic ID of a large number of isolates from dogs with SNA has implicated A. fumigatus as the aetiologic agent
in most cases.17-18 However, molecular ID has been performed on a small number of isolates only.12, 28 In 14 dogs
with clinically confirmed SNA, DNA of Penicillium or Aspergillus spp. was detected in nasal mucosal biopsies
using a genus-specific real-time PCR assay. Species specific PCRs to detect DNA of A. fumigatus, A.niger, A.
terreus or A. flavus were positive for A. fumigatus in seven dogs and negative in the other seven dogs. It is possible
that these isolates may have been Penicillium spp. or another Aspergillus spp. Alternatively there may have been
insufficient A. fumigatus DNA present to be positive with the specific PCR. In another study, ITS sequencing of
archival tissues from the sino-nasal cavity of seven dogs with SNA identified A. fumigatus in all seven cases12.
Further molecular studies are necessary to determine the frequency of involvement of individual species within the
Aspergillus fumigatus complex and from subgenera other than Fumigati.
PATHOGENESIS
Like SNA in dogs, infection in cats starts in the sinonasal cavity. Direct extension of infection into contiguous
structures including the orbit and paranasal tissues occurs in SOA. This is evidenced by progression of SNA to
SOA13, sinonasal cavity involvement on imaging or at necropsy in cases of SOA,7, 11-12 and by isolation of the same
novel species of Aspergillus that causes SOA in a case of SNA. Extension of infection from the sinonasal cavity is
usually through the orbital lamina, situated between the orbit and frontal sinus. Given that only A. fumigatus-mimetic species have been isolated from cats with SOA, infecting fungal species may be a major determinant of
progression. A major difference between SOA in cats and SNA in dogs is the invasiveness of the mycosis. In canine
SNA fungal hyphae do not invade the nasal mucosa and are located in adjacent superficial necrotic plaques.29 By
contrast, SOA in cats is an invasive mycosis. Fungal hyphae invade the respiratory epithelium and form granulomas
within the orbit and paranasal tissues.
EPIDEMIOLOGY
In both cats and dogs URTA typically occurs in young to middle-aged animals. Of 49 reported feline cases the mean
age at diagnosis was 6.5 years with a range from 1.5 to 13 years.2-15, 19-20, 34 In case-series of canine SNA, mean age
at diagnosis was 5 to 6 years.17-18, 30-33 Cats with SNA tend to be older at diagnosis (mean/median 8 y) than those
with SOA (mean 6 y/median 8 y). No sex-predisposition has been identified for feline URTA. Of 47 reported feline
cases where sex was specified, there were 26 males and 21 females. Males appear to be over-represented in canine
SNA. In combined reports of 377 cases there were 245 males and 132 females with a male to female ratio of 1.9:1.
A striking difference between feline and canine URTA is the facial conformation of affected animals. As more cases
of feline URTA are reported an over-representation of brachycephalic breeds has become apparent. Whilst nearly
half of all cases (24) were domestic crossbred cats (22 domestic shorthair, 2 domestic longhair), 40% (21) were of
brachycephalic conformation, mostly Persian (10) or Himalayan (6) breeds. By contrast dolicocephalic and
mesaticephalic breeds of dogs are predisposed to SNA: infection in brachycephalic breeds is rare. In most caseseries comparisons with hospital populations to calculate odds ratios were not performed, thus overt breed
predispositions have not been confirmed. However, breeds repeatedly identified include Rottweilers, Labrador
retrievers, golden retrievers and German shepherd dogs.17,31-33 In the largest study of feline URTA four of six cats
with SNA and five of 17 cats with SOA were brachycephalic, but the difference was not statistically significant12.
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Interestingly, when all published cases are combined, overall 11 of 18 (61%) cats with SNA were brachycephalic
while 10 of 31 (33%) cases of SOA were brachycephalic.
The reasons why brachycephalic cats and dolicocephalic or mesaticephalic dogs are predisposed to URTA remain
elusive. In both dogs and cats the upper respiratory tract is the major site of localised disease. By contrast, in
humans, localised infections are most common in the lower respiratory tract, particularly in immunocompromised
patients. There is no evidence of an association between retrovirus infection and URT aspergillosis, with only one
FeLV positive case reported.4 Most dogs with canine SNA are systemically healthy. When URTA does occur in
humans, risk factors include decreased sinus aeration and drainage of respiratory secretions secondary to infection,
polyps and allergic rhinosinusitis. Reduced drainage of URT secretions due to brachycephalic conformation could
be a risk factor in cats. However, since brachycephalic dogs are under-represented for SNA, it is likely that
additional risk factors are present in cats. These could include heritable defects in mucosal immunity, previous viral
URT infection and previous antibiotic treatment favouring fungal colonisation.34
CLINICAL PRESENTATION
In dogs the triad of muzzle pain, profuse mucopurulent to haemorrhagic chronic nasal discharge and
depigmentation, crusting or ulceration of one or both nares is highly suggestive of SNA. Presenting signs in cats
with SNA are more subtle and include a history of sneezing and unilateral or bilateral serous to mucopurulent nasal
discharge.4,8,9,12,20,34 Intermittent epistaxis occurs in 40% of cases. Occasionally, a discharging sinus or soft-tissue
mass is identified overlying the frontal sinus or the nasal bone as a result of bony lysis and fungal proliferation.12, 19
Stertor is variably present due to excessive nasal secretions or a caudal nasal cavity/nasopharyngeal fungal
granuloma. Nasal depigmentation or ulceration has not been documented in cats with SNA. Cats with SOA are
usually presented for investigation of unilateral exophthalmos. Clinical signs are referable to invasive expansion of a
fungal granuloma in the ventromedial orbit. In addition to exophthalmos, these include dorsolateral deviation of the
globe, conjunctival hyperaemia, third eyelid prolapse and exposure keratitis. An oral mass or ulcer in the ipsilateral
pterygopalatine fossa behind the last molar tooth is usually present. Extension of infection outside the sinonasal
cavity may cause facial distortion, including swelling of the nasal bridge, periorbital tissues and soft tissues adjacent
the maxilla. At the time of presentation, nasal signs are absent in 40% of cases but the medical history will reveal
sneezing or nasal discharge in the previous 6 months in almost all cases.10,12,15 Neurological signs have been
reported in 15% of cases including blindness, circling, facial muscle fasciculation and hyperesthesia.7,10,12,15
DIAGNOSIS
Definitive diagnosis of feline URTA requires cytological or histological ID of fungal hyphae in affected tissue and
ID of the fungal pathogen. Similar to canine SNA, a definitive diagnosis may require various combinations of
diagnostic tests including serology, computed tomography, endoscopy, cytology, histology and fungal culture.
Serum anti-Aspergillus antibodies can be detected by numerous methods including counter-immunoelectrophoresis
(CIE), agar gel immunodiffusion (AGID) or ELISA. These tests have been applied to individual cases of feline
URTA only, thus the sensitivity and specificity of antibody detection for diagnosis of feline aspergillosis is currently
not known. Five of 10 reported cases (9 SNA, 1 SOA) tested seropositive. 4, 8, 12, 20, 34 By contrast, two recent studies
evaluated serology for diagnosis of canine SNA.17, 35 In one study AGID was compared with fungal culture of nasal
biopsies,17 and in the other the AGID and ELISA were compared.35 For both methods a purified aspergillin
preparation composed of extracts of A. fumigatus, A. niger and A. flavus was used. In one study fungal culture was
more sensitive (81%) than serologic testing (67%) while specificity was high for both fungal culture (100%) and
serology (98%).17 In the second study ELISA had higher sensitivity (88%) than AGID (76%) and specificity was
high for both methods (ELISA 97%, AGID 100%). These studies demonstrate that seropositivity for Aspergillus
spp. is highly suggestive of SNA in dogs but that negative test results do not rule out aspergillosis.
Serum galactomannan (GM) measurement for diagnosis of feline URTA was recently evaluated using the PlateliaTM
ELISA.36 GM was measured in healthy cats (n = 44) including juvenile (n = 31) and adult cats (n = 13) as well as in
cats with URTA (n = 13; 6 SNA, 7 SOA), non-fungal upper respiratory tract disease (n = 15) or being treated with
β-lactam antibiotics (n = 14). The overall sensitivity and specificity was 24% and 78% respectively, for a cut-off
optical density index (ODI) of 1.5. High numbers of false positive results were identified in juvenile cats and in cats
receiving β-lactam antibiotics. Using the same ELISA, GM was measured in dogs with SNA.35 Using a cut-off ODI
of 0.5, 24% of dogs with SNA tested positive, as did 11% of dogs with nasal tumours, 9% of dogs with non-fungal
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rhinitis and 24% of healthy dogs. Overall sensitivity was 24% and specificity was 82%. Currently available antigen
tests cannot be recommended in the evaluation of feline or canine patients with URTA.
TREATMENT
In general, the prognosis for treatment of feline and canine SNA is good, but treatment can be challenging. Since
canine SNA is a noninvasive mycosis, topical therapy is considered more effective than systemic therapy because of
direct contact with fungal plaques.29 However, multiple applications are often required to achieve clinical cure. In a
multicentre, retrospective study of 81 dogs with SNA treated with topical clotrimazole or enilconazole using
catheters placed intranasally and/or via sinus trephination, a single treatment was successful in 47%.32 Techniques
reported to improve efficacy of topical antifungals include endoscopic/sinuscopic debridement of sinonasal fungal
plaques prior to therapy,37 endoscopic guidance of infusion catheters into the caudal frontal sinus37 and use of depot
preparations of 1% clotrimazole or1% bifonazole cream.35 Information on treatment of feline SNA is limited. Of 14
feline cases with available follow-up, signs resolved in 11 (78%).4, 8,12,20,34 The most common successful treatment
regimes were systemic antifungal therapy alone (triazole +/- amphotericin-B) (n = 5), systemic triazole therapy
combined with topical intranasal clotrimazole (n = 2) or topical therapy alone (single 1% intranasal clotrimazole
infusions) (n = 2). Similar to canine SNA, the importance of debridement of fungal plaques is illustrated by
resolution of signs in one case34 after rhinoscopy and sinonasal cavity lavage and in another after
sinusotomy/rhinotomy and instillation of iodoform paste.4 Also, debridement of gross fungal plaques in cats with
SNA treated with systemic antifungal therapy could have contributed to treatment success.12 Presence or absence of
orbital involvement in cats with URTA has important prognostic significance. Few cases of SOA have been treated
successfully despite aggressive therapy including orbital exenteration and use of newer generation fungicidal
triazoles (posaconazole or voriconazole), liposomal amphotericin-B and the echinocandin micafungin.5, 7, 10-12, 15
Fluconazole should not be used for treating feline URTA because most species in the Aspergillus fumigatus complex
are resistant in vitro.12, 26 Posaconazole or itraconazole are recommended for first-line therapy. The pharmacology of
posaconazole has not been determined in cats but it is well tolerated after oral administration.12 Although isolates
show in vitro susceptibility to voriconazole, this drug should not be used initially due to the reported high frequency
of adverse neurological events.9-10, 12 Where disease is confined to the nasal cavity topical treatment is also
recommended. For SOA use of triazole antifungals in combination with amphotericin-B may improve outcomes.
Molecular ID of fungal pathogens causing feline URTA will enable development of optimal treatment protocols.
References: 1 Black L, et al. Vet Rec 1973; 92; 447. 2Peiffer R, et al. J Am Vet Med Assoc 1980; 176:449. 3Wilkinson G, et al. J Small Anim
Pract 1982; 23:127. 4Goodall S, et al. J Small Anim Pract 1984; 25:627. 5Kano R, et al. Mycoses 2008; 51:360. 6Karnik K, et al. Vet Radiol
Ultrasound 2009; 50:65. 7Barachetti L, et al. Vet Ophthalmol 2009; 12:176. 8Furrow E, et al. J Am Vet Med Assoc 2009; 235:1188. 9Quimby J, et
al. J Vet Int Med 2010; 24:647. 10Smith L, et al. Vet Ophthalmol 2010:13:190. 11Giordano C, et al. J Fel Med Surg 2010; 12:714. 12Barrs V, et al.
Vet J 2012:191:58. 13Halenda RM, et al. Vet Radiol Ultrasound 1998; 38:208. 14Hamilton H, et al. J Am Anim Hosp Assoc 2000; 36:343.
15
McLellan G, et al. J Am Anim Hosp Assoc 2006; 42:302. 16Samson R, et al. In: Aspergillus: molecular biology and genomics, Caister
Academic Press 2010:19. 17Pomrantz J, et al. J Am Vet Med Assoc 2007; 230:1319. 18Pomrantz J, et al. J Am Vet Med Assoc 2010:236:757.
19
Malik R, et al. J Fel Med Surg 2004; 6:383. 20Whitney B, et al. J Feline Med Surg 2005; 7:53. 21Sharp N. In, Greene C (Ed) Infectious Diseases
of the Dog and Cat, 2nd Ed WB Saunders 1998:404. 22O’Gorman CM et al. Nature 2009; 457:471. 23Miller J, et al. PhytoKeys 2011:5:1. 24Sugui J,
et al. J Clin Microbiol 2010;48:220. 25Vinh D, Emerg Infect Dis 2009; 15:1292. 26Alcazar-Fuoli L, et al. Antimicrob Agents Chem. 2008;
52:1244. 27Barrs V, et al. J Vet Intern Med 2007; 21:579 (abstr). 28Peeters D, et al. Vet Microbiol 2008;128:194. 29Peeters D, et al. J Comp Path
2005; 132:283. 30Johnson L, et al. J Am Vet Med Assoc 2006; 228:738. 31Billen F, et al. Can Vet J 2010:51:164. 32Sharman M, et al. J Sm An
Pract 2010:51:423. 33Mathews K, et al J Am Vet Med Assoc 1998; 213: 501. 34Tomsa K, et al. J Am Vet Med Assoc 2003; 222:1380. 35Billen F,
et al. Vet Microbiol 2009; 133:358. 36Whitney J, et al. ACVSc Science Proceedings 2011; 9. 37Zonderland J, et al J Vet Med Assoc 2002;
221:1421.
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