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Ascites with right heart failure in a dog: Diagnosis and management

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A female Labrador dog presented with a history of distended abdomen was subjected for clinical, physical, hemato-biochemical, eletrocardiographic, and ultrasonographic evaluations. Respiratory distress, weakness, fluid thrill on palpation of abdomen, cough, cyanotic tongue, and syncope were the significant manifestations. Elevated levels of creatine kinase, lactate dehydrogenase, alanine amino transferase, and alkaline phosphatase with normal blood urea nitrogen and creatinine were the common serum chemistry findings. Low voltage QRS complexes were the electrocardiographic abnormalities. Classical ground glass appearance of abdomen, and enlarged heart with increased sternal contact were the radiographic findings of abdomen and thorax. Ultrasonography of abdomen revealed floating viscera in the anechoic effusion with engorged and distended hepatic vasculature. 2-dimensional echocardiography revealed dilated right ventricle both on B- and M-mode. Further, insufficiency in mitral and tricuspid valves were recorded on pulsed and color flow Doppler. Hence, right heart failure due to ascites was confirmed, and the condition was successfully managed with losartas, spiranolactone, co-enzyme Q10 and tricholine citrate, and sorbitol.
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Kumar and Srikala/ J. Adv. Vet. Anim. Res., 1(3): 140-144, September 2014 140
Ascites with right heart failure in a dog: diagnosis and management
Karlapudi Satish Kumar1* and Devarakonda Srikala2
1Veterinary Hospital, Sri Venkateswara Veterinary University, Warangal, India;
2College of Veterinary Science, Sri Venkateswara Veterinary University, Tirupati, India.
*Corresponding author’s e-mail: drsatish.ksk@gmail.com
ABSTRACT
A female Labrador dog presented with a history of
distended abdomen was subjected for clinical,
physical, hemato-biochemical, eletrocardiographic,
and ultrasonographic evaluations. Respiratory
distress, weakness, fluid thrill on palpation of
abdomen, cough, cyanotic tongue, and syncope were
the significant manifestations. Elevated levels of
creatine kinase, lactate dehydrogenase, alanine amino
transferase, and alkaline phosphatase with normal
blood urea nitrogen and creatinine were the common
serum chemistry findings. Low voltage QRS
complexes were the electrocardiographic
abnormalities. Classical ground glass appearance of
abdomen, and enlarged heart with increased sternal
contact were the radiographic findings of abdomen
and thorax. Ultrasonography of abdomen revealed
floating viscera in the anechoic effusion with
engorged and distended hepatic vasculature. 2-
dimensional echocardiography revealed dilated right
ventricle both on B- and M-mode. Further,
insufficiency in mitral and tricuspid valves were
recorded on pulsed and color flow Doppler. Hence,
right heart failure due to ascites was confirmed, and
the condition was successfully managed with
losartas, spiranolactone, co-enzyme Q10 and
tricholine citrate, and sorbitol.
Keywords
Ascites, Co-enzyme Q10, Losartas, Right side heart
failure, Spiranolactone
Received : 09 April 2014, Revised: 30 April 2014,
Accepted : 21 May 2014, Published online: 28 May 2014.
INTRODUCTION
Multiple organ disorders, hypoprotenemia (Dabas et
al., 2011; Turkar et al., 2009), and right side heart failure
(Ettinger and Feldman, 2005) are the common causes
associated with ascites in dogs. Ascites may indicate a
serious underlying condition that requires immediate
and rationale treatment, which depends on proper
diagnosis. Literatures on ascites in dogs are readily
available; however, published reports on its association
with right heart failure are dearth in India. The present
paper illustrated the diagnosis and management of
right heart failure associated ascites and its
management in a dog.
CASE HISTORY
An eight years old female Labrador was presented to
the Teaching Veterinary Clinical Complex of the
College of Veterinary Science, Rajendranagar,
Hyderabad, India with the history of persistent
distended abdomen for over a period of time.
Treatment by local vet did not resolve the problem,
except transient relief. History regarding deworming
and vaccination were obscure. Further, it was reported
that the dog was showing respiratory distress, cough
and syncope.
CLINICAL EXAMINATIONS
Close clinical examination revealed severe abdominal
distension, respiratory distress, lethargy, cyanotic
tongue and coughing. Clinical parameters were found
within the normal range. Blood was collected for
complete blood profiling, and the serum was prepared
J. Adv. Vet. Anim. Res., 1(3): 140-144.
Available at- http://bdvets.org/JAVAR
CASE REPORT
OPEN ACCESS
DOI: 10.5455/javar.2014.a15
eISSN 2311-7710
Volume 1 Issue 3 (September 2014)
Figure 1. Ultrasonographic image showing anechoeic
fluid with floating liver
Figure 2. Ultrasonographic image of liver with
engorged portal veins (PV) and hepatic veins (HV)
Figure 3. B-mode echocardiogram note the dilated
right ventricle (RV).
for biochemical analysis using commercially available
diagnostic kits. Peritoneal fluid was collected
aseptically through paracentesis abdominis using
sterile disposable syringe after administering
dexamethasone at 2 mg/kg body weight, im, to
prevent untoward effects such as shock. The aspirated
fluid was subjected to physical, cytological and protein
analysis by standard methods. Fecal sample was also
analyzed to reveal out severity of endoparasitic
infestation. Further, the dog was subjected to
radiography, electrocardiography, ultrasonography,
and 2-dimensional echocardiography. Using color
Doppler machine in echocardiography, quantitative
dilatation was confirmed comparing with the right
ventricle of apparently healthy dog of same age, breed
and sex that was maintained at similar managemental
practices.
The hemoglobin (Hb; 5.8 g/dL) and total erythrocyte
count (TEC; 7.8x106/mL) were slightly decreased with
a normal level of total leukocyte count (TLC;
10.4x103/mL) and differential leukocyte count (DLC;
neutrophil68, lymphocyte29, monocyte01, and
eosinophill02). Moderately decreased level of total
protein (4.12 g/dL), albumin (3.04 g/dL) and increased
alanine amino transferase (ALT; 78.60 U/L) and
alkaline phosphatase (ALP; 128 U/L) were recorded.
Also, increased levels of creatine kinase MB (72.4 U/L)
and lactate dehydrogenase (LDH; 346.84 U/L) were
noticed; these were suggestive for heart failure
associated ascites. Low levels of TEC and Hb with
eosinophilia could be associated with hook worm
infestation, resulting in microcytic hypochromic
anemia, as the fecal samples of this dog revealed ova of
Ancylostoma sp. (+++). The aspirated peritoneal fluid
was colorless, transparent, and odorless with a mean
protein content of 2.8 g/dL, specific gravity of 1.010
and cellular content of 1350/cmm; these findings
suggested the fluid as transudate (Tarn and Lagworth,
2010).
The electrocadiographic findings revealed low voltage
QRS complexes, which were suggestive of effusion in
body cavities. Abdominal radiograph revealed “ground
glass” appearance, which is considered as a classical
appearance in ascitic abdomen. Further, gross enlarged
heart with increased sternal contact was recorded on
thoracic radiograph; this could be attributed to right
ventricle enlargement. Abdominal ultrasonography
revealed floating viscera in the anechoic abdominal
fluid (Figure 1). No abnormal echogenicity was noticed
with the abdominal organs such as spleen, kidney and
bladder, except liver; where there was presence of
hyperechoic to mixed echogenecity indicative for
hepatic disease. Further, the liver was greatly engorged
with dilated portal and hepatic veins with hyperechoic
focal areas and rounded borders of hepatic lobes
(Figure 2); these were suggestive for hepatomegaly
associated with congestive heart failure.
Figure 4. M-mode echocardiogram of RHF dog note the
dilated right ventricle (RV) on par with left ventricle (LV).
Figure 5. M-mode echocardiogram of healthy dog - note the
lumen of right ventricle (RV), left ventricle (LV).
Figure 6. Pulsed wave Doppler image at mitral valve note
the jet like turbulent flow.
2-d echocardiography revealed enlarged and globose
heart with dilated right ventricle on right parasternal
short axis view on B-mode (Figure 3). Whereas, M-
mode showed a relatively increased right ventricle
lumen in both diastole and systole condition (Figure 4)
as compared to that of healthy dog (Figure 5). Further,
pulsed wave and color flow Doppler of the mitral and
tricuspid valves revealed jet like turbulent flow (Figure
6) and mosaic pattern of color (Figure 7) respectively;
these were suggestive for valvular insufficiency and
regurgitation that might be due to pulmonary
hypertension and right heart failure.
TREATMENT & MANAGEMENT
Based on the above findings, ascitic dog was diagnosed
for hepatic congestion and right side heart failure. The
condition was treated with angiotensin receptor
blockers (losartas, at 25 mg, sid, 90 days), aldosterone
blockers (spiranolactone, at 5 mg/kg, bid, 30 days),
syp. sorbiline (tricholine citrate and sorbital) and
nutriceutacle (co-enzyme Q-10, 1 tab for 90 days). After
5 days of giving therapy, slight improvement in
physical activity, appetite and general health condition
observed. Disappearance of abdominal distension and
complete clinical recovery were recorded on day 90, no
sign of recurrence was noticed within this time.
DISCUSSION
The clinical and hematobiochemical alterations noticed
in the present study were in agreement with Tarn and
Lapworth (2010). Low voltage QRS complexes with
reduced R wave amplitude was considered as
significant electrocardiographic abnormality of ascites
dogs, as described by Ettinger and Feldman (2005). In
many animals with a long history of mitral valve
insufficiency, pulmonary hypertension and right side
heart failure might be developed. In the cases of mitral
valve insufficiency, the right side heart failure might be
occurred as secondary due to persistent elevation of left
atrial and pulmonary venous pressures. As the wall of
right ventricle is thinner and more compliant as
compared to the left ventricle, it can be increased in
volume; however, this caused a decreased stroke
volume.
As a consequence of increased right atrial pressure,
ascites, pleural, pericardial effusion, hepatomegaly and
splenomegaly might be developed. The common
manifestations of right heart failure are respiratory
distress, abdominal distension due to ascites, hepato-
or splenomegaly (Haggstrom, 2010). The disease
process that led to heart failure might not show clinical
sign, as in early heart disease, the heart is often able to
Figure 7. Color Doppler image at mitral valve note the
mosaic pattern of color development.
compensate for changes in volume and pressure.
Congestive heart failure (CHF) occurs when the heart is
no longer able to compensate. Systemic congestion may
result from the impaired blood flow returning to the
right heart from the body. Blood backs up and fluid
leaks through the vessels into other parts of the body
resulting to ascites, pleural and pericardial effusion
(Antran et al., 2005).
Signs of right heart failure (abdominal and pleural
effusion) might be alleviated with diuretics, and two or
more drugs might be used to obtain sequential
blocking of nephron (Antran et al., 2005). When
pumping efficiently of heart is lessened, fluid retention
in the body cavities of dog eventually leads to complete
heart failure. Losartan potassium was the first orally
bioavailable, long-acting, nonpeptide AT-II type 1-
receptor antagonist to be used in humans. The drug is
absorbed rapidly from the gastrointestinal tract.
Losartan undergoes first-pass hepatic metabolism via
cytochrome P-450 (CYP) isoenzymes 2C9 and 3A4 to its
active carboxylic acid metabolite (Raquel and Mahtab,
2000). Administration of losartan per day is possible as
the drug's effects are extended by the EXP-3174
metabolite and has been found to produce consistent
reductions in blood pressure over a 24 h period. The
usual starting dosage of losartan potassium is 25-50 mg
once daily. However, the dosage should be reduced to
25 mg once daily in the patients having liver function
impairement.
Aldosterone receptor blockers (at 0.5 mg/kg) were
used in human for the treatment of heart failure, are
thought to be effective by blocking the remodeling
effects of aldosterone (Borgarelli and Haggstrom, 2010;
Atkins et al., 2009). The aldosterone antagonist,
spironolactone, has received renewed interest with a
report that survival was prolonged in humans with
heart failure when spironolactone (0.3 mg/kg QD) was
administered concurrently with conventional therapy
in NYHA phase IV patients (Clarke, 2007).
Co-enzyme Q10, also known as ubiquinone, is essential
for energy production at the cellular level. It helps the
body to produce energy by two ways; one: by helping
cell to produce enzymes that is used to generate
energy, and two: by creating energy directly. In the
cases of insufficient coenzyme Q10, heart could be
weakening leading to malfunction of heart due to
inadequate blood circulation. In older animals, this is
especially critical as production of coenzyme Q10
drops with the advancement of age (Harkeret al., 2000).
CONCLUSIONS
Right side CHF could be one of the probable causes for
ascites in dogs (as the condition is manifested by
pleural, pericardial and abdominal effusion) that
requires special attention and the suspicion never be
ignored. Aldosterone blockers (diuretics) along with
angiotensin receptor blockers, cardiac neutraceuticles
and hepatoprotectives can be considered as effective
therapeutic agents to treat right heart failure in dog.
ACKNOWLEDGEMENTS
The authors are thankful to the Vice Chancellor, Sri
Venkateswara Veterinary University, Tirupati for
providing research facilities at the Teaching Veterinary
Clinical Complex, Bhoiguda.
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... Owczarek-Lipska et al. (2013) Cerabasi et al. (2013) found that the most prominent and reliable clinical findings in pleural and pericardial mesothelioma were respiratory distress which results from the pleural exudation, impaired cardiac output due to diastolic failure and abdominal distension due to peritoneal fluid accumulation. Kumar and Srikala (2014) reported respiratory distress, weakness, fluid thrill on palpation of abdomen, cough, cyanotic tongue, and syncope as significant manifestations in dogs suffered from right sided heart failure. Lopez-Alvarez et al. (2015) found that data obtained from history and physical examination, specifically history of cough, exercise intolerance, inappetance, dyspnoea and syncope as well as murmur grades louder than III/VI and loss of respiratory sinus arrhythmia were independent indicators of disease progression for DMVD. ...
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ACVIM Consensus Statement Consensus Statements of the American College of Veterinary Internal Medicine (ACVIM) provide the veterinary community with up-to-date information on the pathophysiology, diagnosis, and treatment of clinically important animal diseases. The ACVIM Board of Regents oversees selection of relevant topics, identification of panel members with the expertise to draft the statements, and other aspects of assuring the integrity of the process. The statements are derived from evidence-based medicine whenever possible and the panel offers interpretive comments when such evidence is inadequate or contradictory. A draft is prepared by the panel, followed by solicitation of input by the ACVIM membership, which may be incorporated into the statement. It is then submitted to the Journal of Veterinary Internal Medicine, where it is edited prior to publication. The authors are solely responsible for the content of the statements. © 2009 by the American College of Veterinary Internal Medicine.
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Background: Coenzyme Q10 (CoQ10) is essential for ATP generation and has antioxidant properties. Decreased CoQ10 levels have been reported in human heart failure (CHF), but it remains unclear if this is a conserved feature of CHF. The objective of the study was to determine if tachycardia-induced CHF in the dog is associated with reduced CoQ10 levels. Furthermore, it was hypothesized that CoQ10 supplementation may improve CHF severity by preventing CoQ10 deficiency (if present) or via antioxidant effects. Methods and results: Serum and myocardial levels of CoQ10 were examined in normal dogs (n = 6), dogs with CHF (control, n = 5), and dogs with CHF treated with CoQ10 (CoQ10; 10 mg/kg/day, n = 5). Serum CoQ10 levels did not change with CHF in control dogs, and myocardial levels were similar to those of normal dogs. CoQ10 therapy increased serum but not myocardial levels of CoQ10. In early CHF, CoQ10-treated dogs had lower filling pressures, and, in severe CHF, CoQ10-treated dogs had less hypertrophy as compared with untreated dogs. Other indices of CHF severity were similar in control and CoQ10-treated dogs. Conclusion: These data indicate that CoQ10 deficiency is not present in this model of CHF. Although dramatic effects on hemodynamics were not observed, CoQ10 supplementation did appear to attenuate the hypertrophic response associated with CHF. Key words: enzymes, cardiomyopathy, hormones, antioxidant.
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Myxomatous mitral valve disease is a common condition in geriatric dogs. Most dogs affected are clinically asymptomatic for a long time. However, about 30% of these animals present a progression to heart failure and eventually die as a consequence of the disease. Left atrial enlargement, and particularly a change in left atrial size, seems to be the most reliable predictor of progression in some studies, however further studies are needed to clarify how to recognize asymptomatic patients at higher risk of developing heart failure. According to the published data on the natural history of the disease and the results of published studies evaluating the effect of early therapy on delaying the progression of the disease, it seems that no currently available treatment delays the onset of clinical signs of congestive heart failure (CHF). Although the ideal treatment of more severely affected dogs is probably surgical mitral valve repair or mitral valve replacement, this is not a currently available option. The results of several clinical trials together with clinical experience suggest that dogs with overt CHF can be managed with acceptable quality of life for a relatively long time period with medical treatment including furosemide, an angiotensin-converting enzyme inhibitor, pimobendan, and spironolactone.
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Ascitic fluid samples are frequently sent to the laboratory for analysis. Although the underlying cause of the ascites is often thought to be clinically obvious, it is important to establish a definitive diagnosis. The value of a cell count and bacterial culture of the ascitic fluid is not disputed, but the role of biochemical testing is less clear. The use of ascitic fluid total protein to try to classify ascitic fluids as either an exudate or a transudate has contributed to this. The use of the physiologically based serum ascites albumin gradient to differentiate ascites caused by portal hypertension from other causes provides a better diagnostic approach. We recommend that the serum ascites albumin gradient is performed by laboratories as the first-line test and that interpretative reports are provided. Additional testing should be restricted to specific diagnostic queries and requires close collaboration between the laboratory and the clinician.
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Text book of Veterinary Internal Medicine; Disease of Dog and Cat.VI edn
  • S J Ettinger
  • Feldmanec
Ettinger SJ, FeldmanEC (2005). Text book of Veterinary Internal Medicine; Disease of Dog and Cat.VI edn. WB Saunders, Philadelphia; pp 137-145.
Myxomatous mitral valve disease. In: BSAVA Manual of Canine and Feline Cardiorespiratory Medicine 2 nd Edn
  • J Haggstrom
Haggstrom J (2010). Myxomatous mitral valve disease. In: BSAVA Manual of Canine and Feline Cardiorespiratory Medicine 2 nd Edn., Luis Fuentes V, Johnson LR, Dennis S; pp 186-194. British Small Animal Veterinary Association, Gloucester.
Ascites associated with ancylostomiasis in a pup: A case report
  • Turkars
  • Cs Randhawa
  • Sk Uppal
TurkarS, Randhawa CS, Uppal SK (2009). Ascites associated with ancylostomiasis in a pup: A case report. Intas Polivet, 10:357-359.
Text book of Veterinary Internal Medicine; Disease of Dog and Cat
  • Antran De Morais
  • Helio
  • D S Schwarz
Antran de Morais, Helio, Schwarz DS (2005). Pathophysiology of Heart failure. In. Ettinger SJ and Feldman EC (Edn.). Text book of Veterinary Internal Medicine; Disease of Dog and Cat.VI Edn., WB. Saunders Co., Philadelphia; pp 914-940.