FIRST REPORTED CASE OF SYMPTOMATIC DIROFILARIA IMMITIS INFECTION IN A HOUSOLED DOMESTIC FERRET (MUSTELA PUTORIUS FURO) IN BULGARIA.

32480642_1950070525005966_7673581144482250752_nMihaylova L. DVM1.

1Veterinary surgeon in United Veterinary Clinic Bulgaria Varna 9000,

email: lillyvet@gmail.com

Heartworm disease in dogs and cats is well known in many European countries including Bulgaria. There are furthermore studies confirming dirofilariosis in wild foxes and Canis aureus i reports about heartworm disease in domestic ferrets in our country.

History

A 5 year old male, entire, pet ferret (Mustela putorius furo), weight 0,9 Kg was presented with labored abdominal breathing. The owner reported reduced appetite, difficulty breathing and restlessness. The ferret was not able to sleep or lie down for more than few minutes.  The ferret was used to live mainly indoor and allowed during the summer to be outside in the garden, for just few hours during the day, to be exposed to natural sunlight.

Clinical presentation and collateral exams

On presentation ferret was lethargic with abdominal breathing and breathing rate up to 90/minute. There was clear subcutaneous edema more prominent on the front and hind legs and ventral part of the abdomen. Mucous membranes were pale, while CRT was not possible to be assessed. Heart rate ranged in between 120-180 bpm. Pulses were weak even if assessing on the femoral artery was difficult due to the subcutaneous edema. Abdominal palpation was unremarkable, lymph nodes were normal in size. Thoracic radiograph showed loss of detail into thoracic cavity consistent with pleural effusion. Thoracic US was performed confirming pleural effusion and one hundred and twenty ml of modified transudate was drained. Brief screening echocardiography showed normal left atrium and left ventricle and severely dilated right atrium containing double line hyperechoic objects suggesting the presence of few adult Heartworms. (Fig 1). Right atrium was larger than left atrium. Doppler study and any further detailed investigation of the heart were not possible to be performed due the fact ferret became aggressive and owner declined any sedation or anesthesia. Snap® HTWM Antigen test (Idexx) on blood yielded negative result and at fresh blood smear examination no microfilariae were possible to be identified.  Knott test was not possible to be performed due to limited amount of sampled blood.

Diagnosis

On the basis of echocardiography findings diagnosis of HW disease was done.  Negative HW antigen test was assumed to be due probably due to juvenile D.immitis worms and right atrium localization to the small size of pulmonary arteries as described in cats and ferrets.

Therapy and Follow up

The ferret was treated with Advocate® spot on >4kg (half tube), Furosemide 2mg/kg twice a day and Prednisolone 1mg/kg daily both of them orally. The ferret was stable on that therapy. He was eating and drinking well regain the normal body weight 1.5 kg. no breathing difficulties were reported. He was rechecked 35 days after initial presentation. Echocardiography showed right mildly dilated atrium but no presence of HW (Fig 2). Only 10 ml of fluid was drained from the thoracic cavity. From that time he was stable with no owners complain for 6 month. Suddenly he developed respiratory distress and on presentation was with cyanotic membrane. Pulmonary thromboembolism connects to HW disease was suspected Owner elected euthanasia and no more investigations. Necropsy was declined.

Comments

1

Fig 1

2

fig 2

This case shows the in endemic area even indoor domestic ferrets may be infected by Dirofilaria immitis. and that the disease is difficult to be diagnosed and can lead to death. Suspicion about this problem and monthly chemoprophylaxis should be warranted in this situation as in dogs and cats.

Diagnosis and therapeutic management in a a dog with severe cardiac dilatation associated with complex arrhythmias – A case report.

18033866_664669780384620_7541915442490356035_n

Dr Vasile Vulpe

33023039_1831545640221964_5476404995450470400_n

Dr Andrei Baisan

Radu Andrei BAISAN, Vasile VULPE

Clinics Department, Faculty of Veterinary Medicine, University of Agricultural Sciences and Veterinary Medicine “Ion Ionescu de la Brad”, Iași, Romania

Baisan.andrei_mv@yahoo.com

Cardiac dilatation is a common finding in dogs with heart disease. Chronic myocardial stress and volume overload are the main reasons for cardiac remodeling. These changes are encountered in most of chronic diseases such as dilated cardiomyopathy, mitral valve disease or congenital disease that develop volume overload. Cardiac dilatation should not be confused with dilated cardiomyopathy (DCM), which is known to be a myocardial disease induced by several specific factors such as genetic or familial predispositions. In the absence of specific signs, such as mitral valve degeneration or congenital heart diseases, cardiac dilatation should be carefully evaluated and additional tests must be performed before deciding the diagnosis and therapy. In veterinary medicine, there is insufficient data regarding the differential diagnosis of cardiac dilatation when specific sins are absent.

The aim of this paper is to report and discuss a patient with congestive heart failure due to severe cardiac dilatation associated with multiple arrhythmias and to describe the diagnostic protocol, therapy and evolution of the disease.

Case presentation

An eleven years male, German Shorthaired Pointer dog, weighing 38 kg, was referred for a second opinion to our Cardiology Service from the Teaching Hospital of the Veterinary Faculty of Iași, because of chronic abdominal fluid accumulation, severe effort intolerance and weight loss for the past few months. The dog was receiving cardiac therapy assigned by the referring clinician and consisted of pimobendane (Vetmedin® Boehringer Ingelheim), 0.25 mg/kg P.O. BID and furosemide (Furosoral, Artesan Pharma GmbH & Co.), 2 mg/kg P.O. BID. The owner reported that the dog had been treated for Babesia canis for four times in the past few years.

During the first visit, the dog was subjected for complete cardiologic examination consisting of physical examination, five minutes six leads electrocardiography (PolySpectrum veterinary device), blood pressure measurement (Vet-HDO blood pressure device), cardiac ultrasonography (Logiq V5, General Electric), cardio-thoracic radiography (Intermedical Basic 4006 X-ray machine and Examion X-CR smart digital developing machine) and biochemical and CBC blood analyses as previously described [1-4].

Physical examination showed pink mucosal membranes, with a CRT of 3 seconds, abdominal distension, breathlessness, with a normal respiratory rate (28 bpm), strong and arrhythmic cardiac beats, without precordial thrill. The palpation of the femoral artery revealed weak asynchronous arterial pulse. Auscultation revealed an arrhythmic rhythm and III/VI systolic plateau left apical murmur. Auscultation of the lungs revealed crackles in both sides of the caudal lung lobes.

Electrocardiography revealed an arrhythmic rhythm with a median heart rate of 130 bpm, with more types of arrhythmias present over the five minutes ECG tracing. The predominant rhythm was accelerated idioventricular rhythm, with a heart rate of 168 bpm, interrupted by runs of supraventricular tachycardia, with a heart rate of 240 bpm and sinus tachycardia with a heart rate of 165 bpm (Fig no 1).

Fig no 1

Fig 1. Six leads ECG at 50 mm/sec and 5 mm/mV of an eleven years old dog with signs of congestive heart failure. The main rhythm is represented by an accelerated idioventricular rhythm (black arrowhead), with a heart rate of 168 bpm, interrupted by left ventricular premature complexes (red arrowhead) and fusion beats (star)

Fig no 2

Fig 2. Six leads ECG at 50 mm/sec and 5 mm/mV of the same dog with signs of congestive heart failure. Sequences of supraventricular rhythm are visible, with a heart rate of 240 bpm and sparse sinus complexes (star); also, one left ventricular premature complex is present on the tracing (diamond) and junctional beats with retro-conducted P’-waves (arrow);

Fig no 3-1

Fig 3. Six leads ECG at 50 mm/sec and 5 mm/mV of the same dog with signs of congestive heart failure. An atrial beat is present with a small P-wave (star), followed by 3 RBBB aspect complexes and a fusion beat. The black horizontal arrow marks the beginning and the end of fast supraventricular tachycardia consistent with atrial fibrillation, followed by another fusion beat (diamond);

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

There were also present runs o junctional beats with a retro-conducted P-wave. Between these sequences of arrhythmias, there were present 25 left ventricular premature complexes, with the same morphology, with a negative polarity in DII, DIII, and aVF and positive polarity aVR and aVL. These complexes had a length of 120 msec and a tall, opposed T-wave. Multiple fusion beats were also present (Fig no 2 and 3).

 

 

 

 

 

 

 

 

 

 

 

 

The blood pressure measurement was performed with a D1 cuff placed on the tail and simultaneous recording of the pulsating-wave graphic. However, measurements of the blood pressure were not accurate due to the differences in the pulsating wave.

Fig no 6

Fig nr. 6 Echocardiographic M-mode in right parasternal short axis view through the papillary muscles of the left ventricle of the same dog with signs of congestive heart failure. Arrhythmic contractions of the left ventricle are visible. The free wall and septum appear thinned and the ventricular cavity is enlarged in both systole and diastole. The measurements were performed when the rhythm was supraventricular. The shortening (SF%) and ejection (EF%) fractions are within normal limits.

figg 4

Fig 4

figg 5

Fig 5

Cardiac ultrasonography revealed severe left ventricular dilatation during systole (39.6 mm 95%CI 15.8-17.18 mm) and diastole (64.2 mm, 95% CI 37.64-39.1 mm), with thinned interventricular septum and ventricular free wall and severe left atrial dilatation, with a LA/Ao ratio of 2.54 (normal upper limit 1.6). Also, the left auricular cavity was visibly enlarged. The mitral valve was thin with normal echoic appearance and abnormal motion due to the hemodynamic changes induced by the underlying arrhythmia and a regurgitating jet was observed by color doppler. The left ventricle systolic function was within normal limit, when assessed during supraventricular rhythm (SF%=38, EF%=67). The pulmonary and aortic flow were laminar, within normal ranges. There were no signs of pulmonary hypertension. The pericardium was normal, without fluid accumulation (Fig no 4-6).

Fig nr. 4 Echocardiographic left parasternal long axis apical four chamber view of an eleven years old dog with signs of congestive heart failure. The LA and LV are visible enlarged and the mitral valve leaflets appear normal. LV-left ventricle; LA-left atrium; RV-right ventricle; RA-right atrium;

Fig nr. 5 Echocardiographic right parasternal long axis oblique four chamber view optimized for the left atrium of the same dog with signs of congestive heart failure. The LA and Lau appear visible enlarged. LV-left ventricle; LA-left atrium; LAu-left auricle

 

xray

Fig nr. 7 Left lateral chest radiography of an eleven years old dog with signs of congestive heart failure. The cardiac silhouette is visibly enlarged with dorsal displacement of the trachea and a perihilar pulmonary interstitial and alveolar pattern is visible extending in the caudal lung lobes. A round radiopaque mass is visible on the lower cranial abdomen

A left lateral thoracic X-ray was available for examination and revealed severe cardiomegaly, with a VHS of 13.3v. The trachea was dorsally displaced and a perihilar pulmonary interstitial and alveolar pattern was visible in the caudal lung lobes consistent with moderate cardiogenic pulmonary edema. A round radiopaque area was present over the gallbladder topography and a gallbladder stone was suspected (Fig no 7).

 

Blood biochemical analyses were within normal ranges except a moderate hypoalbuminemia (2.5 g/dL normal ranges 2.6-4 g/dL) and moderate increased alanine aminotransferase (58 UI/L, normal ranges 8-57 UI/L). Cell blood count was within normal ranges.

The diagnosis consisted of idiopathic dilated cardiomyopathy with supraventricular and ventricular arrhythmias. The current therapy was maintained and amiodarone (Amiodaronă LPH, LABORMED PHARMA S.A.), was added as following: 15 mg/kg P.O. BID for 7 days, followed by 7.5 mg/kg P.O. BID for the next seven days and 7.5 mg/kg P.O. QD for the next fourteen days. The dog was released from the hospital the same day with effort and salt restriction. The reevaluation was scheduled after 2 weeks if no event required a sooner visit.

Three weeks later, the owner called for a reevaluation. The medication was administered according to recommendation and no events were observed during this period. aA significant improvement in the quality of life of the patient was reported.

The dog was alert and active during physical examination, with pink mucosal membranes, CRT of 3 seconds, moderate decreased respiratory rate (36 bpm) and effort, and a less distended abdomen. Palpation of the thorax revealed a strong cardiac beat and the arterial pulse was synchronous with the cardiac beat. Cardiac auscultation showed rhythmic rhythm, with a heart rate of 114 bpm and III/VI systolic plateau left apical murmur.

Fig no 8

Fig 8. Six leads ECG at 50 mm/sec and 5 mm/mV of the same dog with signs of congestive heart failure, performed during reevaluation, 3 weeks later. The predominance of sinus rhythm is visible, with a heart rate of 115 bpm, interrupted by one right ventricular premature complex (star) and one supraventricular complex (arrowhead);

The five minutes six lead ECG tracing revealed a predominant sinus rhythm, interrupted by 107 single supraventricular complexes and only one right ventricular premature complex with positive polarity in DII, DIII and aVF and negative in DI, aVR and aVL. No sequences of supraventricular tachycardia or accelerated idioventricular rhythm were present on the five minutes tracing. The abnormalities in morphology of the sinus beats revealed a mitral P-wave (78 msec), increased amplitude of the R-wave (3.34 mV) and increased length of the QRS complex (91 msec) (Fig no 8).

 

There were no improvements seen during the echocardiographic examination. The owners were instructed to administer the therapy with pimobendane and furosemide continuously and amiodarone until the end of protocol. Eight weeks after the first examination, owners reported by telephone that the patient is alive and the quality of life remained improved.

Discussions

Dilated cardiomyopathy (DCM) can occur as a primary cardiomyopathy such as genetic, or familial DCM [5], or secondary to myocardial stress, such as drug- or toxin-induced, infiltrative, ischaemic, metabolic, nutritional, or inflammatory myocardial diseases [6]. In both cases, DCM is expressed through a disease of the myocardium associated with ventricular systolic and diastolic dysfunction and development of congestive heart failure [5]. According to ESVC Taskforce for Dilated Cardiomyopathy, 2003, scoring system, the score in this dog was above 6 points, which is consistent with the presence of DCM  [5]. The left ventricular internal diameter in both systole and diastole were above the 95% CI based on the regression formula [7], the sphericity index was under the lowest recommended limit and left atrial enlargement was present. However, there were some changes that did not seem to be associated with primary DCM. The shortening and ejection fraction were within normal ranges and the large range of arrhythmias was not consistent with specific morphologic and rhythm changes in primary DCM. It has been suggested that atrial fibrillation is the most common arrhythmia in dogs with DCM and also, increased number of ventricular premature complexes may have diagnostic value [5, 8]. Nevertheless, it must be considered that the dog was treated with positive inotropic medication which may have influenced the systolic function of the heart. Another unexpected result was the intense positive response to arrhythmic therapy. Amiodarone is an antiarrhythmic agent with primarily class 3 action, but also potent class one. This agent prolongs the action potential duration and the effective refractory period in all cardiac tissues. It is recommended in dogs with ventricular arrhythmias and has also been used to convert atrial fibrillation to sinus rhythm [9].

The differential diagnosis for cardiac dilatation should include secondary DCM due to cardio-toxicosis, drug-induced, metabolic or nutritional factors, chronic myocarditis or tachycardia-induced cardiomyopathy (TIC). Secondary DCM is difficult to diagnose due to the multiple factors of environment and microclimate. A large series of pathogens have been reported to induce chronic myocarditis, including canine babesiosis [10-15]. However, in most studies, the etiological diagnosis was reached through histopathological examination of the cardiac tissue after patient’s death [16]. Considering the four episodes of clinical manifestation of canine babesiosis in this patient, cardiac enlargement may be related to this. Tachycardia-induced cardiomyopathy is characterized by cardiac dilatation and systolic and diastolic dysfunction due to long-term increased heart rate, however these changes may be easily confused with DCM. Clinical studies in human medicine have suggested that the left ventricle internal diameter and volume are significantly smaller in patients with TIC than in those with DCM [17]. Another difference between the two pathologies is that the ventricle remodeling during TIC may benefit from partial or total reversibility once the arrhythmia control is achieved [18]. In the patient discussed in this paper, we observed a significant improvement in controlling the rhythm and heart rate after the antiarrhythmic therapy but not in the cardiac remodeling. It remains unclear whether the arrhythmias were induced by the myocardial structural changes during the progression of heart remodeling or if the dilatation was induced by a chronic supraventricular tachyarrhythmia which later developed ventricular complexes and accelerated idioventricular rhythm.

Conclusions

Dilated cardiomyopathy is a common cardiac disease in large breed dogs, however differential diagnosis must be considered when cardiac dilatation is present, in the absence of any certain factors. The dog from this report had cardiac dilatation associated with severe arrhythmia. Although an etiologic diagnosis could not be established, we succeeded to improve the quality of life by controlling the heart rate and the rhythm.

The reference list is available at baisan.andrei_mv@yahoo.com

Open heart surgery for a left atrial mass extraction during cardio-pulmonary bypass (CPB) in a 9 yoa Labrador dog

ranko

Dr Ranko Georgiev

Ranko Georgiev1, Stoyan Nikolov2, Nadezhda Petrova3

Georgi Ignatov4, MD Thoracic Surgery

1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria

4 MD, City Clinic Cardiovascular Center, Sofia, Bulgaria

1rankoge@gmail.com

 

Introduction:

 

Open heart surgery during a cardiopulmonary bypass is the only effective approach for some diseases that require an access to the heart chambers or the great vessels; even when a temporary inflow occlusion is chosen as an alternative, only a very few “time restricted” procedures could be done on a beating heart. However, when considering an open heart surgery, the high risk of intra- and post- procedure complications often outweighs the benefits. In veterinary medicine the financial weight of such a procedure is also a limiting factor.

We would like to share a case where a temporary sinus arrest was induced during a cardiopulmonary bypass and a huge mass was successfully extracted from the left atrium of a dog with an open heart approach.

 

Case presentation:

 

Artur 1

This is the patient just before the surgery

Arthur is a 9 year old MC Labrador, trained like a guide dog for a blind person, admitted because of increasingly frequent exercise intolerance episodes during the past few months. Furthermore, the last week the patient was very weak and experienced several syncopal episodes. On a clinical presentation with the referring vet а tachycardia and dyspnea were noted and the patient was referred to us for a Cardiology consult.

On physical examination, the dog weighted 25 kg, with a history of a rapid body mass loss for the last couple of months. His “normal” weight has always been around 32 kg according to the owners. The body condition was poor (score 2/5) and the dog had a grade II/VI left sided apical soft diastolic heart murmur. Lung auscultation was unremarkable, but the respiratory rate (RR) was more than 50 breaths per minute.Artur VD

Artur LLR

 

 

 

 

 

 

 

 

 

 

The X-rays of the chest were highly suggestive for e left sided congestive heart failure and showed mild generalized cardiomegaly with a VHS of 11.5 with enlarged left atrium and left ventricle. The pulmonary veins were slightly larger than the pulmonary arteries; the lung parenchyma with diffuse interstitial pattern in the area of the hilus. The patient was already on Furosemide in a low dose – 2mg/kg twice a day for the last two weeks with no improvement of the clinical signs.

 

 

A transthoracic echocardiography was done with the patient in lateral recumbence through the right and left parasternal windows. A huge echogenic mass with irregular shape was observed in the area of the left atrium – attached to the intra atrial septum and prolapsing through the mitral valve during diastole towards the left ventricle. The mass was creating almost full diastolic obstruction of the valve, allowing only a tiny fraction of the blood in.Artur_Ochi_na_4_lapi_20161116113435_1139400 Artur_Ochi_na_4_lapi_20161116113435_1140250 Artur_Ochi_na_4_lapi_20161116113435_1147090 Artur_Ochi_na_4_lapi_20161116113435_1837270 Artur_Ochi_na_4_lapi_20161116113435_1837510

Complete blood count, electrolytes and biochemical profile were normal. During the abdominal US study no further abnormalities were noted and no more masses found. On the ambulatory ECG a normal sinus rhythm was recorded with multiple atrial premature complexes. The blood pressure was normal. A hemo-culture and a urine culture were obtained and came back negative for a bacterial growth. The bleeding time and the Pt/APtT were normal.

A diagnosis of an intra atrial mass with clinical signs of a progressing left sided congestive heart failure was made and a surgery was discussed. Because of the location of the mass no surgical or interventional approach was possible without the aid of a cardiopulmonary bypass (CPB) and cardioplegia. All the risks and possible complications were discussed with the owner and a decision for such a surgery was made. The team for the surgery was from a veterinary surgeon, human cardiovascular surgeon, cardiovascular perfusionist, veterinary and human anesthetists, and nurses. The procedure was done in Central Vet Clinic, Sofia on 3rd of December 2016.

 

 

 

Artur 3

The heart-lung machine with 4 pumps – one main pump for the oxygenator and the blood, two for collecting the surgical field blood and one for the cardioplegique solution; the model is Sorin 5 with a pediatric small volume oxygenator

Our anesthesia protocol with this patient started routinely for the procedure of a thoracic surgery – premedication with Midazolam and Buprenorphine, induction with Etomidate, intubation and maintenance with Isoflurane. Additionally we put a bladder catheter for urine production measurement, central venous catheter, an intra-arterial catheter for a direct blood pressure measurement and tree peripheral intra-venous catheters. Many more drugs were used during the anesthesia and the long post-operative recovery period like Nitroglycerin, Atracurium, Protamine, Amantadine, Pyracetam, Efedrin, Dopamine, Methylprednisolone, Fraxiparin, Clopidogrel, antibiotics, etc.)

Artur 2

The busy surgical field – left lateral thoracotomy through the 5th intercostal space; visible are the venous, the arterial and the cardioplegique cannulae

Artur 7

the surgical ward during the procedure – a total of 10 people were simultaneously engaged in the procedure

Artur 5

the surgical ward during the procedure – a total of 10 people were simultaneously engaged in the procedure

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Artur 6

he extracted mass from the left atrium – Neurofibrosarcoma with size 8/6/4 cm

The surgical approach was through the left fifth intercostal space with a standard lateral thoracotomy. Additionally the left carotid artery was approached and prepared in case it is needed for the CPB blood return. The pericardium was excised and the left atrium, the big vessels and the left ventricle visualized. Then three cannulas were put – the one collecting the venous blood inside the right atrium (through the right atrium auricle), the one returning the oxygenated blood from the CPB machine into the ascending aorta and one small cardioplegique cannula into the aortic root over the coronary arteries. Then a bolus of Heparin was injected iv in a dose of 800UI/kg and 5 minutes later the patient was switched to the heart-lung machine (Sorin 5 and a pediatric oxygenator with 360 ml prime). Then we started a controlled cooling of the patient using a chiller, connected to the CPB machine. When the target body temperature of 28o C was reached the ascending aorta was cross clamped and a 600 ml of cooled to 4o C crystalloid cardioplegique infusion rich in potassium was infused through the coronary cannula producing complete heart arrest. We stopped the active ventilation of the lungs and the patient became fully dependent of the heart-lung machine. The heart was open through a 5 cm cut into the left atrial wall starting from the auricle tip. The mass was directly visualized and excised. It was connected to the intra atrial septum with a relatively small neck. We removed it without creating an ASD. The air from the heart was evacuated and the surgical cut closed with a 5-0 Polypropylene suture in a continuous way. The mass was a solid and well defined structure with irregular shape and was admitted for histology. The size was 8/6/4 cm.

We started a slow rewarming of the patient with a target body temperature of 38o C. Two epicardial electrodes were embedded and connected with an external pacemaker. Once closed and warmed, the heart was gently massaged manually for a couple of minutes and then hit with a direct pediatric defibrillator. We used 5 to 20J of energy shocks and got a slow and then faster rhythm after the 9th try. The external pacemaker was switched on and put on a 100 bpm rate for the next 12 hours. The surgical closure was uncomplicated and no significant bleeding was noted. The patient received slowly iv Protamin (1mg/100IU Heparin) as a Heparin antidote and the heart-lung machine was gradually restricted and then switched off. Two chest drains were put and connected to a sterile active suction. The total machine time was 130 min, the sinus arrest time – 22 min, total surgery time – close to 5 hours. Immediately after the CPB machine was stopped a hemotransfusion with two units of fresh blood was done.

Artur 10

the first 12 hours post the procedure Artur was kept on a Propofol CRI and with an external pacemaker set at a minimum of 100 bpm rate

Artur 9

the first 12 hours post the procedure Artur was kept on a Propofol CRI and with an external pacemaker set at a minimum of 100 bpm rate

Comments:

 

Arthur recovered from the general anesthesia slowly over the next 12 hours, but he was unable to stand on his feet for additional 5 days. The electrolyte levels, liver and kidney values were monitored almost every hour for the first 2 days and then three to five times a day; our main concern was the potassium blood level and we tried to maintain it stable at all times. The urine production was also constantly monitored and tailored to be in the normal range – with diuretics and blood pressure control drugs. From all the possible complications after a CPB we saw only a transient neurological signs attributed to some degree of brain injury – interpreted after the neurological exam as left sided forebrain lesion – ischemic or hemorrhagic. Arthur recovered completely both physically and mentally for the next two weeks with a lot of supportive care and physiotherapy. On discharge from the clinic he was able again to do all the things a blind person guide dog is trained to do. The histology report was made in a referral laboratory in Germany – Laboklin, and after the immunohistochemistry stain came back as a Neurofibrosarcoma.ran 2 ran 3

 

 

 

 

 

 

Artur 11

Artur reacted very well when in children company and we use this to stimulate his mental state (the authors’ youngest daughter)

Conclusions:

 

Artur 12

two weeks after the surgery with the owner

CPB is a routine everyday procedure in the human hospitals, usually carrying a good to excellent prognosis and very low mortality rate. On the other hand in the veterinary medicine field is still an exotic and very risky one. Although very demanding both for the clinical team and the patient himself, the cardiopulmonary bypass is the only option for cardiac diseases requiring an open heart surgery. We believe that a close relationship between a human medicine cardio surgical team and a small animal hospital team could make this type of procedures safer and better recognized.

We have done regular monthly rechecks on the patient with echocardiography and X-rays since then and now six months later Arthur is doing great, no drugs or any supportive therapy needed. He gained back his usual weight and is working like a guide dog every day.

 

Rupture of the atrial septum in dog with degenerative mitral valve disease

13549281_10207110414020766_1752592814_o

Dr Todor Kalinov

Dr Todor Kalinov

ZaraVet- city of Plovdiv, Bulgaria

Introduction

Degenerative mitral valve disease (DMVD) is the most common cardiologic disorder in canine population. It has been estimated to account for 75% to 80% of canine cardiac disease1. It is common in small breed dogs, but also can be encountered in large breeds like german shepherd and other . The disease characterizes with thickening and enlarging of the mitral leaflets, elongation of chrdae tendineae and mitral regurgitation. Histopathologic  features are expansion of extracellular matrix with glycosaminoglycans and proteoglycans; valvular interstitial cell alteration; and attenuation or loss of the collagen-laden fibrosa layer2. Because of the mitral regurgitation the usual course of this disorder represents volume overloud of the left atrium and left ventricle , eccentric hypertrophy of the left ventricle , dilation of the left atrium ,and  left sided congestive heart failure . Increased pressure in left atrium and pulmonary veins leads to pulmonary edema . Often complication is so called passive pulmonary hypertension , consequence of increased pressure in pulmonary veins. Really rare complication is left atrial rupture .

 

Case presentation

fig 1

Fig. 1

fig 3

Fig.3

fig 2

Fig.2

Richka is 12 years old mixed breed dog with history of DMVD , threated only with enalapril . She was admitted in our clinic for cardiologic examination, because recently increasing in coughing and exercise intolerance. During the examination she was tachypneic , normal mucous membrane color , alert and responsive .She had increased heart rate. Auscultation revealed right and left apex systolic heart murmurs. The abdomen was swollen with palpable fluid thrill. We have made echocardiographic examination, with the patient on left and right lateral recumbency, with all parasternal views according to the accepted standards. We found eccentric hypertrophy of the left and right ventricles, left and right atrial dilation, thickening and prolapse of the mitral valve. Doppler examination shows mitral and tricuspid regurgitation with pressure gradient of 162 mmHg and 62 mmHg respectively (figures 1,2,3) . Abdominal echography revealed ascites. So we diagnosed degenerative mitral valve disease with secondary pulmonary hypertension. We prescribed following: pimobendan – 0.25 mg/kg/bid , furozemid – 4.0 mg/kg/bid , spironolactone – 1.0 mg/kg bid enalapril – 0.5 mg/kg/bid , sildenafil – 1.0 mg/kg/tid.

Week later on control examination Richka was better, ascites resolved , mitral and tricuspid regurgitation was with gradient 125 mmHg and 43 mmHg respectively. So we decreased the dose of furosemide to 2.0 mg/kg/bid, and the other drugs were continued with the same doses.

fig 4

Fig 4

fig 5

Fig 5

fig6

Fig 6

fig 7

Fig 7

fig 8

Fig 8

Several months later the owners noticed again swelling of the abdomen and the dog collapsed after exercise. When they came in the clinic Richka was tachypneic with cyanotic mucous membrane. On auscultation we have found 5/6 systolic murmur on the right haemithorax with palpable precordial thrill. Electrocardiography revealed sinus tachycardia – 156 bpm , with premature supraventricular and multifocal ventricular complexes (fig 4). We have made roentgenography in right lateral (fig 5) and dorsoventral (fig 6) position. There was generalized cardiomegaly with dilation of the pulmonary vessels. On echocardiographic examination we have found eccentric hypertrophy of the left and right ventricles, paradoxical motion of the ventricular septum (fig 7), mitral and tricuspid regurgitation with gradient – 118 mmHg and 42 mmHg respectively. Abdominal ultrasonography showed ascites with no collapse of the caudal vena cava with respiration (fig 8). Despite the medications and lower then before pulmonary pressure in this dog the signs of right heart failure were predominant. Because of that and the palpable precordial thrill on the right side we suggested right to left intracardiac shunt. The presence of ventricular septal rupture is less possible, so we decide to search for rupture of the atrial septum. On the right parasternal 4 chambers view modified for better visualization of the right and left atrium with atrial septum, we have found rupture of the septum in the region of the fossa ovalis with left to right shunt.

 

 

 

Video 1 and 2 are same loops with and without colour Doppler demonstrating the defect and shunt of the blood. In this region very often because of the echo dropout on 2d image can be seen a hole in the atrial septum. To be sure that this is a real defect we decided to make a bubble contrast study. We injected 10 ml of agitated saline in v.cephalica antebrachii thru i.v. catheter.  When there is right to left shunt the microbubbles are seen in left atrim, left ventricle or arterial circulation – usually the abdominal aorta. But in left to right shunt the goal of the bubble study is to notice contrast washout during right atrium passing of the bubbles. Video 3 and 4 show right parasternal short axis view of the base of the heart with cranial vena cava. We can see the entrance of the contrast and the following washout like a flame because of the left to right shunting of the blood.

 

 

In this situation sildenafil makes the pulmonary pressure lower and facilitate the shunt from high pressure left atrium to low pressure right atrium. So we decided to use pulmonary hypertension properly and make the dose of sildenafil lower – 1 mg/kg/24 h. with presumption that higher right ventricle and right atrium pressure will make the amount of the shunt lower. 72 hours after this change the ascites resolves and the condition of the dog became better. On the time of the written of the article Richka is about half year on this medications with sildenafil once per day and no changes in other medications and the only clinical sign is exercise intolerance.

 Discussion

Rupture of the atrial septum is really rare complication of mitral valve disease. Most commonly the rupture occurs in caudal weaker part of atrial wall. In a study of Buchanan JW from 30 dogs only in 4 was found rupture of the interatrial septum with signs of right heart failure3. In another study from the same investigator from 50 dogs 7 have acquired ASD4. The еtiology for rupture of the left atrium is uncleаr , but probably is related with the high pressure in the left and right atrium and the so called jet lesions from the mitral and tricuspid regurgitation. Usually the mitral regurgitation jet is toward lateral wall of the left atrium like in this case (video 5). Tricuspid regurgitation jet was directed to interatrial septum so probably contributed to rupture of the septum. The thin fossa ovalis is weak and suitable place for this kind of lesions. In human medicin rupture of the septum is reported after blunt chest trauma , most often accompanied with rupture of the tricuspid valves 5,6. The proposed reason is that compressivе force occurred during isovolumic contractiоn with maximally dilated ventricles and closed atrioventricular valves5. In humans  right ventriсle is right behind the sternum , and this predispоse it to injury. In those cаses when there is rupture of the tricuspid valve and massive regurgitation , the increased pressure in right atrium leads to rupture of the septum and right to left shunt. In canine patients with degenerative mitral valve disease after the rupture of caudal atrial wall and following haemopericardium the clinical signs are collapse and sudden death. After rupture of the atrial septum the predominant signs are of right heart failure. In this case the right atrium and ventricle serves as a low pressure “sink” for severely dilated left atrium.

There are several publications about echocardiographic diagnosis of acquired atrial septal defect and rupture of the atrial septum with haemopericardium3,4. The bubble contrast study has been validated in veterinary echocardiography for diagnosis of congenital and acquired intra and extra cardiac defect and shunt7,8. In this case we have demonstrated the usefulness of so called contras washout – result of bubbles free blood entering contrast rich compartment.

In conclusion in any dog with degenerative mitral valve disease and predominated signs of right heart failure we have to look echocardiographically for atrial septal rupture. More we scan , more we find , and more we learn.

 

Pacemaker implantation (PMI) as treatment for AVB III and very slow ventricular escape rhythm in a geriatric canine patient

2 д-р Ранко Георгиев

Dr Ranko Georgiev

Ranko Georgiev1, Hristina Shukerova2, Nadezhda Petrova3

1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria

Introduction:

Pacemaker implantation is the most effective treatment for ‘syncope and severe exercise intolerance’ – related arrhythmias; however when searching for the best clinical decision for some older dogs, the risk of anesthesia often outweighs the benefits. We would like to share a case where the old age was not a problem.

Case presentation:

Larry was a 17-year old MI mix breed dog admitted because of increasingly frequent exercise intolerance episodes during the past few months. Furthermore, the last week the patient was very week, unable to stand on his feet and with a depressed overall clinical status. On a clinical presentation with the referring vet а bradycardia was noted and the patient referred to us for a Cardiology consult.fig 1 Lari-Ro-LLR

During auscultation, a slow regular rhythm was detected with heart rate of 20 bpm classified as ventricular escape rhythm during the normal ECG. A 24hour Holter monitor revealed complete AV block (AVB III) throughout the study with an average rate of 31 bpm, occasional VE beats with some pairs, triplets and short runs; no pauses greater than 5 sec were noted. The slowest heart rate detected was 20 bpm.fig 3 echocardio

Complete blood count and biochemical profile were normal. Radiography and echocardiography revealed generalized cardiomegaly, with mild-to-moderate mitral and tricuspid regurgitation and decreased contractility. During the abdominal FAST study a small amount of free fluid was noted – defined as a transudate on diagnostic abdominocenthesis. Lari_20150811163929_1640560

A diagnosis of complete AV block with clinical signs of right sided congestive heart failure was made and pacemaker implantation was decided. A VVI, bipolar, passive lead was fluoroscopically placed, under anesthesia, through the right jugular vein into the right ventricle, where it was successfully lodged.Lari_20150814181226_1819550 The lead was connected to a generator, which was later fixed in the subcutaneous tissue dorsally to the cervical vertebrae. A temporary pacemaker was used when the dog developed asystole during the procedure. Recovery from the surgery was uneventful, with the pacemaker capturing normally. The pacing rate was set to 100 bpm. The system used was a ‘St Jude’ one.r1

Our anesthesia protocol with this patient was routine for the procedure of a PMI – premedication with Midazolam and Buprenorphine, induction with Etomidate, intubation and maintenance with Isoflurane. The post procedure treatment was only with Cefazolin iv for the next few days.fig 4 PMI-procedure-1fig 5 PMI-procedure-2

The use of a temporary lead and/or an external pacemaker is highly advisable in patients who are depended on their escape rhythm.

Comments:

Even though Larry recovered from the general anesthesia normally he was unable to stand on his feet for additional 5 days. He was bright, alert and responsive, with good appetite and normal consciousness, but with an impaired proprioception. We attributed this to the long period with severe bradycardia (HR of 20 bpm) and potential vasoconstriction/reperfusion complications. There is some data in the human medicine literature concerning PMI in old people with preexisting severe bradycardia, who reported pain in the extremities post the procedure.

Other factors such as chronic joint and spinal diseases could have been the cause of the slow recovery as well. The myoglobin levels were not checked prior to the PMI unfortunately.fig 6 flororfig 8 Lari-Ro-LLR-post-PMI

Conclusions:

Pacemaker implantation may be warranted even in older dogs with ‘syncope and severe exercise intolerance’ – related arrhythmias.r2

7 months post the procedure Larry is still doing great; in this period he underwent two additional major surgeries for a prostate abscess – with no anesthesia complications.581708_10201218994737586_1026692492_n