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

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Dr Vasile Vulpe

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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.

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Fig 4

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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

Patent Ductus Arteriosus in adult dog

 

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Todor Kalinov, DVM, Zaravet veterinary clinic

Todor Kalinov, DVM, Zaravet veterinary clinic, city of Plovdiv, Bulgaria, e-mail drkalinov80@gmiail.com

INTRODUCTION

 

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Patent Ductus Arteriosus(PDA) is one of the most frequently encountered congenital heart disease in dogs , ranging in prevalence from about 25 to 32 % from reported malformations 1 , and lest frequently in cats – about 11 % .  The ductus arteriosus is normal foetal structure  that  shunts blood from  pulmonary artery to aorta 2. Before the birth , it divers approximately 80 to 90 % of the right ventricular output back to the left side of the circulation. After parturition and the onset of breathing , pulmonary vascular resistance falls, flow in the ductus reverses , and the resulting rise in arterial oxygen tension inhibits local prostaglandin release causing constriction of the vascular smooth muscle within the vessel wall and functional closure of  the ductus arteriosus3.

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The ductal wall usually contains a loose branching pattern of circumferential smooth muscle in normal pups. The increasing genetic liability to PDA represents extension of the noncontractile wall structure of the aorta to an increasing segment of the ductus arteriosus, progressively impairing its capacity to undergo physiologic closure1.

In typical cases because of the lower pressure in pulmonary circulation there is continuous flow thru the ductus arteriosus from aorta to pulmonary artery. Clinical impact from this is volume overload of the structures in the shunt pathway : the main pulmonary artery, lungs, left atrium, left ventricle, and back to the ascending aorta up to the level of the ductus4. In that shunt direction the dogs show signs of left-sided congestive heart failure – exercise intolerance, coughing, eventually pulmonary edema. In rare instances when the ductus still wide after birth, the flow is really enormous and this leads to increase in pulmonary vascular resistance and change in direction of the shunt, so-called Eisenmengers physiology and reversed PDA . This pattern of pulmonary hypertension and reversed (right to left) shunting usually develops within the first few weeks of life3. Clinical signs in reversed PDA are shortness of breath, differential cyanosis – pink mucous membranes in cranial part of the body and cyanosis in caudal membranes, polycythemia , pelvic limb weakness, collapse, and seizures. The changes in pulmonary vasculature are irreversible and closure of the PDA is not suggested.

Many dogs with left to right PDA do not show any clinical signs, but if left heart failure has developed in first year of life, up to 65 % would die if left untreated. In most of the dogs clinical signs are apparent before the third year of age. The appearance of signs in older dogs is unusual2.

 

CASE PRESENTATION

 

Buky was 7 years old springer spaniel admitted in our clinic with severe respiratory distress. He had history of heart murmur noted on routine examination , several episodes with increasing respiratory rate, and one presyncopal event with rear limb weakness. All clinical signs were apparent past several months.

The dog breathed with open mouth, mucus membranes were cyanotic , respiration rate increased, and on auscultation we have founded continued heart murmur, and crackles on the both side of the thorax. On the X-ray there was severe generalized cardiomegaly, pulmonary overcirculation with dilation if the pulmonary arteries and veins, interstitial to alveolar lung pattern (Figure 1 – L/L projection, Figure 2 – D/V projection). We have applied initial therapy for congestive heart failure with:

Furozemide – 4mg/kg/hour i.v.

Pimobendan – 0.25mg/kg p.os.

Enalapri – 0.5mg/kg p.os.

Sodium nitroprusside – i.v.  constant rate infusion

Oxygen – via mask .

After several hours there was a reduction in respiratory rate, and efforts and an ECG and echocardiography were made.

ECG findings :

Sinus tachycardia – 163 bpm

Wide and tall P wave – suggestive of left atrium enlargement

Tall R wave – suggestive of left ventricular enlargement (Figure 8)

Atrial premature complexes (Figure 3)

Ventricular  premature complexes(VPC) with origin in left ventricle (Figure 4)

Fusion beats – intermediate morphology between normal complexes and VPC (Figures 5, 6, 7).

 

ECHOCARDIOGRAPHY

 

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We have made echocardiography at left and right lateral recumbency of the patient with all parasternal  views according to accepted standards. From the exam we have found severe left heart volume overloud with eccentric hypertrophy of the left ventricle. Left atrium was dilated with rightward excursion of the atrial septum. Left ventricle was dilated with thin free wall and interventricular septum, dooming of the septum to the right ventricle, and reduced systolic motion of the free wall and the septum (video 1).

 

 

 

Left atrium and aorta  was measured on right parasternal short axis view at the heart base and the ratio LA/AO was estimated with results showing at Figure 11. Normal LA/AO ratio have to be < 1,6. Main pulmonary artery was dilated compared to aortic root (video 2)

 

, and blowing of the pulmonary valve was noted (Figure 12).

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On Color Doppler exam there was mild mitral regurgitation with central jet , probably because the dilation of the mitral annulus (Figure 13), and in pulmonary artery was noted typical for PDA continuous flow (video 3).

 

 

With  CW Doppler the aortic flow velocity was measured 2,19 m/s , with normal speed les then 2.0 m/s. In pulmonary artery CW Doppler show typical continuous bidirectional flow (Figure 14).

On the  basis of this findings the dog was diagnosed with Patent Ductus Arteriousus with left to right shunt. Because of the dramatic structural and functional changes in heart, the already developed left heart failure and increased anesthetic risks the owners refused surgical ligation of the ductus. At the time of the diagnosis in our country we did not have the chance for transcatheter coil embolisation. So the only opportunity was to treat congestive heart failure with medications. We have prescribed :

Pimobendan – 0.25 mg/kg/12 h. p.os

Enalapril – 0.5 mg/kg/12 h. p.os

Furozemid – 1.0 mg/kg/12 h. p.os

Spironolacton  – 1.0 mg/kg/12 h. p.os

Supplements with L carnitine, taurine, and coenzyme q10.

The dog was very well after the beginning of the therapy and had only exercise intolerance. After about 1 year he had improvement in some echocardiographyc parameters of systolic function – normal fractional shortening, normal pre ejection period, normal ejection time, but the left atrium was bigger then year ago (Figures 15, 16, 17).

 

 

 

Video 4 – right parasternal  four and five chamber view year after diagnosis ,

 

 

 

 

 

 

video 5 – modified left parasternal short axis view of heart base with color Doppler of the pulmonary artery showing continuous flow with small turbulent jet in opposite direction.

COMMENTS

 

The treatments for Patent Ductus Arteriosus are surgical ligation or transcatheter device closure. Because of the technical factors and price in our country no one does make device closure but in many clinics surgical procedure can be done with great success. In this case the owners decline surgery, but mine opinion is also that the dog was not appropriate candidate for operation. Despite the fact that in most cases there is dramatic improvement in clinical status and cardiac function after surgical closure, the age ,the already developed  heart failure, and concurrent heart disease, affect negatively survival period after PDA closure5. In adult dogs one of the major surgical complications is haemorrhage due to ductus friability2. Mitral valve endocardiosis is also an important factor affecting the survival period. On video 1 and 4 we can see the slight thickening and prolapsed mitral valve leaflets, so I supposed that the dog had degeneration of the mitral valve. Conduction instability of the heart is another reason for anesthetic complications. Actually the dog has died suddenly during routine walk without any other signs, about two years after the diagnosis,  so malignant arrhythmia can be the reason. Despite this facts in most of the literature, the authors suggest closure of the PDA, even in adult dogs, only important contraindication for not closing is right to left shunt.

CONCLUSION

It is not known why some animals with PDA do not show any signs until adulthood. One of the reasons could be the small diameter of the ductus. In human medicine the maintenance of normal pulmonary vascular resistance is important factor for survival of the older patients2. It is certain that the adult dogs with congenital heart diseases are more then we expect, and always  when we examine adult animal for some heart disease, we have to think not only for degenerative valve disease and cardiomyopathies but also for congenital and inherited problems. And of course rare things do happen everyday.

 

 

 

Surgical extraction of adult D. immitis filariae from the pulmonary arteries of a patient with stage III heartworm disease

ranko

Dr Ranko Georgiev

Ranko Georgiev1, Hristina Shukerova2, Nadezhda Petrova3(anesthetist)

1,2,3 DVM, Central Veterinary Clinic, Sofia, Bulgaria; 2016

 

Introduction:

 

An “exotic” diagnosis for Bulgaria just 5 years ago, Heartworm Disease (HWD) is a parasitic infestation that we nowadays see regularly in our small animal practice. Due to climate change and spreading of intermediate vectors, ever more dogs are getting affected. Other major contributing factors are the infrequency of preventive measures in the country and the high number of undiagnosed and subclinical patients, leading to a reservoir of hosts in the general canine population.

The aim of this article is to report a case where the heavy worm burden of the patient warranted surgical extraction prior to adulticide therapy.carcar3

 

Case presentation:

 

Rem is a 25kg, 10 years old MC mix breed dog admitted because of ascites and exercise intolerance during the past few weeks. Most prominent of the clinical signs was the severely distended, fluid-filled abdomen – assessed as modified transudate on abdominocenthesis (more than 4 liters were drained because of the labored breathing).

Thoracic X-rays revealed right-sided cardiomegaly and severely distended tortuous and blunt-ended pulmonary arteries. On echocardiography, right heart pathology was mainly observed – including a distended right atrium and ventricle, dilated pulmonary artery and evidence of pulmonary hypertension, as well as many tubular echoic structures in the lumen of the main pulmonary artery, typically identified as adult parasites.car1

Serology was positive for D. immitis (IDEXX 4D snap test) and the dog was classified as stage III HWD.

Because of the high worm burden and ascites, the possibility of interventional removal of the worms, before the adulticide treatment, was suggested to the owner, who gave his informed consent.

The patient was scheduled for surgery several days after hospitalization and treatment of right congestive heart failure and pulmonary hypertension using the following therapeutic protocol:

Torasemide: 0.2mg/kg/12h, IV and PO

Sildenafil: 2mg/kg/12h, PO

Ivermectin: 6ug/kg monthly, subcutaneously

Surgical extraction of worms was routinely performed using the right jugular vein approach. The area was scrubbed aseptically and a small skin incision was made over it. The vein was dissected free from the surrounding tissue and ligated proximally. A small transverse cut in its wall was made, through which a forceps was advanced into the heart under fluoroscopic control.

Video:   http://dox.bg/files/dw?a=f058367161

 

An Ishihara Flexible Alligator Forceps (Fujinon TypeL FK-480L) was used, which is a vet instrument designed in Japan, especially for Dirofilaria extraction.car2

The anesthetic protocol we used was typical for this procedure; in particular premedication with Atropine, Butorphanol and Midazolam; induction with Etomidate; and finally Isoflurane maintenance.

After nearly 20 attempts, we extracted 25 adult worms. The overall fluoroscopic time of the procedure was less than 5 minutes. The recovery of the patient was uneventful and a day later we started the adulticide protocol for HWD treatment, as recommended by the American Heart Worm Association.car4car5

 

Comments:

 

In all cases with stage III or IV HWD it is advisable to discuss the possibility of surgical extraction of some of the worms as a pre-adulticide step. This will lower the risk of fatal pulmonary thromboembolism after the injection of Immiticide and will likely improve the symptoms of existing pulmonary hypertension.

It should be noted that if a different extraction device is used (endoscopic loops and baskets, rigid or semi-rigid alligator forceps, different types of graspers, etc.), the success rate of the procedure is much lower, at least in our experience. The Ishihara forceps could be actively maneuvered into the RVOT, hence providing faster and easier access to the PA.car6

 

Conclusions:

 

Surgical extraction of a heavy worm burden is possible and clinically important before adulticide treatment, in patients with end-stage HWD.

Rem, the dog of our study, successfully completed the treatment protocol for HWD without any evidence of pulmonary thromboembolism; meanwhile the symptoms of RCHF have slowly abated.

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