Proceeding of the SEVC Southern European Veterinary Conference

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1 Close this window to return to IVIS Proceeding of the SEVC Southern European Veterinary Conference Oct. 2-4, 2009, Barcelona, Spain Next conference : October 1-3, Barcelona, Spain Reprinted in the IVIS website with the permission of the SEVC

2 PATENT DUCTUS ARTERIOSUS: CLINICAL MANAGEMENT Jordi Manubens HOSPITAL VETERINARI MOLINS, Barcelona, España EMBRYOLOGY AND ANATOMICAL DEVELOPMENT The ductus arteriosus is a muscular blood vessel originating embryologically from the 6th aortic arch and runs from the bifurcation of the main pulmonary artery to the ventral aspect of the descending aorta. During gestation, the foetus receives oxygen supply through the placenta. The lungs remain collapsed and pulmonary vascular resistance is high enough to cause the blood circulating through the right ventricle to deviate directly towards the descending aorta through the duct. At the moment of birth there is an increase in the oxygen pressure, the lungs expand and vascular resistance decreases when pulmonary arterioles dilate. In normal patients, the increased oxygen pressure stimulates the contraction of the smooth muscle of the wall of the ductus and causes its closure. Within few weeks, this muscle will transform into fibrous tissue, leaving the ligamentum arteriosum. Due to the different degrees of hypoplasia of the smooth muscle, the closure can be incomplete to develop into Patent Ductus Arteriosus (PDA). According to Kittleson, and depending on the extent and distribution of the muscular hypoplasia, PDAs can be divided into 6 groups: Groups 1 and 2: The smooth muscle is insufficient to close the aortic end but enough to result in closure at the end communicating with the pulmonary artery, forming an aortic aneurysm. Groups 3, 4 and 5: It can result in small, medium or large PDAs. The ductal musculature is absent in the aortic end of the duct, with some muscle along the duct, which will lead to partial closure at the pulmonary end and the PDA will adopt the shape of a funnel. Group 6: There is no contraction of the duct and with time it will develop into a reversed PDA (right-to left shunt). According to Buchanan, depending on anatomy and function of the PDA, we find 4 different types: Type 1: small PDA. Asymptomatic left-to-right shunt. With mild or non-existent precordial thrill at the left heart base. Heart rate and pulses are normal. X-rays and ECG are initially normal. Surgery is advisable but not urgent. Type 2: medium PDA. Asymptomatic left-to-right shunt PDA. There is a continuous murmur at the base, mainly audible at the apex. Pulse is normal or slightly stronger. Presenting mild to moderate cardiomegaly before one year of age. The aneurysm of the duct is small. Pulmonary vasculature is within higher end of normal levels. In lead II, the voltage of the R wave is greater than 3 mv. Surgery is recommended but can be postponed few weeks. Type 3a: PDA with no pulmonary congestion. The murmur is continuous at the left heart base with a mitral murmur at the apex. The aneurysm is medium to large. There is cardiomegaly before the age of 6 months and pulmonary vessels are dilated. Pulses are bounding. In lead II, the R wave is greater than 5 mv. Surgery is urgent. Type 3b: PDA with congestive heart failure. The patient usually presents with cachexia, atrial fibrillation and pulmonary oedema. It should be stabilised before surgery.

3 Type 4: PDA with pulmonary hypertension. Compensated PDA with right-to-left shunt. It has been reported in patients of even 12 years of age which present with weakness in hind quarters or syncope during exercise, cyanosis on the hind quarters, normal pulses, polycythaemia (Hct >80%). They do not present with murmur or thrill. Right ventricular hypertrophy on echocardiography. Right axis shift on ECG. On x-ray, right-sided cardiomegaly and prominent pulmonary artery. Surgery is contraindicated. Prevalence and incidence: PDA is the most commonly diagnosed cardiac disease in dogs. It is a congenital condition with polygenic heritability and does not follow simple mendelian genetics. Some predisposed breeds are: Border collie, Cocker spaniel, Collie, German shepherd, Irish Setter, Keeshound, Pomeranian, Shetland sheepdog, Yorkshire terrier, Labrador, English Springer spaniel, Kerry blue terrier, Bichon frise and Chihuahua. The incidence in females in respect to males is 2:1 3:1. A referral centre like U.C. Davis will diagnose an average of 20 cases per year. Out of 215 cases in 10 years, only 14 presented with reversed PDA. Pathophysiology: Due to the pressure difference between systemic and pulmonary circulation, the presence of a PDA allows the shunting of blood from the aorta into the pulmonary artery. The shunt volume causes volume overload on the left side with a subsequent dilatation of the atrium and ventricle. If the defect is very large and the pulmonary resistance is normal, it could lead to congestive heart failure with pulmonary oedema. Pulmonary overperfusion can increase excessively pulmonary vascular resistance which with time can develop into pulmonary hypertension, compensation of the pressure between the right and left side and reversal of the blood flow (reversed PDA) allowing the flow of non-oxygenated blood towards systemic circulation. Diagnosis: 1.- Clinical history: Puppies with PDA tend not to show clinical signs as long as the vascular pulmonary resistance remains within normal limits. The defect is often diagnosed during a routine physical examination during the first few months of life. If the patient presents clinical signs, the most common include dyspnoea. In cases of reversed PDA, the symptoms are more evident and include tachypnoea, lethargy, pain, anorexia, cough, dyspnoea, collapse, syncope, hind-limb weakness during exercise, Physical examination: A grade IV-VI / VI continuous murmur is usually detected with higher intensity on the caudal left scapular region of the thorax, being more intense during systole. If the heart rate is slow, it may not be detected in telodiastole. A continuous thrill can be palpated craniodorsally at the heart base. It is also occasionally possible to auscultate a murmur on the area of projection of the mitral valve, originating as a consequence of the dilatation of the mitral annulus which usually disappears within a few weeks after surgery, once the left ventricle has reduced in size. If the communication is very large in size, an increase in femoral artery pulse pressure can be palpated. In cases of reversed PDA there is usually no murmur detected but occasionally differential cyanosis can be identified as a consequence of the non-oxygenated blood flow entering the descending aorta caudal to the origin of brachiocephalic trunk and left subclavian artery and is directed towards the caudal body. As a consequence, we can see a pink coloration of the oral mucous membranes together with cyanosis of the caudal mucous membranes. 3.- Laboratory tests: In left-to-right shunts, the results of laboratory tests can be completely normal but in cases of reversed PDA we can commonly see hypoxaemia (partial oxygen pressure < 40 mmhg), when non-oxygenated blood mixes with oxygenated blood originating from the left ventricle, leading to a marked renal hypoperfusion causing polycythaemia (haematocrit > 65%) 4.- Radiography: It is characteristic to see an increase in size of the left side of the heart (left-sided cardiomegaly) due to volume overload. If there is congestive heart failure we can observe an increased diameter of the pulmonary veins and oedema formation. There is also an increased size of the main pulmonary artery and excessive pulmonary overperfussion. On the DV view we may see the aneurysmic protrusion of the descending aorta. In cases of reversed PDA, an increased pulmonary vascular resistance leads to right ventricular enlargement and increased

4 diameter of the pulmonary arteries as well as reduced diameter of peripheral pulmonary vessels. 5.- Electrocardiogram: The alterations observed on the ECG may include the presence of a P mitrale (because of dilatation of the left atrium), increased amplitude of the R waves (due to dilatation of the left ventricle) and of the Q wave (due to hypertrophy of the right ventricle) in the leads II, III and avf. In any case, it is important to recognize that it is not possible to reach a diagnosis of chamber enlargement based on an ECG; it should always be confirmed with echocardiography. 6.- Echocardiography: The diagnosis of PDA does not always have to be confirmed by echocardiography but it is very useful to confirm the diagnosis and rule out other anomalies. Due to the course of the blood flow, there is volume overload of the pulmonary artery, left atrium, left ventricle and aorta. This volume overload can occasionally lead to a bulging of the interatrial septum and interventricular septum to the right. The right side of the heart tends not to be affected but the diameter of the left ventricle is usually increased in telodiastole. The shortening fraction tends to remain within normal limits. The main pulmonary artery and its branches have an increased diameter. We should avoid confusion with other pathologies also presenting with dilatation of the pulmonary artery which can easily be differentiated from PDA. Left-to-right shunting does not result into hypertrophy of the right ventricle, unlike in cases of pulmonary hypertension. We should not mistake it either with pulmonic stenosis as in this case there is no dilatation of the main pulmonary artery at valvular level. We do not require visualizing the PDA to confirm its existence. By performing a Doppler study of the main pulmonary artery, we can observe an aliasing of blood flow originating near the bifurcation with a jet striking the pulmonic valve. Spectral Doppler shows a continuous flow. In normal dogs, the pressure within the aorta is of 120 mmhg and of 20mmHg in the main pulmonary artery. Therefore, within the PDA the gradient should be of approximately 100mmHg, which is equivalent to a peak systolic flow velocity of 5 m/s. If pulmonary hypertension is already present, this gradient could be less. It is also common to detect a higher velocity in the aortic flow due to an increased preload. In patients without subaortic stenosis, an increased velocity in the left ventricular outflow tract usually rules out PDA. If there has been a longstanding reversed PDA, we can see on echocardiography a clear hypertrophy of the right ventricle and dilatation of the main pulmonary artery. The right atrium tends to be of a normal size except in cases of insufficiency of the tricuspid valve and the left side is smaller due to reduced preload. To differentiate this from primary pulmonary hypertension or pulmonary thromboembolism we need to perform a contrast echocardiographic study, injecting agitated saline into the cephalic vein and observing how the bubbles move from the right side to the descending aorta bypassing the left side of the heart. This test is also useful to rule out intracardiac right-to-left shunting defects (e.g. Eisenmenger syndrome). 7.- Catheterisation and angiography: These two techniques aid to identify the type of PDA and help differentiate it from other congenital defects such as aorticopulmonary window, abnormal shunts between systemic and pulmonary circulation, arteriovenous fistulae, stenosis of a branch of the pulmonary artery, interventricular septal defects with aortic regurgitation, or pulmonary stenosis with pulmonary regurgitation. In the majority of these cases, the anomalies are not only evident during angiography and echocardiography, but the type of murmur is also different. Treatment: 1.- Medical: During gestation the ductus arteriosus remains functional attributed to the effect of prostaglandins. In premature children, the administration of non-steroidal anti-inflammatories such as aspirin, indometacine or ibuprofen causes inhibition of the synthesis of prostaglandins and subsequently induce the closure of the duct. However, the effect of these drugs is not the same in veterinary medicine, because the duct lacks enough smooth muscle for this effect to occur. In cases where congestive heart failure has developed, we can administer frusemide, ACEi, digoxin,... in order to reduce the associated complications of the PDA. The case is different with reversed PDAs, as surgery is not recommended. The only method of control is

5 therefore phlebotomies or the administration of hydroxyurea at doses of 30mg/kg/day during 7-10 days to be then reduced to half that dose every 24hours to achieve myelopsuppresion and reduce haematocrit to below 65%. Haemograms will have to be carried out every 7-14 days and treatment should be interrupted if there is evidence of leukopenia, thrombocytopenia or anaemia. 2.- Surgical: Ligation of PDA: This technique has to be carried out between the first 8 to 16 weeks of life. The prognosis is excellent and the mortality rate is below 2%. It should not be performed if patients with congestive heart failure, where surgery will have to be postponed until the patient has been medically stabilised. Surgery is performed in right lateral recumbence. The approach is by thoracotomy at the level of the 4th intercostal space. We place rib retractors and separate the lung with a moist gauze. Once the heart has been exposed, we have to identify, dissect and ventrally retract the vagal nerve with a stay suture. We should also identify the phrenic nerve. It is rare that we see a persistent left vena cava. If that was the case, we should dissect it and retract with sutures. The dissection of PDA is carried out bluntly and avoiding the pericardial sac. Once the duct is dissected we will place two nylon sutures. The first we ligate is the one nearer the aorta. Like this we will achieve a reduction in the existing pressure inside the ductus and the ligation of the second suture will be easier. We can then proceed to reposition the lung lobes and inflate them to reverse atelectasia. To close the thorax we will place tension sutures from the anterior aspect of the 4th rib until the posterior aspect of the 5th rib. Before we place the last suture, we should perform overinflation of the lungs to reduce the degree of pneumothorax, and we will suture the latissimus dorsi with a continuous suture. The subcutaneous tissue and skin is closed in routine manner. The air will then be aspirated from inside the thoracic cavity and a control x-ray is taken to assess the need of the placement of a thoracic drain. The patient will need to remain hospitalised for 3 to 5 days and receive suitable antibiotic therapy. The most serious complication we may encounter is the rupture of the duct during dissection. A small tear can be controlled with gentle pressure. If the tear is more severe we will need to use vascular clamps. The first clamp will be placed obliquely to the aorta at the base of the duct to sufficiently reduce haemorrhage to repair the tear. It is also helpful that this method does not interrupt circulation completely. If the haemorrhage is still not fully controlled we will have to proceed to open the pericardium and clamp the descending aorta and pulmonary artery. This method will completely interrupt the circulation and is therefore only used in case of major haemorrhage. Once the haemorrhage is under control, the surgeon will have to decide whether to proceed with the intervention or postpone it altogether. It is often not possible to perform second surgeries due to the amount of adhesions forming at the site Percutaneous closure: This technique consists of the occlusion of the PDA by means of devices (coils, Amplatzer or Nitocclud coils,...) which cause the formation of thrombi to occlude the duct interrupting the blood flow. The decision of which method to use in each case will depend on the size and shape of the ductus, as well as the expertise of the clinician and supporting team. In general, to achieve occlusion, with interventionist technique, the patient must be of a bodyweight above 2,5 kg to allow vascular access and catheterisation. Conventional echocardiography allows to determine the size of the duct but presents certain limitations. The use of trans-oesophageal echocardiography is currently recommended intraoperatively. The technique used for the classification of the duct is angiography, which tends to be applied before the occlusion of the duct and at the end of surgery, to evaluate the residual flow. There are two classifications to use: the classification for human patients and the one suggested for canine PDA. The information available for feline patients is very limited, due to the low incidence of the defect in this species. The following table gives an orientation regarding the choice of occlusion method:

6 Coil The coil is a device with the shape of a spring with thrombogenic fibres. There are different varieties, being the coils of platinum (Tornado Coils, Cook ) and stainless steel (Stainless Steel Coils, Cook ) the most commonly used. The latter require a delivery system but the separable embolisation coils have a screwing system which allows the controlled release of the coil as well as the repositioning of the device with lower risk of embolism. The classification is made according to size and number of turns (i.e. 5/3.2, 5 mm diameter with 3.2 turns) or of larger or smaller diameter, depending on the model. For the placement of the coil, we catheterise the femoral artery with the technique of cut-down and the use of vascular introducers. Angiography is performed to obtain the size of the duct. After the selection of the suitable coil has taken place (only one coil with PDA 2.5 mm or multiple coils with PDA > 2.5< 4 mm) we will proceed to place the device aided by fluoroscopy. The diameter of the coil has to be double the diameter of the ostium pulmonale (pulmonary opening of the PDA). Finally, an aortogram is performed to evaluate the presence of residual flow and to assess the need of additional coils. There are two techniques for the insertion of multiple coils (via artery or vein), but it is generally recommended to anchor the first turn at the ostium pulmonale to avoid embolisms. There are various publications about the occlusion of PDA by means of coils, as well as regarding the use of transoesophagial echocardiography to reduce the fluoroscopy time but it is not commonly used. One of the most common complications with this technique is the formation of emboli in the pulmonary arteries but it does not seem to be associated to adverse clinical signs. The presence of residual flow is usually not haemodynamically significant. Other less frequent complications are aberrant embolisation, haemolysis, etc. - Amplatzer Duct Occluder (ADO) Autoexpandible device made of Nitinol (nickel and titanium allow) with the shape of a mushroom incorporating structures of polyester to stimulate thrombogenesis inside the device. It has an area of larger diameter (the retention fold) which will be placed on the aortic end of the duct. For its placement we require a system of load and release. For the selection of the size of ADO, the retention fold has to be greater than 20-30% of the diameter of the ostium pulmonale of the PDA (approximately 2mm greater). The ADO is placed via intravenous route (femoral vein) with the aid of fluoroscopy, for which we have to catheterise the femoral vein. We can use a venous (catheterisation of the duct through the pulmonary artery) or arterial (femoral artery) approach for angiography. Post-placement angiography of the Amplatzer can also be carried out from the femoral artery or through one of the lateral ports of the release system of the ADO. Although the realease technique of the ADO is difficult, the risk of embolisation of the device is lower because it is released by a system of a thread and can be replaced with ease inside the realease system once expanded. The risk of residual flow is also relatively low compared to the system of Coils. The price, however, will be the main limiting factor. - Amplatzer Vascular Plug (AVP) Autoexpandible nitinol device with thread system aimed for the arterial or venous occlusion of the peripheral circulation. Although it lacks thrombogenic structures, it is formed by a more dense wire mesh (144 versus 72 in ADO) to avoid residual flow. The use for PDA occlusion is not approved but, due to its lower cost, it has been used in dogs. It does require the same system of loading and release as the ADO and it is place via venous or arterial route. The size of the AVP has to be at least 1,5 times the diameter of the ostium pulmonale of the PDA. The information about its use is limited but it has been successfully used in dogs with medium sized PDAs, although seems to have a higher incidence of residual flow.

7 - Amplatz Canine Ductal Occluder (ACDO) This new device represents a more affordable alternative to ADO in canine patients. It is made of an autoexpandible nitinol mesh formed by two discs connected by a thin waist which will anchor at the aortic and pulmonary opening of the PDA. It does require the same loading and release system than ADO and is placed via arterial route. The size of the waist of the ACDO has to be 2 times greater than the diameter of the ostium pulmonale of the PDA. Although the system is promising, there are still publications regarding its use. After releasing the occluding device it is necessary to carry out another angiocardiography to confirm the correct closure. One of the possible complications that can be observed after the release of ACDO is the incorrect conformation of the shape of a cobra-head. This can be due to having chosen a too big Amplatzer in relation to the PDA. Once released, the ACDO, the device tends to adopt a normal conformation. To summarise, interventional surgery to occlude a PDA is routinely used in cardiology referral centres as it offers a high success rate and an excellent postoperative recovery, compared with conventional surgery. However it has its limitations such as high cost, equipment needed (fluoroscopy, occlusion devices, angiographic injectors, etc) and expertise in catheterisations Thoracoscopy and closure with haemoclips: It has recently been described a new surgical technique for the closure of PDA. It has been reported in few cases that the occlusion of PDAs by means of minimally invasive approach such as thoracoscopy with the use of titanium hemoclips is a reliable and feasible technique in dogs. This new technique does have however limitations because it requires very sophisticated equipment and technology and has not been tested in patients of less than 7 Kg bodyweight or with a PDA diameter larger than 12 millimetres. It also requires an exact measurement of the duct for a complete closure of the communication prior to surgery. Prognosis: According to studies carried out, 64% of cases with left-to-right PDAs die during the first year of life if no treatment is given. The most common complications are mitral regurgitation and pulmonary oedema due to left ventricular congestive failure, atrial fibrillation of the left atrium and pulmonary hypertension secondary to overload of the left side of the heart. As previously mentioned, the prognosis after surgery is excellent. On occasions a systolic murmur can be detected associated to mitral valve regurgitation but tends to disappear after few days as the closure of the duct reduces considerably the preload on the left side, the volume and thickness of the left ventricular free wall as well as the dimensions of the valvular annulus. Cases of reversed PDA tend to survive a period of 2 to 5 years as long as they can lead a quiet life and the haematocrit can be kept below 65%. Acknowledgements: This presentation would not have been possible without the collaboration of our colleagues Jordi Manubens, Rodrigo Paiva and Roberto Gaztañaga from Servicio de Cardiología y Respiratorio del Hospital Veterinari Molins, and Anne T French from the Cardiopulmonary Service of the Hospital for Small Animals, University of Edinburgh. Reference: 1. Abbott JA: Patent Ductus Arteriosus. En: Abbott JA: Small Animal Cardiology Secrets, Philadelphia, Hanley & Belfus, 2000; Bonagura JD, Lehmkuhl LB: Congenital Herat Disease. En: Fox PR, Sisson D, Moïse NS (eds): Textbook of Canine and Feline Cardiology 2nd Ed, WB Saunders, 1999; Boon JA: Manual of Veterinary Echocardiography, Philadelphia, Lippincott Williams & Wilkins, 1998; Borenstein N, Behr L, Chetboul V et al.: Minimally invasive patent ductus arteriosus occlusion in 5 dogs. Vet Surg 33[4], Jul-Aug 2004; Buchanan JW: Small Animal Cardiac Surgery - Patent Ductus Arteriosus. En: 6. Campbell FE, Thomas WP, Miller SJ, Kittleson MD: Immediate and late outcomes of transarterial coil occlusion of patent ductus arteriosus in dogs. Proceeding 14th ECVIM-CA Congress Barcelona 2004; Campbell, F.E., Thomas, W.P., Miller, S.J., Berger, D., Kittleson, M.D. Immediate and Late Outcomes of Transarterial Coil Occlusion of Patent Ductus Arteriosus in Dogs (2006) Journal of Veterinary Internal Medicine, 20: Cote E, Ettinger SJ: Long-Term Clinical Management of Right-to-Left ("Reversed") Patent Ductus Arteriosus in 3 Dogs. J Vet Intern Med 15[1], Jan-Feb 2001; Doménech, O. Novedades en el tratamiento del conducto arterioso persistente (2007) En Proceedings del Sexto Congreso de Especialidades Veterinarias de AVEPA, GECAR, pag

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