CARDIAC SURGERY IN VETERINARY MEDICINE

Theresa W. Fossum DVM, MS, PhD, Diplomate ACVSTom and Joan Read Chair in Veterinary Surgery, Professor of Surgery

Texas A&M University College of Veterinary Medicine, College Station, TX 77843-4474tfossum@cvm.tamu.edu

SURGICAL MANAGEMENT OF CONGENITAL CARDIAC DISEASEREQUIRING BYPASS

Cardiopulmonary bypass and inflow occlusion

Cardiac surgery includes procedures performed on the pericardium, cardiac ventricles, atria,venae cavae, aorta, and main pulmonary artery. Closed cardiac procedures (i.e., those that do notrequire opening major cardiac structures) are most commonly performed; however, someconditions require open cardiac surgery (i.e., a major cardiac structure must be opened toaccomplish the repair). Open cardiac surgery necessitates that circulation be arrested during theprocedure by inflow occlusion or cardiopulmonary bypass. Venous inflow occlusion providesbrief circulatory arrest, allowing short procedures (less than 5 min) to be performed. Longer opencardiac procedures require establishing an extracorporeal circulation by cardiopulmonary bypassto maintain organ perfusion during surgery.

Cardiac surgery is not fundamentally different from other types of general surgery and similarprinciples of good surgical technique (i.e., atraumatic tissue handling, good hemostasis, and secureknot tieing) apply. Consequences of poor surgical technique are often devastating. Cardiac surgerydiffers from other surgeries in that motion from ventilation and cardiac contractions adds to thetechnical difficulty of performing these procedures. Approaches that provide limited access to dorsalstructures require that surgeons incise, suture, and/or ligate structures located deep within the thorax.Ligature placement using hand ties are useful in such situations and the ability to place hand-tiedknots (vs. instrument tieing) should be considered a fundamental skill for cardiac surgeons. Secureknot tieing is critically important to successful cardiac surgery. Hand tieing knots is fast and producestighter and more secure knots than instrument tieing. The one-handed knot tie technique is best suitedto the fine sutures used in cardiac surgery. Tight knots are facilitated by throwing the first two or threethrows in the same direction before finishing with square knots for security.

Inflow OcclusionInflow occlusion is a technique used for open heart surgery where all venous flow to the heart is

temporarily interrupted. Because inflow occlusion results in complete circulatory arrest, it allowslimited time to perform cardiac procedures. Ideally, circulatory arrest in a normothermic patientshould be less than 2 minutes, but can be extended to 4 minutes if necessary. Circulatory arrest timecan be extended up to 6 minutes with mild, whole-body hypothermia (32 to 34 C). Temperatures˚ ˚below 32 C may predispose to fibrillation and should be avoided. The advantage of inflow occlusion˚

is that it does not require specialized equipment; however, the limited time available to perform thesurgery requires that the procedure be well planned and executed with speed and expertise. We haveused this technique primarily for right atrial tumors and cor-triatriatum dexter.

Depending on the cardiac procedure being done, a left or right thoracotomy or mediansternotomy is performed. With a right thoracotomy or median sternotomy, the cranial and caudalvena cava and azygous vein are occluded with vascular clamps or Rumel tourniquets which can bemade by passing umbilical tape around the vessel, then threading umbilical tape through a piece ofrubber tubing that is 1 to 3 inches long. When the umbilical tape has been adequately tightened toocclude the vessel, a clamp is placed above the rubber tubing to hold it securely in place. Caremust be taken to avoid injuring the right phrenic nerve during placement of the clamps ortourniquets. For left thoracotomies, separate tourniquets are passed around the cranial and caudalvenae cavae. Then, dissecting dorsal to the esophagus and aorta, the azygous vein is occluded byplacing a tourniquet around it.

Cardiopulmonary Bypass Cardiopulmonary bypass is a procedure whereby an extracorporeal system provides flow of

oxygenated blood to the patient while blood is diverted away from the heart and lungs. This greatlyextends the time available for open cardiac surgery. Several advances (i.e., development of membraneoxygenators, improved methods of myocardial protection, increased availability of monitoringtechnologies, and improved veterinary critical care) have made cardiopulmonary bypass increasinglyfeasible in dogs. Cardiopulmonary bypass can be used to treat dogs with congenital or acquiredcardiac defects. Readers are referred to a cardiovascular surgery text for details of performingcardiopulmonary bypass.

Preoperative concernsAnimals requiring cardiac surgery often have prior cardiovascular compromise that should be

stabilized medically when possible, prior to anesthetic induction. Congestive heart failure, particularlypulmonary edema, should be managed with diuretics (e.g., furosemide) and ACE inhibitors (e.g.,enalapril, lisinopril) before surgery. Cardiac arrhythmias should be recognized and treated (see alsopostoperative care below). Ventricular tachycardia should be suppressed before surgery with class Iantiarrhythmic drugs (i.e., lidocaine, procainamide). Lidocaine is effective for management ofventricular tachyarrhythmias during and immediately after surgery. Supraventricular tachycardia mayrequire management with digoxin, beta-adrenergic blockers (e.g., esmolol, atenolol), or calciumchannel blocking drugs (e.g., diltiazem) prior to surgery. Atrial fibrillation should be controlled priorto surgery with digoxin to lower the ventricular response rate below 140 bpm. This may require theaddition of beta-adrenergic blockade or calcium channel blocking drugs if digoxin alone does notdecrease the ventricular rate sufficiently. Animals with bradycardia should undergo an atropineresponse test before surgery. If bradycardia is not responsive to atropine, temporary transvenouspacing or may be required.

Most animals should undergo evaluation by echocardiography prior to cardiac surgery as anincomplete or inaccurate diagnosis can have devastating consequences. With the advent of Dopplerechocardiography, cardiac catheterization is no longer routinely necessary prior to cardiac surgery.

SUB-AORTIC STENOSISTo date, surgical treatment of sub-aortic stenosis (SAS) in dogs has been successful in the

short term in reducing the systolic pressure gradient across the aortic valve, but has not beenshown to decrease the incidence of sudden death in this population. Reports of closedtransventricular dilation showed marked post-operative decreases in pressure gradients, butrestenosis is common, usually within three months. This restenosis is consistent with reports inthe human literature following transventricular dilation. The most promising results thus far arefound in techniques investigating the use of cardiopulmonary bypass and open surgicalcorrection. The traditional approach to resection of the subvalvular stenosis is through anaortotomy made above the coronary ostia. Tearing of the aortic incision during resection is apotential complication of this approach. The typical defect is a discrete fibrous membranelocated 1-5 mm below the base of the cusps of the aortic valve that reflects onto the septal cuspof the mitral valve from the septum. This portion of the ring must be excised to adequatelyreduce the pressure gradient but care must be taken not to damage the mitral valve during theresection. Varying degrees of muscular hypertrophy of the interventricular septum accompanythis lesion. Removal of partial thickness sections of hypertrophied septum (septal myectomy)has been reported in the veterinary literature but a significant difference in survival using thistechnique was not demonstrated. Due to the continued problem of late recurrence of stenosis,alternate techniques are used in people to resect full thickness portions of septum and reconstructthe septal defect with a patch graft. The proximity of the conduction system is the primaryconcern when performing a septal myectomy.

To date, one dog with subaortic stenosis has undergone cardiopulmonary bypass and open-heart correction of this defect at Texas A&M University. The patient had severe SAS with aDoppler-derived gradient in excess of 200 mmHg and moderate to severe left ventricularhypertrophy without significant ventricular ectopy or mitral regurgitation. Through a mediansternotomy, a right ventriculotomy was performed. An initial incision into the hypertrophiedseptum allowed exploration of the left ventricular outflow tract (LVOT). An aortotomy was alsoperformed to improve visualization of the LVOT and aortic valve. A large portion (1.5 x 2 cm)of the dorsal septum was removed and the subvalvular fibrous tissue resected without damage tothe mitral valve. The septal defect was repaired with autologous pericardium harvested atsurgery and treated with glutaraldehyde to improve its handling characteristics. Full thicknessresection was performed in an attempt to alleviate the late restenosis noted with alternate partialthickness resection techniques. Although not substantiated in dogs, it is hoped that this will, at aminimum, delay the progression of disease and decrease the chance of sudden death.

PULMONIC STENOSISAlthough supra and subvalvular lesions have been seen, the most common cause of pulmonic

stenosis in dogs is valvular dysplasia. Dogs with moderate to severe stenosis may experience

syncope or changes leading to congestive heart failure and are at risk for sudden death. Surgeryor balloon valvuloplasty should be considered if the pressure gradient is above 80 mmHg.Valvuloplasty may be beneficial for primarily valvular lesions, but it efficacy may be reduced inthose cases with significant subvalvular muscular hypertrophy. Restenosis, presumably due toscarring, has been reported.

Alternatively a patch graft technique, using PTFE or Gortex material, may be more likely toprovide a greater and longer standing reduction in the pressure gradient, although survival datahave not been previously evaluated. Patch grafting techniques may be performed under inflowocclusion and mild hypothermia; however, the use of cardiopulmonary bypass affords thesurgeon more time for precise placement of the graft and thus may allow for improved post-operative outcomes.

Dogs with an aberrant coronary artery contributing to their pulmonic stenosis are notconsidered candidates for balloon valvuloplasty or patch grafting techniques due to the risk ofdisturbance of that coronary vessel. Surgery in these animals would generally requirecardiopulmonary bypass and placement of a conduit from the right ventricle to the pulmonaryartery to circumvent the stenosis.

SEPTAL DEFECTS

Ventricular septal defect (VSD) is the second most common congenital heart defect in cats andaccounts for 5% to 10% of congenital heart defects seen in dogs. Most ventricular septal defects insmall animals occur in the membranous septum. Perimembranous defects are located in themembranous septum, medial to the septal tricuspid leaflet, and inferior to the crista supraventricularis.Infundibular or supracristal defects are located in the right outflow tract superior to the cristasupraventricularis. The pathophysiology of VSD depends on the size of the defect and on pulmonaryvascular resistance. VSD typically causes a left-to-right shunt. A typical VSD overloads the left heartand, depending on its size and location, may overload the right heart as well. A large VSD canprogress to left-sided congestive heart failure. Chronic overcirculation of the lungs can causeprogressive pulmonary vascular remodeling leading to severe pulmonary hypertension and right-to-left shunting of blood (Eisenmenger’s physiology). Aortic insufficiency is a fairly common secondaryabnormality associated with VSD, particularly infundibular VSD. Aortic insufficiency results fromprolapse of an aortic leaflet into the defect. This prolapse is due to the Venturi effect associated withVSD flow and loss of support of the aortic annulus. Aortic insufficiency adds to the left ventricularvolume overload and is usually progressive. Definitive patch closure of VSD can be accomplishedwith the aid of cardiopulmonary bypass in dogs over 4 kg in body weight. A perimembranous VSD iscorrected from the right side via a right atriotomy approach. An infundibular VSD is corrected via aright ventriculotomy from a left thoracotomy or median sternotomy approach.

. Atrial defects can easily be fixed using bypass. We have performed surgery in several dogs withseptal defects where we have used glutaraldehyde fixed pericardium to repair the defect. Theprogrnosis is generally excellent.

SURGICAL MANAGEMENT OF CONGENITAL CARDIAC DISEASE NOTREQUIRING BYPASS

PATENT DUCTUS ARTERIOSUS

The ductus arteriosus is a fetal vessel that connects the main pulmonary artery anddescending aorta. During development it shunts blood away from the collapsed fetal lungs.Normally it closes shortly after birth during the transition from fetal to extrauterine life.Continued patency of the ductus arteriosus for more than a few days after birth is termed "patentductus arteriosus".

PDA is the most common congenital heart defect of dogs; it also occurs in cats. PDAcauses a left-to-right shunt that results in volume overload of the left ventricle and produces leftventricular dilation and hypertrophy. Progressive left ventricular dilation distends the mitralvalve annulus causing secondary regurgitation and additional ventricular overload. This severevolume overload leads to left-sided congestive heart failure and pulmonary edema, usuallywithin the first year of life. Atrial fibrillation may occur as a late sequela due to marked leftatrial dilation.

Rarely, dogs with PDA develop suprasystemic pulmonary hypertension that reverses thedirection of flow through the shunt causing severe hypoxemia and cyanosis (Eisenmenger’sphysiology). Right-to-left PDA can occur as a late sequela to untreated PDA. When right-to-leftPDA is noted in very young animals it may be due to persistent pulmonary hypertension afterbirth. Reversal of PDA lessens the risk for developing progressive left-sided heart failure, butcauses severe debilitating systemic hypoxemia, exercise intolerance, and progressivepolycythemia.

DiagnosisCLINICAL PRESENTATION

Signalment - PDA is seen more commonly in purebred, female dogs. Maltese,Pomeranians, Shetland sheepdogs, English springer spaniels, keeshonds, bischon frise, miniatureand toy poodles, and Yorkshire terries are at increased risk to develop PDA. A genetic basis hasbeen established in poodles.

History - Most young animals with PDA are asymptomatic or have only mild exerciseintolerance. The most common complaint in symptomatic animals with left-to-right shunts arecough or shortness of breath (or both) due to pulmonary edema. Animals with right-to-left orreverse PDA may be asymptomatic or have exercise intolerance and hindlimb collapse onexercise.

Physical examination findings

The most prominent physical finding associated with PDA is a characteristic continuous(machinery) murmur heard best at the left heart base. The left apical cardiac impulse isprominent and displaced caudally and a palpable cardiac A “thrill” often is present. Femoralpulses are strong or hyperkinetic (water hammer pulse) due to a wide pulse pressure caused bydiastolic runoff of blood through the ductus. Tall R waves (> 2.5 mV) or wide P waves on a leadII electrocardiogram are supportive of the diagnosis, but not always present. Atrial fibrillation orventricular ectopy may be present in advanced cases.

The physical examination findings in animals with right-to-left or reverse PDA differfrom those with left-to-right shunts. “Differential” cyanosis is typically present (i.e., cyanosis ismost apparent in the caudal mucous membranes), but cyanosis may also be noted in the cranialhalf of the body in some animals. Cyanosis occurs because there is admixture of non-oxygenatedblood (from the pulmonary artery) with the oxygenated aortic blood. Femoral pulses are normal.A systolic cardiac murmur, rather than a machinery murmur, is often present. However, amurmur may not be ausculted if polycythemia is present or if left and right sided pressures arenearly equal and shunting of blood through the ductus is minimal.

Radiography/EchocardiographyThoracic radiographs typically show left atrial and ventricular enlargement, enlargement

of pulmonary vessels, and a characteristic dilation of the descending aorta on the dorsoventralview. Echocardiography provides information that further confirms PDA and helps ruleconcurrent cardiac defects, but is not invariably required to establish the diagnosis.Echocardiographic findings that support a diagnosis of PDA include left atrial enlargement, leftventricular dilation and hypertrophy, pulmonary artery dilation, increased aortic ejectionvelocity, and a characteristic reverse turbulent Doppler flow pattern in the pulmonary artery.

With right-to-left PDA, thoracic radiographs show evidence of biventricular enlargementand marked enlargement of the pulmonary artery segment. Pulmonary arteries may also appeartortuous. A right-to-left PDA can be documented by performing a saline bubble contrastechocardiogram. Observing bubbles in the descending aorta, but not in any left sided cardiacchamber, is diagnostic.

Laboratory findings

Laboratory abnormalities are uncommon in animals with left-to-right shunting PDA;however, animals with right-to-left shunts are commonly polycythemic. Polycythemia occurs inresponse to increased erythropoietin production due to chronic hypoxemia.

Differential diagnosis

The characteristic physical examination findings (i.e., continuous murmur, boundingarterial pulses) makes diagnosis of PDA straightforward in most affected animals. Acombination of aortic stenosis/aortic insufficiency or ventricular septal defect/aortic insufficiencyresults in a to-and-fro murmur which may be difficult to differentiate from continuous PDAmurmurs. In some animals where the diastolic component of the PDA murmur is difficult todetect, other differentials would include subaortic stenosis, pulmonic stenosis, atrial septaldefect, and ventricular septal defect. Differentials for dogs with right-to-left PDA includetetralogy of Fallot, right-to-left shunting atrial or ventricular septal defects, or other complexforms of cyanotic heart disease (rare).

Medical management

Animals with pulmonary edema should be given furosemide for 24 to 48 hours prior tosurgery. If atrial fibrillation is present, the ventricular response rate should be controlled usingdigoxin (with or without - adrenergic blockers or calcium channel blockers) prior to surgery. Ifhemodynamically significant arrhythmias are present they must be controlled. Completeresolution of clinical signs of congestive heart failure may be difficult with medical managementalone.

Surgical treatment

Surgical correction of PDA is accomplished by ligation of the ductus arteriosus. Ligationof PDA is considered curative and should be performed as soon as possible after diagnosis.Secondary mitral regurgitation usually regresses after surgery due to reduction in left ventriculardilation. Inadvertent ductal rupture during dissection is the most serious complication associatedwith PDA repair. The risk of this complication decreases as the surgeon's experience increases.Small ruptures, especially those on the back side of the ductus, often respond to gentletamponade, but will enlarge and worsen if dissection is continued. Large ruptures must becontrolled immediately with vascular clamps and then repaired with pledget-buttressed mattresssutures. Once bleeding is controlled, a decision must be made whether to continue surgery, or toabandon surgery in favor of repair at a later time. Second surgeries are more difficult due toadhesions at the surgical site, so complete occlusion should be attempted during the initialprocedure, if possible. Often, simple ductal ligation is not possible after a rupture has occurred.In such instances, surgical alternatives include ductal closure with pledget-buttressed mattresssutures or ductal division and closure between vascular clamps. The divided ductal ends areclosed with a continuous mattress suture oversewn with a simple continuous pattern. Ductal

closure without division is safer than surgical division, but re-cannulation of the ductus mayoccur. Because ductal division requires added technical expertise, it should be undertaken onlyby experienced surgeons.

Surgical anatomy

The ductus arteriosus in dogs and cats is usually wide (- 1 cm), but relatively short (< 1cm). It is located between the aorta and main pulmonary arteries, caudal to the origin of thebrachycephalic and left subclavian arteries. As a result, most mixing of oxygenated and non-oxygenated blood occurs in the descending aorta in dogs with reverse PDA. Thus, normallyoxygenated blood is supplied to the head and neck, while desaturated blood is presented to thecaudal half of the body (see comments on differential cyanosis above). The left vagus nervealways passes over the ducts arteriosus and must be identified and retracted during dissection.The left recurrent laryngeal nerve can often be identified as it loops around the ductus.

SURGICAL TECHNIQUE

Perform a left 4th space intercostal thoracotomy. Identify the left vagus nerve as it courses overthe ductus arteriosus and isolate it using sharp dissection at the level of the ductus. Place asuture around the nerve and gently retract it. Isolate the ductus arteriosus by bluntly dissectingaround it without opening the pericardial sac. Pass a right-angle forceps behind the ductus,parallel to its transverse plane, to isolate the caudal aspect of the ductus. Then, dissect the

cranial aspect of the ductus by angling the forceps caudally approximately 45 degrees. Completedissection of the ductus by passing forceps from medial to the ductus in a caudal to cranialdirection. Grasp the suture with right-angle forceps. Slowly pull the suture beneath the ductus.If the suture does not slide easily around the ductus, do not force it. Regrasp the suture andrepeat the process, being careful not to include surrounding soft tissues in the forceps. Pass asecond suture using the same maneuver. Alternatively, the suture may be passed as a doubleloop and the suture cut so that you have 2 strands. Slowly tighten the suture closest to the aortafirst. Then, tighten the remaining suture.

Suture materials/special instruments

Heavy silk (No. 1 or 0) or cotton tape are suitable materials for ductal ligation. Rightangle forceps are best suited for blunt dissection of the PDA and passing ligatures. Angled ortangential vascular clamps are required for surgical division of PDA, or for repair of inadvertentruptures. Polypropylene mattress sutures (4-0), buttressed with Teflon pledgets, are used forrepair of ruptured PDA.

Postoperative care and assessment

Postoperative pain should be treated with systemic opioids and local anesthetictechniques. Bupivicaine may be used intercostally or intrapleurally to supplement analgesia.Young animals should be fed as soon as they are fully recovered from surgery. Thoracostomytubes are occasionally placed prior to thoracic closure (e.g., if intraoperative bleeding occurred).They can generally be removed within 12 to 24 hours after surgery.

Prognosis

Dogs with untreated PDA usually develop progressive left-sided congestive heart failureand pulmonary edema. Seventy percent of dogs with untreated PDA die before 1 year of age.Dogs with PDA may also develop suprasystemic pulmonary hypertension that reverses thedirection of the shunt causing severe hypoxemia, cyanosis, and exercise intolerance. Ligation ofa completely reversed PDA is contraindicated.

VASCULAR RING ANOMALIES

Vascular ring anomalies are congenital malformations of the great vessels and theirbranches that cause constriction of the esophagus and signs of esophageal obstruction.

The most common type of vascular ring anomaly is a persistent fourth right aortic arch, rightdorsal aortic root, and rudimentary left ligamentum arteriosum (left sixth arch). The leftpulmonary artery and the descending aorta are connected by the ligamentum arteriosum. Theesophagus is encircled by the ligamentum arteriosum (or patent ductus arteriosus) on the left, thebase of the heart and pulmonary artery ventrally, and the aortic arch on the right. The esophagusis constricted by this vascular “ring” and begins to dilate cranially as food accumulates. Food notpassing beyond the constriction is intermittently regurgitated. Chronic regurgitation predisposesto aspiration pneumonia. Approximately 95% of those diagnosed with vascular ring anomalieswill have a persistent right aortic arch (PRAA). Persistent left vena cava occurs in conjunctionwith PRAA in about 40% of the cases.

Abnormal location of the great vessels mechanically interferes with function of the esophagusand sometimes the trachea and other adjacent structures. The severity of clinical signs and degree

of esophageal stricture depend upon the vascular structures involved. Other types of vascular ringanomalies include: (1) persistent right aortic arch with persistent left subclavian artery, (2)persistent right aortic arch with persistent left ligamentum arteriosum and left subclavian artery,(3) double aortic arch, (4) normal left aortic arch with persistent right ligamentum arteriosum, (5)normal left aortic arch with persistent right subclavian artery, and (6) normal left aortic arch withpersistent right ligamentum arteriosum and right subclavian artery.

Six pairs of aortic arches surround the esophagus and trachea during early fetal life. Normalmaturation and selective regression of these arches form the adult vasculature. All vascular ringanomalies have resulted from abnormal development of arches three, four, and six. Themechanism of inheritance is thought to involve single or multiple recessive genes. In the embryothe first and second aortic arches disappear and the fifth arches are incomplete and inconsistent.The third arch joins the dorsal aortic arch and continues anteriorly as the right and left internalcarotid arteries. The third arch also forms the brachiocephalic trunk. The dorsal aortas disappearbetween the third and fourth arches. Normally the left fourth aortic arch and the dorsal aortic rootpersist to form the permanent aortic arch. The left sixth arch becomes the ductus arteriosus andthe right fourth arch contributes to the right subclavian artery.

Diagnosis

Signalment. Vascular ring anomalies occur in both dogs and cats, but are more common indogs. German shepherds, Irish setters, and Boston terriers are the most commonly affected dogbreeds. Siamese and Persian cats have been diagnosed more often than other cat breeds. Malesand females are equally affected. The condition may affect multiple animals in a litter. Vascularring anomalies are present at birth. Clinical signs are usually evident at the time of weaning,most being diagnosed between 2 and 6 months of age. The condition may not be recognized untillater in life if obstruction is partial and signs are mild. Early diagnosis and treatment of PRAAmay improve the prognosis.

History. The classic history is acute onset of regurgitation when solid or semisolid food is firstfed. Regurgitation of undigested food occurs soon after eating early in the disease; later it mayoccur at variable times (minutes to hours). Affected animals may grow slower than litter matesand appear malnourished. They often have a voracious appetite, some immediately eating theregurgitated food. Coughing with respiratory distress may be a result of aspiration pneumoniaand/or tracheal stenosis secondary to a double aortic arch.

Physical Examination Findings

Affected animals are often thin and small. An enlarged esophagus may sometimes be palpatedat the thoracic inlet and neck. The thoracic inlet and caudal neck area may bulge when the chestis compressed. Murmurs are rare; an occasional patient may have a continuous murmurassociated with concurrent patent ductus arteriosus. Pneumonia may be suggested byauscultating coarse crackles or finding fever.

Radiography/Ultrasonography/Endoscopy

Thoracic radiographs may reveal a dilated esophagus cranial to the heart containing air, water,or food. The trachea may be displaced ventrally and the esophagus may overlap it. Signs ofpneumonia may be identified. Positive contrast radiography using a barium suspension or bariumwith food will demonstrate esophageal constriction at the base of the heart with varying degreesof esophageal dilatation extending cranially. The caudal esophagus is usually a normal size,although sometimes it is dilated. Fluoroscopy is beneficial in evaluating esophageal motility. Thedilated esophagus does not usually demonstrate normal peristaltic contractions. Although notroutinely performed, angiography is beneficial in preoperatively identifying the type of vascularring anomaly and other cardiac anomalies. Echocardiography may also be beneficial. Endoscopicexamination of the esophagus helps rule out other causes of esophageal stricture or obstructionand may reveal esophageal ulceration. Tracheoscopy is not routinely performed, but maydocument tracheal lumen narrowing secondary to external compression.

SURGICAL TREATMENT

Surgical treatment of PRAA is described below. Other types of vascular ring anomalies can bemanaged in a similar fashion. A persistent left vena cava often covers the left ventral area of thevascular ring. A persistent right ligamentum arteriosum and some aberrant right subclaviansshould be approached from the right side. Angiograms are helpful in patients with double aorticarches to determine which arch is dominant and if adequate circulation can be maintained aftertransection of the other arch. It may not be possible to relieve constrictions caused by a doubleaortic arch. If the animal is severely debilitated, place a gastric feeding tube for several daysbefore surgery.

Some surgeons attempt to decrease esophageal lumen size if the esophagus is severely dilatedand not expected to return to normal size. This is accomplished by placing a series ofnonpenetrating “plication” or “gathering” sutures in the accessible lateral esophageal wall.

Alternatively a portion of the esophagus may be resected. These techniques are notrecommended routinely because they increase the risk of complications.

Surgical transection of the constricting structure(s) is recommended before esophagealdilatation becomes severe. Transection is feasible with most vascular ring anomalies with theexception of some double aortic arches. Perform a lateral thoracotomy at the left fourth (fifth)intercostal space for patients with PRAA. Pack the cranial lung caudally to expose themediastinum dorsal to the heart. Identify the aorta, pulmonary artery, ligamentum arteriosum,vagus, and phrenic nerves . Identify the anomalous structure(s). If a persistent left cranial cava ispresent, dissect and retract the vena cava to improve visualization. If a prominent hemiazygousvein is also present, dissect, ligate, and divide it. If a constricting subclavian artery is identified,isolate, ligate, and transect it. Incise the mediastinum, dissect, and elevate the ligamentumarteriosum. Double ligate the ligamentum arteriosum and then transect it. Pass a balloonedcatheter or large orogastric tube through the constricted esophagus to aid identification ofconstricting fibrous bands and to dilate the site. Dissect and transect these fibrous bands from theesophageal wall. Lavage the area, reposition the lung lobes, place a thoracostomy tube ifnecessary, and close the thorax routinely.

Postoperative care and assessment

Postoperative analgesics should be provided. The patient should be closely monitored fordyspnea and the chest tapped if necessary. Nasal oxygen may benefit dyspneic patients. If athoracostomy tube has been placed, the thorax should be aspirated at regular intervals (initiallyevery 15 to 30 minutes) and the volume of air and fluid collected at each interval noted.Thoracostomy tubes can generally be removed the day of surgery or by the next morning in thesepatients. Antibiotics should be continued in debilitated patients if thoracic contaminationoccurred or if pneumonia exists.

Pediatric patients should be closely monitored for hypoglycemia in the postoperative period.Oral intake can be resumed within 12 to 24 hours of surgery. Initially a canned food gruel shouldbe fed with the animal in an upright posture. This stance should be maintained for 10 to 20minutes after eating to help prevent distention of the dilated esophagus and help reestablishesophageal muscle tone and esophageal size. Owners may gradually reduce the amount of waterin the food 2 to 4 weeks after surgery if minimal regurgitation has occurred with gruel feeding.Hopefully, addition of water can ultimately be eliminated without increased regurgitation.Animals who can eat solid food without regurgitation should be allowed to eat with the bowl onthe floor while standing normally. This feeding practice is continued unless regurgitationfrequency increases. Some animals can eventually be fed any type food from a normal stance,while others must continue eating gruel from an elevated stand.

The esophagus should be reevaluated with an esophogram 1 to 2 months after surgery toassess persistent dilatation and motility. Sometimes the esophagus returns to a normal size andfunction. Other times the esophagus remains severely dilated with poor motility. If esophageal

constriction occurs, balloon dilation may be beneficial. Owners should be advised againstbreeding affected animals because it is believed to be a genetic disorder.