Theresa W. Fossum DVM, MS, PhD, Diplomate ACVS Tom and Joan Read Chair in Veterinary Surgery, Professor of Surgery Texas A&M University College of Veterinary Medicine, College Station, TX 77843-4474

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 not require opening major cardiac structures) are most commonly performed; however, some conditions require open cardiac surgery (i.e., a major cardiac structure must be opened to accomplish the repair). Open cardiac surgery necessitates that circulation be arrested during the procedure by inflow occlusion or cardiopulmonary bypass. Venous inflow occlusion provides brief circulatory arrest, allowing short procedures (less than 5 min) to be performed. Longer open cardiac procedures require establishing an extracorporeal circulation by cardiopulmonary bypass to maintain organ perfusion during surgery. Cardiac surgery is not fundamentally different from other types of general surgery and similar principles of good surgical technique (i.e., atraumatic tissue handling, good hemostasis, and secure knot tieing) apply. Consequences of poor surgical technique are often devastating. Cardiac surgery differs from other surgeries in that motion from ventilation and cardiac contractions adds to the technical difficulty of performing these procedures. Approaches that provide limited access to dorsal structures 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-tied knots (vs. instrument tieing) should be considered a fundamental skill for cardiac surgeons. Secure knot tieing is critically important to successful cardiac surgery. Hand tieing knots is fast and produces tighter and more secure knots than instrument tieing. The one-handed knot tie technique is best suited to the fine sutures used in cardiac surgery. Tight knots are facilitated by throwing the first two or three throws in the same direction before finishing with square knots for security. Inflow Occlusion Inflow 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 allows limited time to perform cardiac procedures. Ideally, circulatory arrest in a normothermic patient should be less than 2 minutes, but can be extended to 4 minutes if necessary. Circulatory arrest time can 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 the surgery requires that the procedure be well planned and executed with speed and expertise. We have used this technique primarily for right atrial tumors and cor-triatriatum dexter. Depending on the cardiac procedure being done, a left or right thoracotomy or median sternotomy is performed. With a right thoracotomy or median sternotomy, the cranial and caudal vena cava and azygous vein are occluded with vascular clamps or Rumel tourniquets which can be made by passing umbilical tape around the vessel, then threading umbilical tape through a piece of rubber tubing that is 1 to 3 inches long. When the umbilical tape has been adequately tightened to occlude the vessel, a clamp is placed above the rubber tubing to hold it securely in place. Care must be taken to avoid injuring the right phrenic nerve during placement of the clamps or tourniquets. For left thoracotomies, separate tourniquets are passed around the cranial and caudal venae cavae. Then, dissecting dorsal to the esophagus and aorta, the azygous vein is occluded by placing 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 greatly extends the time available for open cardiac surgery. Several advances (i.e., development of membrane oxygenators, improved methods of myocardial protection, increased availability of monitoring technologies, and improved veterinary critical care) have made cardiopulmonary bypass increasingly feasible in dogs. Cardiopulmonary bypass can be used to treat dogs with congenital or acquired cardiac defects. Readers are referred to a cardiovascular surgery text for details of performing cardiopulmonary bypass. Preoperative concerns Animals requiring cardiac surgery often have prior cardiovascular compromise that should be stabilized medically when possible, prior to anesthetic induction. Congestive heart failure, particularly pulmonary 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 also postoperative care below). Ventricular tachycardia should be suppressed before surgery with class I antiarrhythmic drugs (i.e., lidocaine, procainamide). Lidocaine is effective for management of ventricular tachyarrhythmias during and immediately after surgery. Supraventricular tachycardia may require management with digoxin, beta-adrenergic blockers (e.g., esmolol, atenolol), or calcium channel blocking drugs (e.g., diltiazem) prior to surgery. Atrial fibrillation should be controlled prior to surgery with digoxin to lower the ventricular response rate below 140 bpm. This may require the addition of beta-adrenergic blockade or calcium channel blocking drugs if digoxin alone does not decrease the ventricular rate sufficiently. Animals with bradycardia should undergo an atropine response test before surgery. If bradycardia is not responsive to atropine, temporary transvenous pacing or may be required. Most animals should undergo evaluation by echocardiography prior to cardiac surgery as an incomplete or inaccurate diagnosis can have devastating consequences. With the advent of Doppler echocardiography, cardiac catheterization is no longer routinely necessary prior to cardiac surgery.

SUB-AORTIC STENOSIS To 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 been shown to decrease the incidence of sudden death in this population. Reports of closed transventricular dilation showed marked post-operative decreases in pressure gradients, but restenosis is common, usually within three months. This restenosis is consistent with reports in the human literature following transventricular dilation. The most promising results thus far are found in techniques investigating the use of cardiopulmonary bypass and open surgical correction. The traditional approach to resection of the subvalvular stenosis is through an aortotomy made above the coronary ostia. Tearing of the aortic incision during resection is a potential complication of this approach. The typical defect is a discrete fibrous membrane located 1-5 mm below the base of the cusps of the aortic valve that reflects onto the septal cusp of the mitral valve from the septum. This portion of the ring must be excised to adequately reduce the pressure gradient but care must be taken not to damage the mitral valve during the resection. Varying degrees of muscular hypertrophy of the interventricular septum accompany this 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 this technique 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 reconstruct the septal defect with a patch graft. The proximity of the conduction system is the primary concern when performing a septal myectomy.

To date, one dog with subaortic stenosis has undergone cardiopulmonary bypass and openheart correction of this defect at Texas A&M University. The patient had severe SAS with a Doppler-derived gradient in excess of 200 mmHg and moderate to severe left ventricular hypertrophy without significant ventricular ectopy or mitral regurgitation. Through a median sternotomy, a right ventriculotomy was performed. An initial incision into the hypertrophied septum allowed exploration of the left ventricular outflow tract (LVOT). An aortotomy was also performed 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 to the mitral valve. The septal defect was repaired with autologous pericardium harvested at surgery and treated with glutaraldehyde to improve its handling characteristics. Full thickness resection was performed in an attempt to alleviate the late restenosis noted with alternate partial thickness resection techniques. Although not substantiated in dogs, it is hoped that this will, at a minimum, delay the progression of disease and decrease the chance of sudden death. PULMONIC STENOSIS Although 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. Surgery or 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 in those cases with significant subvalvular muscular hypertrophy. Restenosis, presumably due to scarring, has been reported. Alternatively a patch graft technique, using PTFE or Gortex material, may be more likely to provide a greater and longer standing reduction in the pressure gradient, although survival data have not been previously evaluated. Patch grafting techniques may be performed under inflow occlusion and mild hypothermia; however, the use of cardiopulmonary bypass affords the surgeon more time for precise placement of the graft and thus may allow for improved postoperative outcomes. Dogs with an aberrant coronary artery contributing to their pulmonic stenosis are not considered candidates for balloon valvuloplasty or patch grafting techniques due to the risk of disturbance of that coronary vessel. Surgery in these animals would generally require cardiopulmonary bypass and placement of a conduit from the right ventricle to the pulmonary artery to circumvent the stenosis. SEPTAL DEFECTS Ventricular septal defect (VSD) is the second most common congenital heart defect in cats and accounts for 5% to 10% of congenital heart defects seen in dogs. Most ventricular septal defects in small animals occur in the membranous septum. Perimembranous defects are located in the membranous 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 crista supraventricularis. The pathophysiology of VSD depends on the size of the defect and on pulmonary vascular resistance. VSD typically causes a left-to-right shunt. A typical VSD overloads the left heart and, depending on its size and location, may overload the right heart as well. A large VSD can progress to left-sided congestive heart failure. Chronic overcirculation of the lungs can cause progressive pulmonary vascular remodeling leading to severe pulmonary hypertension and right-toleft shunting of blood (Eisenmenger’s physiology). Aortic insufficiency is a fairly common secondary abnormality associated with VSD, particularly infundibular VSD. Aortic insufficiency results from prolapse of an aortic leaflet into the defect. This prolapse is due to the Venturi effect associated with VSD flow and loss of support of the aortic annulus. Aortic insufficiency adds to the left ventricular volume overload and is usually progressive. Definitive patch closure of VSD can be accomplished with the aid of cardiopulmonary bypass in dogs over 4 kg in body weight. A perimembranous VSD is corrected from the right side via a right atriotomy approach. An infundibular VSD is corrected via a right ventriculotomy from a left thoracotomy or median sternotomy approach. . Atrial defects can easily be fixed using bypass. We have performed surgery in several dogs with septal defects where we have used glutaraldehyde fixed pericardium to repair the defect. The progrnosis is generally excellent.

PATENT DUCTUS ARTERIOSUS The ductus arteriosus is a fetal vessel that connects the main pulmonary artery and descending 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 "patent ductus arteriosus". PDA is the most common congenital heart defect of dogs; it also occurs in cats. PDA causes a left-to-right shunt that results in volume overload of the left ventricle and produces left ventricular dilation and hypertrophy. Progressive left ventricular dilation distends the mitral valve annulus causing secondary regurgitation and additional ventricular overload. This severe volume overload leads to left-sided congestive heart failure and pulmonary edema, usually within the first year of life. Atrial fibrillation may occur as a late sequela due to marked left atrial dilation. Rarely, dogs with PDA develop suprasystemic pulmonary hypertension that reverses the direction of flow through the shunt causing severe hypoxemia and cyanosis (Eisenmenger’s physiology). Right-to-left PDA can occur as a late sequela to untreated PDA. When right-to-left PDA is noted in very young animals it may be due to persistent pulmonary hypertension after birth. Reversal of PDA lessens the risk for developing progressive left-sided heart failure, but causes severe debilitating systemic hypoxemia, exercise intolerance, and progressive polycythemia. Diagnosis CLINICAL PRESENTATION Signalment - PDA is seen more commonly in purebred, female dogs. Maltese, Pomeranians, Shetland sheepdogs, English springer spaniels, keeshonds, bischon frise, miniature and toy poodles, and Yorkshire terries are at increased risk to develop PDA. A genetic basis has been established in poodles. History - Most young animals with PDA are asymptomatic or have only mild exercise intolerance. The most common complaint in symptomatic animals with left-to-right shunts are cough or shortness of breath (or both) due to pulmonary edema. Animals with right-to-left or reverse PDA may be asymptomatic or have exercise intolerance and hindlimb collapse on exercise. 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 is prominent and displaced caudally and a palpable cardiac A “thrill” often is present. Femoral pulses are strong or hyperkinetic (water hammer pulse) due to a wide pulse pressure caused by diastolic runoff of blood through the ductus. Tall R waves (> 2.5 mV) or wide P waves on a lead II electrocardiogram are supportive of the diagnosis, but not always present. Atrial fibrillation or ventricular ectopy may be present in advanced cases. The physical examination findings in animals with right-to-left or reverse PDA differ from those with left-to-right shunts. “Differential” cyanosis is typically present (i.e., cyanosis is most apparent in the caudal mucous membranes), but cyanosis may also be noted in the cranial half of the body in some animals. Cyanosis occurs because there is admixture of non-oxygenated blood (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, a murmur may not be ausculted if polycythemia is present or if left and right sided pressures are nearly equal and shunting of blood through the ductus is minimal. Radiography/Echocardiography Thoracic radiographs typically show left atrial and ventricular enlargement, enlargement of pulmonary vessels, and a characteristic dilation of the descending aorta on the dorsoventral view. Echocardiography provides information that further confirms PDA and helps rule concurrent cardiac defects, but is not invariably required to establish the diagnosis. Echocardiographic findings that support a diagnosis of PDA include left atrial enlargement, left ventricular dilation and hypertrophy, pulmonary artery dilation, increased aortic ejection velocity, and a characteristic reverse turbulent Doppler flow pattern in the pulmonary artery. With right-to-left PDA, thoracic radiographs show evidence of biventricular enlargement and marked enlargement of the pulmonary artery segment. Pulmonary arteries may also appear tortuous. A right-to-left PDA can be documented by performing a saline bubble contrast echocardiogram. Observing bubbles in the descending aorta, but not in any left sided cardiac chamber, 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 in response to increased erythropoietin production due to chronic hypoxemia. Differential diagnosis The characteristic physical examination findings (i.e., continuous murmur, bounding arterial pulses) makes diagnosis of PDA straightforward in most affected animals. A combination of aortic stenosis/aortic insufficiency or ventricular septal defect/aortic insufficiency results in a to-and-fro murmur which may be difficult to differentiate from continuous PDA murmurs. In some animals where the diastolic component of the PDA murmur is difficult to detect, other differentials would include subaortic stenosis, pulmonic stenosis, atrial septal defect, and ventricular septal defect. Differentials for dogs with right-to-left PDA include tetralogy of Fallot, right-to-left shunting atrial or ventricular septal defects, or other complex forms of cyanotic heart disease (rare). Medical management Animals with pulmonary edema should be given furosemide for 24 to 48 hours prior to surgery. If atrial fibrillation is present, the ventricular response rate should be controlled using digoxin (with or without - adrenergic blockers or calcium channel blockers) prior to surgery. If hemodynamically significant arrhythmias are present they must be controlled. Complete resolution of clinical signs of congestive heart failure may be difficult with medical management alone. Surgical treatment Surgical correction of PDA is accomplished by ligation of the ductus arteriosus. Ligation of 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 ventricular dilation. Inadvertent ductal rupture during dissection is the most serious complication associated with 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 gentle tamponade, but will enlarge and worsen if dissection is continued. Large ruptures must be controlled immediately with vascular clamps and then repaired with pledget-buttressed mattress sutures. Once bleeding is controlled, a decision must be made whether to continue surgery, or to abandon surgery in favor of repair at a later time. Second surgeries are more difficult due to adhesions at the surgical site, so complete occlusion should be attempted during the initial procedure, 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 mattress sutures or ductal division and closure between vascular clamps. The divided ductal ends are closed 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 may occur. Because ductal division requires added technical expertise, it should be undertaken only by experienced surgeons. Surgical anatomy The ductus arteriosus in dogs and cats is usually wide (- 1 cm), but relatively short (< 1 cm). It is located between the aorta and main pulmonary arteries, caudal to the origin of the brachycephalic and left subclavian arteries. As a result, most mixing of oxygenated and nonoxygenated blood occurs in the descending aorta in dogs with reverse PDA. Thus, normally oxygenated blood is supplied to the head and neck, while desaturated blood is presented to the caudal half of the body (see comments on differential cyanosis above). The left vagus nerve always 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 over the ductus arteriosus and isolate it using sharp dissection at the level of the ductus. Place a suture around the nerve and gently retract it. Isolate the ductus arteriosus by bluntly dissecting around 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. Complete dissection of the ductus by passing forceps from medial to the ductus in a caudal to cranial direction. 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 and repeat the process, being careful not to include surrounding soft tissues in the forceps. Pass a second suture using the same maneuver. Alternatively, the suture may be passed as a double loop and the suture cut so that you have 2 strands. Slowly tighten the suture closest to the aorta first. Then, tighten the remaining suture.

Suture materials/special instruments

Heavy silk (No. 1 or 0) or cotton tape are suitable materials for ductal ligation. Right angle forceps are best suited for blunt dissection of the PDA and passing ligatures. Angled or tangential vascular clamps are required for surgical division of PDA, or for repair of inadvertent ruptures. Polypropylene mattress sutures (4-0), buttressed with Teflon pledgets, are used for repair of ruptured PDA. Postoperative care and assessment Postoperative pain should be treated with systemic opioids and local anesthetic techniques. Bupivicaine may be used intercostally or intrapleurally to supplement analgesia. Young animals should be fed as soon as they are fully recovered from surgery. Thoracostomy tubes 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 failure and 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 the direction of the shunt causing severe hypoxemia, cyanosis, and exercise intolerance. Ligation of a completely reversed PDA is contraindicated.

VASCULAR RING ANOMALIES Vascular ring anomalies are congenital malformations of the great vessels and their branches 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, right dorsal aortic root, and rudimentary left ligamentum arteriosum (left sixth arch). The left pulmonary artery and the descending aorta are connected by the ligamentum arteriosum. The esophagus is encircled by the ligamentum arteriosum (or patent ductus arteriosus) on the left, the base of the heart and pulmonary artery ventrally, and the aortic arch on the right. The esophagus is constricted by this vascular “ring” and begins to dilate cranially as food accumulates. Food not passing beyond the constriction is intermittently regurgitated. Chronic regurgitation predisposes to aspiration pneumonia. Approximately 95% of those diagnosed with vascular ring anomalies will have a persistent right aortic arch (PRAA). Persistent left vena cava occurs in conjunction with PRAA in about 40% of the cases. Abnormal location of the great vessels mechanically interferes with function of the esophagus and 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 ring anomalies 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 with persistent right ligamentum arteriosum and right subclavian artery. Six pairs of aortic arches surround the esophagus and trachea during early fetal life. Normal maturation and selective regression of these arches form the adult vasculature. All vascular ring anomalies have resulted from abnormal development of arches three, four, and six. The mechanism of inheritance is thought to involve single or multiple recessive genes. In the embryo the 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 internal carotid arteries. The third arch also forms the brachiocephalic trunk. The dorsal aortas disappear between the third and fourth arches. Normally the left fourth aortic arch and the dorsal aortic root persist to form the permanent aortic arch. The left sixth arch becomes the ductus arteriosus and the right fourth arch contributes to the right subclavian artery.

Diagnosis Signalment. Vascular ring anomalies occur in both dogs and cats, but are more common in dogs. German shepherds, Irish setters, and Boston terriers are the most commonly affected dog breeds. Siamese and Persian cats have been diagnosed more often than other cat breeds. Males and females are equally affected. The condition may affect multiple animals in a litter. Vascular ring 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 until later in life if obstruction is partial and signs are mild. Early diagnosis and treatment of PRAA may improve the prognosis. History. The classic history is acute onset of regurgitation when solid or semisolid food is first fed. Regurgitation of undigested food occurs soon after eating early in the disease; later it may occur at variable times (minutes to hours). Affected animals may grow slower than litter mates and appear malnourished. They often have a voracious appetite, some immediately eating the regurgitated food. Coughing with respiratory distress may be a result of aspiration pneumonia and/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 palpated at the thoracic inlet and neck. The thoracic inlet and caudal neck area may bulge when the chest is compressed. Murmurs are rare; an occasional patient may have a continuous murmur associated with concurrent patent ductus arteriosus. Pneumonia may be suggested by auscultating 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 of pneumonia may be identified. Positive contrast radiography using a barium suspension or barium with food will demonstrate esophageal constriction at the base of the heart with varying degrees of esophageal dilatation extending cranially. The caudal esophagus is usually a normal size, although sometimes it is dilated. Fluoroscopy is beneficial in evaluating esophageal motility. The dilated esophagus does not usually demonstrate normal peristaltic contractions. Although not routinely performed, angiography is beneficial in preoperatively identifying the type of vascular ring anomaly and other cardiac anomalies. Echocardiography may also be beneficial. Endoscopic examination of the esophagus helps rule out other causes of esophageal stricture or obstruction and may reveal esophageal ulceration. Tracheoscopy is not routinely performed, but may document tracheal lumen narrowing secondary to external compression.

SURGICAL TREATMENT Surgical treatment of PRAA is described below. Other types of vascular ring anomalies can be managed in a similar fashion. A persistent left vena cava often covers the left ventral area of the vascular ring. A persistent right ligamentum arteriosum and some aberrant right subclavians should be approached from the right side. Angiograms are helpful in patients with double aortic arches to determine which arch is dominant and if adequate circulation can be maintained after transection of the other arch. It may not be possible to relieve constrictions caused by a double aortic arch. If the animal is severely debilitated, place a gastric feeding tube for several days before surgery. Some surgeons attempt to decrease esophageal lumen size if the esophagus is severely dilated and not expected to return to normal size. This is accomplished by placing a series of nonpenetrating “plication” or “gathering” sutures in the accessible lateral esophageal wall.

Alternatively a portion of the esophagus may be resected. These techniques are not recommended routinely because they increase the risk of complications. Surgical transection of the constricting structure(s) is recommended before esophageal dilatation becomes severe. Transection is feasible with most vascular ring anomalies with the exception 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 the mediastinum 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 is present, dissect and retract the vena cava to improve visualization. If a prominent hemiazygous vein 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 ligamentum arteriosum. Double ligate the ligamentum arteriosum and then transect it. Pass a ballooned catheter or large orogastric tube through the constricted esophagus to aid identification of constricting fibrous bands and to dilate the site. Dissect and transect these fibrous bands from the esophageal wall. Lavage the area, reposition the lung lobes, place a thoracostomy tube if necessary, and close the thorax routinely. Postoperative care and assessment Postoperative analgesics should be provided. The patient should be closely monitored for dyspnea and the chest tapped if necessary. Nasal oxygen may benefit dyspneic patients. If a thoracostomy tube has been placed, the thorax should be aspirated at regular intervals (initially every 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 these patients. Antibiotics should be continued in debilitated patients if thoracic contamination occurred 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 should be fed with the animal in an upright posture. This stance should be maintained for 10 to 20 minutes after eating to help prevent distention of the dilated esophagus and help reestablish esophageal muscle tone and esophageal size. Owners may gradually reduce the amount of water in 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 on the floor while standing normally. This feeding practice is continued unless regurgitation frequency 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 to assess persistent dilatation and motility. Sometimes the esophagus returns to a normal size and function. Other times the esophagus remains severely dilated with poor motility. If esophageal

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