Ann Thorac Surg 2000;70:971-973
© 2000 The Society of Thoracic Surgeons
Case report
L
R shunt: a serious consequence of TAPVC repair without ligation of vertical vein
Maully J. Shah, MBBSa,
Shaunak Shah, MCha,
Shreyans Shankargowda, MDa,
Usha Krishnan, DMa,
Kottoorathu M. Cherian, MS, FRACSa
a Division of Cardiology and Cardiothoracic Surgery, Institute of Cardiovascular Diseases, Madras Medical Mission, Madras, India
Address reprint requests to Dr Shah, Heart Center, Children’s Hospital, 4800 Sandpoint Way, NE, Seattle, WA 98105
e-mail: mshah{at}chmc.org
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Abstract
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It has been suggested that concomitant ligation of the vertical vein (VV) is not necessary in the repair of total anomalous pulmonary venous connection. The patency of the VV is desirable in the presence of noncompliant left heart chambers that may not be able to accommodate acute increases in pulmonary blood flow, leading to hemodynamic instability after repair. Complete cessation of flow through the previously patent VV has been observed, obviating the need for a second-stage operation. We report 2 infants who were operated using this strategy, in which the VV continued to function as a conduit for a significant left to right shunt.
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Introduction
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T he surgical technique for correction of supracardiac total anomalous pulmonary venous connection (TAPVC) has undergone several modifications, with most surgeons preferring to ligate the ascending vertical vein (VV) [1, 2]. Leaving the VV open may be considered when the left atrium (LA) is judged to be small and noncompliant [2, 3]. In the latter approach, the unligated VV has been reported to atrophy spontaneously [3]. We report a different experience in 2 patients who underwent repair of supracardiac TAPVC without concomitant ligation of VV. Both developed significant symptoms due to a left to right (L
R) shunt through the persistently patent venous channel.
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Case reports
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Patient 1
A 2.5-month-old (3.5 kg) infant with unobstructed supracardiac TAPVC underwent surgical correction at our institution. Echocardiography showed the pulmonary venous confluence (PVC) draining through a VV to the innominate vein and into the superior vena cava. Under deep hypothermic circulatory arrest, an incision was made from the base of the right atrial appendage extending posteriorly along the interatrial groove, the foramen ovale, and the posterior wall of the LA to the LA appendage. The PVC was opened along its long axis and anastomosed to the LA using continuous 7-0 absorbable polyglyconate sutures. The foramen ovale was closed and the patient was weaned off cardiopulmonary bypass. Upon ligation of the VV, there was an acute increase in pulmonary artery pressures (PAP) to suprasystemic levels. The VV was subsequently left open. Postoperative echocardiograms showed unobstructed pulmonary venous return into the LA. The VV remained distended with ascending flow into the innominate vein. Following discharge to home, the patient continued to have tachypnea and failure to thrive. Cardiac catheterization was performed 10 months (wt = 5.4 kg) after the initial operation (Fig 1A, Table 1). Subsequently, the VV was ligated by a left posterolateral thoracotomy. Representative LA pressures were measured through a cannula introduced into the proximal part of VV (mean = 12 mm Hg). After snaring the VV, mean LA pressure increased to 28 mm Hg. With hyperventilation and 100% FiO2, mean LA pressures decreased to 20 mm Hg. The VV was doubly ligated with 2-0 silk. The patient was ventilated mechanically with FiO2 0.8 and 10 ppm of nitric oxide (NO) for 24 hours, at the end of which mean LA pressures decreased to 18 mm Hg. This patient had an uneventful recovery. At 7 months follow-up, the patient is asymptomatic (wt = 8.2 kg) and doing well.
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Fig 1. Angiograms in patient 1 (A) and patient 2 (B) showing a catheter from the superior vena cava through the In.V into the LVV. The LVV is seen draining the PVC. Note that the LUPV is draining separately into the LVV in patient 2. (In.V = innominate vein; LUPV = left lower pulmonary vein; LVV = left vertical vein; PVC = pulmonary venous confluence.)
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Patient 2
A 2-month-old (4.0 kg) infant with unobstructed supracardiac TAPVC underwent surgical repair as described in the previous case. A left upper pulmonary vein draining separate from the PVC into the VV was identified preoperatively. Upon ligation of the VV, the PAP increased to suprasystemic levels. The ligature was removed and the VV left patent. Postoperative echocardiographic findings and symptomatology were similar to the previous case. Cardiac catheterization (Fig 1B, Table 1) was performed after 12 months (wt = 6.5 kg) following which the VV was ligated close to its junction with the innominate vein. At 5 months follow-up (wt = 9.0 kg), the child is asymptomatic.
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Comment
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Several recent perioperative modifications including the use of NO have improved outcome of patients undergoing repair of TAPVC [4–6]. Diminished LA volume, compliance, and reservoir function may be factors limiting survival despite an adequate surgical repair, because the noncompliant LA cannot accommodate an acute increase in pulmonary venous flow [7, 8]. Providing a temporary pulmonary venous reservoir by leaving the VV open may offer an advantage in the early postoperative period [3].
In both patients, the decision to keep the VV patent was made after the occurrence of elevated PAP upon ligating the VV. In the absence of pulmonary venous obstruction, this undesirable effect can be explained by decreased unloading of the PVC due to diminished LA compliance causing postcapillary pulmonary hypertension. In this situation the patent VV is beneficial, serving to decompress the noncompliant LA. However, it is important to recognize that the advantage is temporary. Contrary to the report by Cope and coworkers [3], in which the patent venous pathway atrophied, the follow-up of our 2 patients demonstrated that the VV was not a "temporary" pulmonary venous reservoir but continued to function as a conduit for a large LR shunt. This increases volume work on the right ventricle leading to significant symptoms.
We conclude that leaving the VV open at time of supracardiac TAPVC repair may afford a smoother early postoperative period in patients with severely noncompliant LA, but the benefit is transitory. Significant elevation in PAP or LA pressures upon snaring or ligating the VV after achieving an adequate anastomosis between the PVC and the LA are useful indicators of impaired LA compliance. Patients who have undergone this approach should be followed closely for persistent LR shunt through the patent VV. The residual shunt can be safely interrupted by surgical ligation of the VV at a later stage without adverse hemodynamic sequelae.S0003-4975(00)01501-0
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References
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Kirklin J.W., Barrett-Boyes B.G. Total anomalous pulmonary venous connection. In: Kirklin J.W., Barret-Boyes B.G., eds. Cardiac surgery, 2nd ed. New York: Churchill-Livingstone, 1993:645-673.
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Mustard W.T., Keith J.D., Trusler G.A. Two stage correction of total anomalous pulmonary venous drainage in childhood. J Thorac Cardiovasc Surg 1962;44:477-485.
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Cope J.T., Banks D., McDaniel N.L., Shockley K.S., Nolan S.P., Kron I.L. Is vertical vein ligation necessary in repair of total anomalous pulmonary venous connection?. Ann Thorac Surg 1997;64:23-29.[Abstract/Free Full Text]
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Hyde J.A.J., Stumper O., Barth M.J., et al. Total anomalous pulmonary venous connection. Eur J Cardiothorac Surg 1999;15:735-741.[Abstract/Free Full Text]
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Lupinetti F.M., Kulik T.J., Beekman R.H., Crowley D.C., Bove E.L. Correction of total anomalous pulmonary venous connection in infancy. J Thorac Cardiovasc Surg 1993;106:880-885.[Abstract]
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Graham T.P., Jr, Jarmakani J.M., Canent R.V., Jr Left heart volume characteristics with a right ventricular volume overload. Circulation 1972;45:389-396.[Abstract/Free Full Text]
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Mathew R., Thilenius O.G., Replogle R.L., Arcilla R.A. Cardiac function in total anomalous pulmonary venous return before and after surgery. Circulation 1977;55:361-370.[Abstract/Free Full Text]
Accepted for publication December 23, 1999.
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Abstract
Introduction
