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J Thorac Cardiovasc Surg 2007;134:1397-1405
© 2007 The American Association for Thoracic Surgery

Surgery for Congenital Heart Disease

Subdiaphragmatic venous hemodynamics in patients with biventricular and Fontan circulation after diaphragm plication

Tain-Yen Hsia, MDa,*, Sachin Khambadkone, MD, MRCPb, Scott M. Bradley, MDa, Marc R. de Leval, MD, FRCSb

a Medical University of South Carolina, Charleston, SC
b Great Ormond Street Hospital for Children, NHS Trust, London, United Kingdom.

Received for publication May 4, 2007; revisions received July 17, 2007; accepted for publication July 24, 2007.

* Address for reprints: Tain-Yen Hsia, MD, Cardiothoracic Surgery, Medical University of South Carolina, 96 Jonathan Lucas St, CSB 409, Charleston, SC, 29425. (Email: hsiaty{at}musc.edu).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
Objective: Diaphragm paralysis owing to phrenic nerve injury can result in significant morbidity in children undergoing surgical management of congenital cardiac defects. Diaphragm plication is the accepted therapy for diaphragm paralysis. We have investigated subdiaphragmatic venous hemodynamics in patients with biventricular and Fontan circulation after diaphragm plication.

Methods: Doppler ultrasound was used to evaluate flows in the hepatic vein, portal vein, and subhepatic inferior vena cava under respiratory monitoring and with a tilt table. Twenty-nine patients with biventricular circulation were studied: 19 with normal diaphragms and 10 after diaphragm plication. Twenty-eight patients with total cavopulmonary connections after the Fontan procedure were also studied: 19 with normal diaphragms and 9 with plicated diaphragms. Inspiratory/expiratory flow ratios in supine and upright positions were calculated to investigate respiratory effects, and upright/supine flow ratios were calculated to assess gravity effects.

Results: In patients with biventricular circulation and normal diaphragms, hepatic venous flow was augmented by inspiration; this effect was reduced in patients with a plicated diaphragm (upright inspiratory/expiratory flow ratios: 2.4 vs 1.4, respectively; P = .01). Portal venous flow was higher during expiration; this effect was lost in patients with a plicated diaphragm (supine inspiratory/expiratory flow ratios: 0.8 and 1.0; P < .05). In Fontan patients with normal diaphragms, hepatic venous flow depended heavily on inspiration. This effect was blunted in patients with a plicated diaphragm (supine inspiratory/expiratory flow ratios: 3.2 vs 2.3; P < .05). Expiratory augmentation of portal flow was absent in Fontan patients with normal diaphragms and reversed in patients a plicated diaphragm (supine inspiratory/expiratory flow ratios: 1.0 vs 1.6; P = .02). Gravity reduced Fontan portal venous flow; having a plicated diaphragm did not alter this effect (upright/supine flow ratios: 0.7 vs 0.7).

Conclusions: In patients with biventricular and those with Fontan circulation with a paralyzed diaphragm, plication does not completely restore normal subdiaphragmatic venous hemodynamics. In Fontan patients with a plicated diaphragm, important inspiration-derived hepatic venous flow is suppressed, and portal venous flow loses its normal expiratory augmentation. These flow dynamics share similarities with those observed in patients with failing Fontan circulation. This suboptimal splanchnic circulation may contribute to early problems of prolonged pleural effusions and ascites and potentially may promote late Fontan failure. Phrenic nerve injury should consequently be avoided at all costs before or at the time of the Fontan operation.

Abbreviations and Acronyms IVC = inferior vena cava; NYHA = New York Heart Association; Qex = expiratory flow rate; Qin = inspiratory flow rate; Qsup = flow rate in the supine position; Qup = flow rate in the upright position; TCPC = total cavopulmonary connection


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Discussion
 Conclusions
 References
 
GoRespiration and gravity constantly exert important and, at times, negative influences on venous return dynamics. Classic physiologists, such as Brecher,1Go Guyton,2Go and Moreno and Burchell,3Go have demonstrated that the biventricular heart compensates for these influences so that they are normally unnoticed. Fontan circulation places additional stress on venous return, especially in the subdiaphragmatic region where hydrostatic pressure and interposition of the liver pose further challenges to the passive venous hemodynamics.4Go In several studies focusing on subdiaphragmatic venous hemodynamics, we5-7Go have demonstrated that the splanchnic venous circulation is a particularly vulnerable part of the Fontan circulation. In patients with the Fontan circulation, hepatic venous flow is primarily driven by inspiration.7Go A loss of hepatic–portal circulatory autoregulation results in a portal venous system that is unprotected from elevated hepatic venous pressure and subject to exaggerated gravitational stress.5Go These anomalies are amplified in "failing" Fontans or in patients with elevated Fontan pressures.5Go On the basis of these observations, we postulated that patients who have had the Fontan operation are likely to be highly susceptible to disturbances of respiratory mechanics, such as diaphragm paralysis owing to phrenic nerve injury, and thus may benefit from early diaphragm plication.5Go

Two retrospective case-control analyses of patients with Fontan circulation have shown that diaphragm paralysis significantly increases postoperative morbidity, including prolonged pleural effusions, longer hospital stay, chronic ascites, and higher rate of hospital readmission.8,9Go Both studies suggested that early diaphragm plication would improve and reoptimize Fontan flow dynamics and potentially avoid late complications.

In children with biventricular circulation, early surgical plication has been recognized to limit the morbidity associated with diaphragm paralysis and its resultant respiratory disturbance.10-12Go However, it remains unknown whether diaphragm plication restores venous flow dynamics to normal. The purpose of this study is to examine whether the effects of respiration and gravity on subdiaphragmatic flow dynamics are normalized in patients with biventricular and Fontan circulation after diaphragm plication for phrenic nerve palsy.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Discussion
 Conclusions
 References
 
Study Groups
Twenty-nine patients with biventricular circulation were studied: 10 had undergone surgical diaphragm plication for diaphragm paralysis (group BV-DP). They were in self-reported New York Heart Association (NYHA) functional class I or II (9:1, respectively) and were 7 to 17 years of age (mean 11 ± 3 years). Nine BV-DP patients had undergone previous surgery: 2 tetralogy of Fallot repairs, 1 arterial and 1 atrial switch operation for transposition of the great arteries, 1 interrupted aortic arch repair, 1 open pulmonary valvotomy for pulmonary stenosis, 1 orthotopic heart transplant, 1 atrioventricular septal defect repair, and 1 mediastinal teratoma resection. One BV-DP patient with no structural heart defect required right hemidiaphragm plication for phrenic nerve palsy as a complication of pneumonia/emypema. Nine had plication of a unilateral diaphragm (6 left, 3 right), and 1 patient underwent bilateral diaphragm plications. Nineteen age- and sex-matched normal volunteers were studied as controls for the biventricular analysis (group BV).

Twenty-eight patients were studied 1 to 13 years (mean 7 ± 4 years) after a total cavopulmonary connection (TCPC: lateral tunnel or extracardiac conduit). Nine had previously undergone a unilateral diaphragm plication (group TCPC-DP) for diaphragm paralysis (8 right and 1 left); 5 were in NYHA class I, 1 in class II, and 3 in class III. The remaining 19 TCPC patients with no diaphragm plication were in self-reported NYHA functional class I (group TCPC); none had clinical signs of congestive heart failure, arrhythmia, major pulmonary arteriovenous malformations, protein-losing enteropathy, or other known complications of the Fontan circulation. Six patients in the TCPC-DP group had a fenestrated inferior pathway and 5 in the TCPC group.

For both BV-DP and TCPC-DP groups, the diagnosis of diaphragmatic paralysis was confirmed by either ultrasonongraphic or fluoroscopic interrogation in the immediate postoperative period or before hospital discharge. Diaphragm plications were used before discharge or to assist mechanical ventilatory weaning. In all cases, the surgical method used involved a limited lateral thoracotomy on the affected side and the diaphragm was plicated by the standard central pleating technique. There was no formal interval study of diaphragm function.

All subjects underwent hepatic venous, portal venous, and infrahepatic inferior vena caval (IVC) Doppler ultrasonographic interrogation under simultaneous dynamic respiratory and electrocardiographic monitoring. A tilt table was used to allow measurements in the supine and upright (85°-90° from horizontal plane) positions. In addition, ultrasonographic examination of bilateral diaphragmatic excursion was performed in all subjects to document diaphragm function. The study protocol was approved by the hospital research ethics committee, and informed consent was obtained for all subjects.

Doppler Ultrasound Recordings
The methodology, mathematical background, and flow rate calculations used in this study were described in detail previously.5-7Go In brief, pulsed-wave Doppler recordings in the hepatic vein, portal vein, and IVC were made with each subject breathing quietly in the supine and then the upright position. Recordings were made in the left or middle hepatic vein (approximately 1 cm proximal to the junction with the IVC) and the infrahepatic IVC (1–2 cm proximal to the junction with the hepatic vein). The portal flow signal was obtained in the main portal trunk before its division into the right and left branches, following previously published protocols.13Go Volumetric flow rates in hepatic vein, portal vein, and IVC were calculated from velocity time integrals and the measured vessel diameters from the Doppler recording.

Gravity Effect
The effect of gravity on net flow rate was evaluated. Net flow rate was defined as the absolute total flow during a complete respiratory cycle obtained by subtracting the retrograde velocity time integral from the antegrade velocity time integral. The effect of gravity on flow rate was represented as the ratio of flow rate in the upright position over that in the supine position, Qup/Qsup. A ratio of less than 1 signifies reduced flow in the upright position.

Respiratory Effect
The Doppler signal was evaluated during inspiration, during expiration, and throughout a complete respiratory cycle.5-7Go Flow rates during the inspiratory phase, Qin, of the respiratory cycle were determined, as well as during the expiratory phase, Qex. The effect of respiration on flow was expressed as a ratio of Qin/Qex and was measured in both supine and upright positions for all 3 venous regions of interest. When Qin is higher than Qex, Qin/Qex ratio is greater than 1, and vice versa.

Statistical Analysis
All data are expressed as mean ± standard deviation. Comparisons of (1) normal against biventricular patients with plicated diaphragms (BV vs BV-DP) and (2) TCPC patients against those with plicated diaphragms (TCPC vs TCPC-DP) were performed with 2-tailed t tests. To evaluate the influence of upright posture on Qin/Qex, we conducted intragroup examinations of Qin/Qex in the supine versus Qin/Qex in the upright position using paired t tests.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Discussion
 Conclusions
 References
 
Study Group Characteristics
There were no significant differences in age and male/female distribution between BV-DP and BV subjects. Among TCPC patients, those with a plicated diaphragm were slightly younger than those without (11 ± 3 years TCPC-DP vs 15 ± 5 years TCPC; P = .04) and all were male (9:0 TCPC-DP vs 14:5 TCPC; male/female). In addition, a greater proportion had undergone an extracardiac conduit versus lateral tunnel TCPC (5:4 TCPC-DP vs 2:17 TCPC; extracardiac conduit/lateral tunnel). Similar to our previous study,7Go there were no quantitative differences between the extracardiac conduit and lateral tunnel TCPC patients within each study group, so their data are presented together.

There were no differences in room air oxygen saturation between (1) BV-DP and BV subjects (98% ± 1%, vs 97% ± 2%) and between (2) TCPC-DP and TCPC patients (89% ± 5% vs 89% ± 4%).

All BV and TCPC patients had normal bilateral diaphragm excursion under ultrasonographic interrogation. Patients with a previous diaphragm plication all had severely limited or absent diaphragm mobility on the affected side(s) throughout the respiratory cycle. None had paradoxical diaphragm movement.

Flow Dynamics
Gravity effects on flow: Qup/Qsup
The results of the Doppler flow rate calculations for gravity effects on flow are summarized in Table 1. In the BV patients, gravity reduced hepatic and portal venous flows by 20% and had no significant influence on IVC flow. Diaphragm plication did not alter these effects significantly. In TCPC patients, gravity reduced flows in the hepatic and pulmonary veins and in the IVC. TCPC-DP patients showed similar effects (Table 1).


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  		TABLE 1 Gravity effects on flows in biventricular and Fontan patients
 
Respiratory effects on flow: Qin/Qex
Tables 2 and 3 Go present the Doppler calculations for respiratory effects on flow. Respiratory effects in the supine and upright positions are compared between biventricular subjects with or without a plicated diaphragm (Table 2) and between TCPC patients with or without a plicated diaphragm (Table 3).


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  		TABLE 2 Respiratory effects on flows in biventricular patients
 

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  		TABLE 3 Respiratory effects of flows on Fontan patients
 
Biventricular patients (Table 2)
Hepatic venous flow was higher during inspiration in both BV and BV-DP patients. In the supine position, this effect was similar in the 2 groups. In the upright position, BV patients exhibited higher inspiratory flow augmentation than BV-DP patients (Figure 1). In BV patients, portal venous flow was higher during the expiratory phase of the respiratory cycle. This effect was lost in BV-DP patients, in whom inspiratory flow was equal to expiratory flow in the supine position (Figure 2). Augmentation of IVC flow during inspiration was similar in BV and BV-DP patients.


Figure 1
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  		Figure 1. Respiratory effect on hepatic venous flow in biventricular patients (BV) and biventricular patients with diaphragm plication (BV-DP). The data obtained in supine and upright positions are depicted. Qin, Inspiratory flow rate; Qex, expiratory flow rate. P values by unpaired and paired t tests as appropriate.

 

Figure 2
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  		Figure 2. Respiratory effect on supine portal venous flow in biventricular and Fontan (TCPC) patients with and without a diaphragm plication. BV, Biventricular subjects; BV-DP, biventricular patients with diaphragm plication; TCPC-DP, Fontan patients with diaphragm plication; Qin, inspiratory flow rate; Qex, expiratory flow rate. P values by unpaired t tests.

 
TCPC patients (Table 3)
Hepatic venous flow in TCPC patients occurred primarily during the inspiratory phase of the respiratory cycle. In both the supine and upright positions, this mechanism was significantly blunted in TCPC patients with a plicated diaphragm (Figure 3).


Figure 3
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  		Figure 3. Respiratory effect on hepatic venous flow in Fontan patients (TCPC) and Fontan patients with diaphragm plication (TCPC-DP). Qin, Inspiratory flow rate; Qex, expiratory flow rate. P values by unpaired and paired t tests as appropriate.

 
The expiratory augmentation of portal venous flow seen in BV patients was absent in TCPC patients. In TCPC-DP patients, the portal venous flow pattern was the reverse of normal, with higher flow during inspiration in both the supine and upright positions (Qin/Qex = 1.6 ± 0.9 supine and 1.2 ± 0.3 upright) (Figure 2). IVC flow was augmented by inspiration in TCPC patients, an effect that was maintained in TCPC-DP patients.

Coupled gravity and respiratory effects: Upright (Qin/Qex) versus supine (Qin/Qex) biventricular patients (Table 2)
In BV patients, upright posture enhanced inspiratory hepatic venous flow augmentation (Qin/Qex: 1.7 ± 0.5 supine vs 2.4 ± 1.2 upright) (Figure 4). In BV-DP patients, this accentuation of the respiratory effect by the upright posture is lost (Qin/Qex: 2.0 ± 0.9 supine vs 1.4 ± 0.3 upright) (Figure 1). In the portal vein, upright posture appeared to partially restore expiratory augmentation toward normal (Qin/Qex: 1.0 ± 0.4 vs 0.9 ± 0.3), but this did not reach statistical significance (P =.09). Postural change did not affect the respiratory effect on IVC flow in either BV or BV-DP patients.


Figure 4
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  		Figure 4. Respiratory effect on hepatic venous flow in biventricular subjects (BV). Each line joins supine to upright values in a single patient. P value by paired t test. Qin, Inspiratory flow rate; Qex, expiratory flow rate.

 
TCPC PATIENTS (Table 3)
In both TCPC and TCPC-DP patients, upright posture resulted in a suppression of hepatic venous inspiratory drive (Figures 3 and 5).Go This effect was similar to that in BV-DP patients. Posture change did not affect the respiratory effect on portal venous or IVC flow in either group of TCPC patients.


Figure 5
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  		Figure 5. Respiratory effect on hepatic venous flow in Fontan patients (TCPC). Each line joins supine to upright values in a single patient. P value by paired t test. Qin, Inspiratory flow rate; Qex, expiratory flow rate.

 

   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
Conclusions
 References
 
The diaphragm is the most important inspiratory muscle.14Go Unilateral diaphragm paralysis reduces inspiratory muscle force. Combined with its paradoxical upward displacement, this leads to inability of the patient to inspire to total lung capacity and substantially decreases pulmonary function.15,16Go By eliminating paradoxical movement and increasing kinetics of the unaffected hemidiaphragm, plication of the paralyzed diaphragm improves tidal volume and maximum breathing capacity. This is because stabilization of the paralyzed diaphragm improves the ability of the unaffected hemidiaphragm to act as a pressure generator and increases diaphragmatic contribution to breathing.17Go However, studies have shown that diaphragm plication does not completely restore the impaired respiratory mechanics to normal.15,17Go

Diaphragm paralysis owing to phrenic nerve injury has long been known to be a serious complication of cardiac surgery in children.10,11,18Go The resulting respiratory insufficiency can lead to prolonged mechanical ventilation and its associated comorbidities: pulmonary infection, longer intensive care unit and hospital stay, and potentially higher mortality. Consequently, it has been recognized that early surgical plication can reverse some of these risks and prevent related morbidity.12,18,19Go Subdiaphragmatic venous return, especially the portal–hepatic venous axis, is constantly affected by the dynamic interactions among the liver, diaphragm, and intrathoracic pressure changes. It remains unknown whether surgical plication of a paralyzed diaphragm restores the systemic venous flow dynamics.

This question is particularly relevant in patients undergoing the Fontan operation. The negative intrathoracic pressure generated by normal respiration is responsible for a majority of splanchnic venous drainage; hepatic venous flow during inspiration is more than 3 times that during expiration.7Go Therefore, Fontan patients would be expected to poorly tolerate the impaired respiratory mechanics resulting from a paralyzed diaphragm, a maladaptation that is likely to be most evident within the hepatic–portal circulation. Unfortunately, perhaps owing to the necessity of multiple operations, up to 9% of Fontan patients have diaphragm paralysis as a result of inadvertent phrenic nerve injury during surgery.9Go In 2 recent series, diaphragm paralysis increased the risk of early and midterm complications, including prolonged hospital stay, pleural effusions, readmission rates, and incidence of ascites.8,9Go Although definitive conclusions could not be made, both articles reported anecdotal experience of improved outcomes and reversal of ascites with diaphragm plication. On the basis of these observations, the authors advocated heightened suspicion for diaphragm paralysis after a Fontan operation and early surgical plication once the diagnosis is made. However, the question remains of whether diaphragm plication can restore optimal Fontan hemodynamics.8Go

Patients With Biventricular Circulation
In a series of investigations, we5-7Go have reported that respiration and gravity are two important factors affecting subdiaphragmatic venous flow in patients with normal and Fontan circulation. Normally, gravity and respiration are associated intimately in their influence on the subdiaphragmatic venous circulation. By adopting diaphragm plication as a proxy for a deranged respiratory mechanic, the current study established a clinical model that decouples respiratory and gravity influences and examined their effects individually and together.

The present investigation found that biventricular patients with a plicated diaphragm (group BV-DP) have altered venous flow dynamics. This is the first study of which we are aware that has reported this finding. Our data demonstrate that when diaphragm function is normal, the negative intrathoracic pressure created by inspiration augments hepatic venous return, and upright posture accentuates this phenomenon. Two synergistic mechanisms are responsible for this observed postural effect. First, in the supine position and during quiet tidal breathing, the lower rib cage behaves as if it is driven by transabdominal rather than intrathoracic pressure.14Go Thus, in the supine position, most breathing is abdominal; in the upright position, rib cage motion is greater.16Go The consequence is that lung volume change is higher and the negative intrathoracic pressure generation is more pronounced in the upright position. Second, in the upright position, other accessory muscles are recruited to aid inspiration. For example, abdominal muscle contraction actively raises and stretches the diaphragm to maximize its caudal displacement and pressure generation during inspiration. This ventilatory mechanical advantage only operates in the upright position, where gravity aids passive diaphragmatic descent.14Go Studies in normal subjects have shown that vital capacity drops by 20% in the supine position.14Go This figure corresponds closely to the 29% loss of hepatic venous respiratory effect calculated from our data (BV hepatic venous Qin/Qex: 2.4 upright to 1.7 supine). In biventricular patients with a plicated diaphragm, augmentation of hepatic venous flow by the "respiratory pump" has lost this upright postural advantage.

Having a plicated diaphragm also alters the portal venous flow characteristics. As reported previously, normal portal venous flow decreases during inspiration, as the descending diaphragm compresses the compliant hepatic sinusoids and portal venules to displace portal inflow.3,5Go The hepatic sinusoids are the site of both resistance and compliance in the portal–hepatic circulation, and normal portal flow is augmented during expiration.20Go The loss of expiratory portal flow augmentation in biventricular patients with a plicated diaphragm implies a decreased hepatic compressibility and reserve, a finding that is similar to our previous observation in Fontan patients.5,20-22Go

Patients With Fontan Circulation
In patients with the Fontan circulation, pulmonary vascular resistance and systemic venous resistance are in series. This circulatory arrangement amplifies respiratory and gravitational modulations of venous return in Fontan patients.23Go We have previously demonstrated in TCPC patients that hepatic venous flow is primarily driven by inspiration. This phenomenon is observed whether the patient is well or in a failing state, is independent of Fontan pressure levels, and is enhanced by fenestration in the TCPC pathway.5-7Go Our current findings demonstrate that the inspiratory drive of hepatic venous return in TCPC patients is significantly blunted after diaphragm plication, despite a greater proportion of TCPC-DP patients having a fenestrated pathway. Therefore, the present study not only confirms the importance of the "respiratory pump" in TCPC patients but also points out that altered respiratory mechanics, exemplified in patients with a plicated diaphragm, can suppress this major energy source for hepatic venous drainage. Such a deficit can potentially further impair a splanchnic physiology that is already abnormal in Fontan patients. For example, the suppression of hepatic venous respiratory effect by upright posture is exacerbated in TCPC-DP patients (Qin/Qex: 2.3 supine vs 1.7 upright).

The consequences of suboptimal respiratory mechanics on the splanchnic circulation are also seen in the portal venous flow, which is vulnerable to upstream disturbances in the hepatic venous or central caval systems.21,24Go Our data show that even in TCPC patients with functioning diaphragms, portal flow has lost its normal expiratory augmentation. Furthermore, in TCPC-DP patients with a plicated diaphragm, portal flow is reversed from normal, so that flow is higher during inspiration than during expiration. This is a phenomenon that we have previously observed in Fontan patients in poor functional status or with elevated Fontan pressures, and it is a reflection of increased hepatic congestion and decreased hepatic compliance and reserve.5Go In such patients, congested hepatic sinusoids become dilated and are recruited into an open tube system, which allows portal flow to occur during the same phase of respiration as the hepatic venous flow.3,22,25Go The fact that portal dynamics in TCPC patients with a plicated diaphragm are similar to those in patients with failing Fontan circulation suggests that, despite improving ventilatory mechanics, surgical plication does not completely restore splanchnic flow dynamics. Therefore, even with surgical plication, diaphragm paralysis is not completely compensated in TCPC patients and may increase the risk of late complications, such as ascites and protein-losing enteropathy, both of which have been linked to splanchnic venous congestion.26Go

The initial research question of this study was to find out the impact of diaphragmatic paralysis in the Fontan circulation. Unfortunately, we could not answer this question because, similar to other groups,9,18Go our institution adopted a proactive approach of performing early surgical plication in Fontan patients when a paralyzed diaphragm was diagnosed. Therefore, we do not have data from Fontan patients with a paralyzed diaphragm before plication. However, our data suggest that disturbances in ventilatory mechanics may have a more detrimental effect on the splanchnic venous return in Fontan patients than in biventricular patients. It is also evident that patients with a plicated diaphragm have some generalized defects in their splanchnic venous return that are present in either biventricular or Fontan physiology. In other words, even with a biventricular circulation, some of the splanchnic flow dynamics are abnormal and resemble those seen in Fontan patients.

The current study shed light on subdiaphragmatic venous flow anomalies that persist despite diaphragmatic plication, which is a consequence of phrenic nerve injury. Therefore, protection of the phrenic nerve before and during the Fontan operation is paramount. Because of its long course from the neck to the diaphragm, the phrenic nerve is susceptible to inadvertent damage during operations for congenital cardiac disease owing to topical cold injury, traction injury resulting from tension, vena caval annulations, and direct trauma from electrocute dissection.11,27-29Go The necessity of multiple reoperations in patients with single ventricle likely increases their risk of phrenic nerve injury.9Go The left phrenic nerve is vulnerable during aortic arch reconstruction for the stage I Norwood operation or when a left modified Blalock–Taussig shunt is dissected before its closure. The right phrenic nerve is at risk during dissection and cannulation of the superior vena cava or IVC for the stage II cavopulmonary anastomosis or TCPC completion. One can speculate that surgical strategies that minimize operative dissection during these 2 latter stages of single ventricle palliation, such as deep hypothermic circulatory arrest, may be beneficial in reducing the incidence of iatrogenic phrenic nerve injury. It is more important to prevent diaphragmatic paralysis than to treat it.30Go


   Conclusions
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
References
 
In both biventricular and Fontan patients, diaphragm plication does not completely restore normal subdiaphragmatic venous fluid dynamics. In Fontan patients with a plicated diaphragm, inspiration-derived hepatic venous flow is suppressed and portal venous flow loses its normal expiratory augmentation. These flow dynamics share similarities with those observed in patients with failing Fontan circulation. This suboptimal splanchnic circulation may contribute to early problems of prolonged pleural effusion and ascites and potentially promote late Fontan failure. Phrenic nerve injury should consequently be avoided at all costs before or at the time of the Fontan operation.

We thank the consultants and staff of the Cardiothoracic Unit at Great Ormond Street Hospital for Children for their support and cooperation.


Earn CME credits at http://cme.ctsnetjournals.org

 


   Footnotes
 
Supported by a National Science Foundation International Postdoctoral Research Fellowship Award, Grant No. INT-9802808.

Read at the Eighty-seventh Annual Meeting of The American Association for Thoracic Surgery, Washington, DC, May 5-9, 2007.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 Conclusions
 References
 

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Discussion
J. Thorac. Cardiovasc. Surg. 2007 134: 1405. [Extract] [Full Text] [PDF]



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