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LETTER TO EDITOR  
Year : 2012  |  Volume : 15  |  Issue : 1  |  Page : 90-92
Decompression of superior vena cava during bidirectional Glenn shunt: A simple but risky technique


Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India

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Date of Web Publication5-Jan-2012
 

How to cite this article:
Neema PK, Manikandan S, Singha SK, Rathod RC. Decompression of superior vena cava during bidirectional Glenn shunt: A simple but risky technique. Ann Card Anaesth 2012;15:90-2

How to cite this URL:
Neema PK, Manikandan S, Singha SK, Rathod RC. Decompression of superior vena cava during bidirectional Glenn shunt: A simple but risky technique. Ann Card Anaesth [serial online] 2012 [cited 2019 Nov 22];15:90-2. Available from: http://www.annals.in/text.asp?2012/15/1/90/91475


The Editor,

We read with interest the paper [1] "Decompression of superior vena cava during Bidirectional Glenn Shunt"; we congratulate the authors for describing a very simple and innovative method for decompression of superior vena cava (SVC) during bi directional Glen (BDG) anastomosis. However, we express our concerns regarding neurologic safety and adequacy of cerebral perfusion during the BDG shunt construction and doubts about the efficacy of the method of decompression of SVC.

The patients scheduled for BDG shunt construction are cyanotic and generally have their oxygen saturation in a range of 65-85%. In these patients oxygen delivery is maintained by increase in total hemoglobin. Many of these patients have abnormal magnetic resonance imaging and one or other kind of neurologic deficit. [2] Apparently, these patients have no room for any further neurologic insult. For surgeons and anesthesiologists, spontaneous eye opening or moving all four limbs or patient's response to command signify complete neurologic recovery. However, there are various neurologic testing methods [3] available, which alone can assess and diagnose neurologic functional recovery or loss. Without proper scientific assessment one cannot emphatically state that there were no neurologic issues.

The method of decompression of SVC described by the authors needs scientific scrutiny. As the authors have correctly described cerebral perfusion depends on the difference between mean arterial pressure and central venous pressure (SVC pressure for the patients described in this paper). Arguably, allowing SVC pressure to increase up to 45 mmHg (Case 1) and 38 mmHg (Case 2) can seriously impair cerebral perfusion. Drastic reductions in arterial pressure to about 30-60 mmHg that usually occur during cardiopulmonary bypass (CPB) can further reduce effective cerebral perfusion pressure and cerebral blood flow. Conceivably, the adequacy of cerebral perfusion would be seriously impaired if the mean gradient (arterial pressure minus SVC pressure) decreases to just 15 mmHg (60-45 mmHg). Further, the authors should have started active SVC decompression the moment a rising trend was confirmed; waiting for the mean SVC pressure to increase up to 45 mmHg should have been avoided.

We believe the mean SVC pressure measured during decompression is unlikely to be correct; the mean SVC pressure was transduced through the 20G cannula placed in the right internal jugular vein and the same cannula was used for active and passive decompression. During active decompression, a negative pressure is created at the tip of the cannula, conceivably during active decompression the pressure measured at the tip of the cannula will be sum total of mean SVC pressure and the negative pressure transmitted at the tip of the cannula and will not represent the true cerebral venous pressure. Additionally, the measured mean SVC pressure is likely to be affected by integrity of the internal jugular vein which may collapse if the negative pressure applied is excessive. Arguably, the measured mean SVC pressure will not represent the true cerebral venous pressure.

The authors state that for a 6 kg child one need to aspirate 35 times using a 10 ml syringe; however, they could aspirate for 20 times only. To put it differently, there would be cerebral venous congestion, and because of back pressure a decrease in cerebral blood flow may follow. In a bigger child, the build-up of back pressure would be even greater. The neurologic risk can be even higher if the technique is applied in patients where CPB is not utilized during shunt construction. During on pump (CPB) procedures 100% arterial O2 saturation is ensured, whereas, during off pump BDG construction saturation decreases further as the pulmonary blood flow on the side of BDG construction is shut off because of application of side clamp on the pulmonary artery. Further, during these procedures hemodynamic compromise is common because of manipulation of heart and great vessels. Compromised hemodynamics, decreased oxygen saturation, and cerebral venous congestion combined together can seriously jeopardize adequacy of cerebral perfusion, cerebral O2 delivery, and the neurologic outcome of the patient. Evidently, for ensuring adequate cerebral perfusion during BDG shunt construction the SVC should be adequately decompressed; in our institute during BDG shunt construction our surgeons routinely cannulate the SVC or the innominate vein for its decompression by using a right angled DLP cannula. We do perform BDG without CPB in presence of bilateral SVC; however, before committing ourselves, we ensure that on test clamping the surgical SVC the central venous pressure does not rise above 12-15 mmHg.

 
   References Top

1.Kulkarni V, Mudunuri R, Mulavisala K, Byalal RJ. Decompression of superior vena cava during bidirectional Glenn shunt. Ann Card Anaesth 2009;12:146-8.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.Mahle WT, Tavani F, Zimmerman RA, Nicolson SC, Galli KK, Gaynor JW, et al. An MRI study of neurological injury before and after congenital heart surgery. Circulation 2002;106:109-14.  Back to cited text no. 2
    
3.Andropoulos DB, Stayer SA, Diaz LK, Ramamoorthy C. Neurological Monitoring for Congenital Heart Surgery. Anesth Analg 2004;99:1365-75.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  

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Correspondence Address:
Praveen Kumar Neema
B 9, Sree Chitra Quarters, Poonthi Road, Kumarapuram, Trivandrum 695 011
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.91475

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Kulkarni, V., Mudunuri, R., Mulavisala, K., Jagannath Byalal, R.
Annals of Cardiac Anaesthesia. 2012; 15(1): 92
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