Friday, July 15, 2011

This is Dr Kiran welcoming all to the new post of the blog.

This time, the delay in the posting was not my usual laziness, but it was because of some tight rope walking! It was arrival of my second baby. He was in a hurry and the delivery happened 18 days prior to the due date. We were obviously not well prepared and had to do some circus to get the things settled. Now that all iz well, I am posting this update on the blog. Hope I will get some comments this time, for right or wrong reasons!!


I think we have discussed this issue earlier, but without much clarity. I wish someone replies this time. In cases of single ventricles with borderline high PA pressures, is the recommendation of PA tightening valid? One side of the logic is, by tightening the PA, flow into PAs would be lesser and thereby the pressure. Also, adding BD Glenn shunt in this situation would improve the saturation and off-load the ventricle.
On the other hand, tightening the PA would increase the afterload on the single ventricle and would nullify the effect of offloading the ventricle. Also, when the baseline PVR itself is less (baseline PA pressures in range of 18-20mmHg), what more improvement would PA tightening achieve in PVR/SVR ratio? When the long term threat is failure of single pump, is volume load better or pressure load?
Please let me know your takes on this issue.


Sometimes, we decide to cath some borderline cases for objectiveness and end up cursing our decision to cath!! We had one-and-a-half year old with ASD and VSD with severe PAH, with saturation of 93%. His LV looked non-compacted and the extent of pulmonary hypertension was higher than expected for the extent of lesions. One of the consultants thought of acquiring more data on the issue and decided to cath. Data on cath showed a PVRI of 11wood units! Since the child had all the features of operability on clinical evaluation and baseline investigations, these numbers looked shocking. It is not easy to convince the surgical team to operate when the cath produces such results! However, one of the senior surgeons was kind enough to ignore the cath data and operated the baby! The learning was: when in doubt, don’t just cath. You may get unexpected turn in the way!! Please share your experiences in this issue.


Many places follow the rule of diagnostic cath in Down syndrome babies with congenital heart defects older than 1 year. We had a 2-year-old baby with Down syndrome, who had a large inlet VSD. Although operability on clinical grounds was never an issue, it was sought by someone as ‘knee-jerk’ response. The LV EDP was documented to be 25mmHg. The tracings were verified and found correct. Barring that, the data on operability showed operability. One of the senior surgeons showed his reluctance in operating babies with high EDP. Our recommendation of leaving an ASD open also did not go well. What is the take of readership? Is high EDP a detriment in surgery? Can you recall having seen a similar situation and outcome of that baby? Please share your experiences and expertise in this.


As a matter of convention, I have heard many centers have different PVRI cutoffs for ASD and VSD operability. One convention was: less than or equal to 7 wood units for VSD/PDA and less than or equal to 10 wood units for ASD. The question was- when the PVRI is between 7 and 10 wood units in cases of VSD, can we convert the physiology into an ASD? In other words, can we close the VSD and create a sizable ASD in that patient? On long run, the progress of disease might be better with a pre-tricuspid shunt than a post-tricuspid one. However, our surgical team opined that giving another disease for one even after a major heart surgery is useless and worthless. Are there any studies on these lines? What would your personal opinion on this be? Please let me know. I would be interested if this issue can raise a debate.


In cases of toddlers with moderate to large ASD and near normal PA pressures, how frequently would one witness cyanosis? Even the sinus venosus defects of SVC type where the SVC straddles over both atriae, we rarely see cyanosis. I have seen 3 cases of sinus venosus defect of IVC type and not even one of those three had cyanosis. However, my experience in the latter is obviously less. It is said that a long, redundant Eusthecian valve can some times direct the IVC blood towards LA in low secundum ASDs with deficient IVC rim. In the absence of systemic venous anomalies and unroofed CS, is it possible to have cyanosis in ASD with normal PA pressures? We had one of such kids in our hospital. Conventional and saline contrast echo was not useful in deducing the picture. Cath study is unlikely to yield much. How would you go about in such cases? Please share your experiences on this.

That brings us to the end of the present post. Please send your criticisms and suggestions typed in the comments box or directly to my email: If you wish to contribute your experiences, please type them in a word document and send the attachment to my mail. I shall publish them on your behalf with full credit to the writer! See you shortly with few more learning scenarios.