Wednesday, September 8, 2010

This is Dr Kiran welcoming all the readership to the present post. Thanks for all the response I received for the new idea of book review. Please note that the introduction to the book neither serves as a criticism nor a publicity material! I am quoting those books which no longer require any publicity. Whenever you come across these books (pavement, bookshops, library, friends’ house etc), if it kindles your memory cells and instigates you to read through, the purpose stands served. With this, let us get back to the post contents: Another book, interesting learning scenarios and pearls.

In this post, we shall see one of the all time bestseller. It is read by millions, discussed in forums and one of the books that has actually made an impact on the corporate world. It is authored by Dr Spencer Johnson. He used to work for a company called Medtronic, which manufactures cardiac pacemakers and prosthetic heart valves. His other works include “One minute manager” (coauthored with Kenneth Blanchard). Dr Johnson used to tell a motivational story to groups of people over 20 years. On insistence from Blanchard, Dr Johnson wrote the story in the form of book. It is claimed to have sold 12 million official copies (and lots of pirated ones!) The book is titled “Who moved my cheese?”

The story of the book is simple. It all happens in a maze with four characters: Two mice: Scurry and Sniff, and two “little-people,” Hem and Haw. In the beginning of the story, they have found a huge source of their favourite food, cheese and all iz well! Hem and Haw move their houses to be near the cheese and made the cheese centre of their lives. What they fail to notice is that the cheese is getting smaller. One fine day they come to see that the entire cheese is gone and get devastated.

The story bifurcates from this point into two perspectives. The mice, Scurry and Sniff, quickly accept the loss of the cheese and start exploring the maze for other sources. The little-people, however, refuse to accept the fact. They have built far too much around the source and find it difficult to move on. They start feeling that they are the victims of some kind of fraud or theft. The more they stick on and crib, worse the matters become for them. They achieve nothing better than hunger.
Meanwhile, the mice move on and find new cheese.

The message of the story or “Take home points” is nicely represented as Graffiti that the mice write on the walls of maze.

The simplicity of the book is in not taking oneself seriously. One should develop an ability to laugh at themselves in the moments of predicament. It will have a surprising effect of liberation from the situation. The book, in a way, reiterates the Buddhist philosophy of attachments making oneself weaker and the need for dissociating from one’s attachments!

Everyone’s afraid of change, more for the people who think some point is final and try to “settle down” at the place. However, change is perhaps one of the basic facts of existence. Everyone would like to assume that change would not happen to them. Denial of this basic rule prevents them from sniffing the cheese often and making way for the search of new cheese. A certain level of risk and adventure makes the life worth living. By letting the life adapt to new risks, one would involve change and the latter loses its horror. The mice in the story realize that breaking through the fears makes them free. Ironically, the little-people continuously seek security and always live with the fear that they may lose it!

The book less than 100 pages is something worth a read and contemplation. Try getting your hands on it!

Let us get back to our routine section: Interesting learning scenarios

UNDOING TRAGEDY

I have discussed this in earlier blogs also. But the question keeps coming back. If the cardiac lesion is perfectly suitable for 2-pump repair, but someone earlier has already put the child on single pump pathway by Glenn few years back, how successful can we be in undoing the problem and bringing the patient back to 2-pump pathway? Our surgical team feels that the chances of undoing a Glenn go down with time. Thus, once the child has spent a couple of years with Glenn, it may no longer be fit for 2-pumps. How is the experience in other centres? Is this scenario seen often? Please let me know your ideas and experiences on it.

DELAYED UNMASKING

Shones complex is something that has been haunting us for a long time. Someone quoted recently that Shone was either a nobody or a fictional person, for despite describing such a complex array of disorders, his name does not feature anywhere else in history! We had a 6-month-old with Shones physiology. The supramitral membrane was resected, LVOT cleared and Coarctation repair done. Immediate post-op period did not show any major issue on echo. However, after few days, the mitral valve problem slowly started unmasking itself. We found a small gradient across the mitral valve inflow, which kept increasing with time. The hemodynamics kept on deteriorating. We could virtually think of no other solution than opening again. The general condition of baby did not permit a major undertaking again. Is this phenomenon known? Why does such a thing happen? How do the inflow gradients across mitral valve change in such scenario with time when the LV function all along was reasonably good? Is there anything that we might have missed? Please let us know your experiences.

COLLATERAL EFFECT

We had a 4-year-old boy with a strange issue. This boy had TAPVC with very limited echo windows. SO2 was 60%. One of the consultants felt a possibility of superior-inferior ventricles and possible single ventricle physiology. On cath, we found multiple collaterals from proximal SVC! The RV levophase showed the pulmonary venous confluence draining into distal SVC with no obstruction throughout the course. How to explain the SVC collaterals? Were they pop-offs of the high pressures in proximal SVC, as seen with borderline Glenn shunts? Why should there be such a picture at all prima-facie? One explanation was from TAPVC draining to distal SVC. There may be a possible high pressure at distal SVC resulting in collateral formation proximally. However, cath failed to demonstrate any pressure gradient. Since the PA pressures were high, he could not go on Glenn, more so in the setting of pre-existing SVC collaterals! If you have seen SVC collaterals in a non-Glenn setting, please share your experiences and causes.

GOOD REGURGITATIONS

One cause for prepared LV in cTGA intact IVS is said to be severe TR. But, in practicality, how many times do we come across this as cause? There may be stray case reports of this event. Considering that virtually every cTGA develops TR, can it be taken as a cause? Should we not take this as an exception than a rule? Should we not evaluate for other reasons for LV preparation? We do see many MR children in OPD. How many sever MR do we recall having caused severe hypertension? Don’t we teach the students to check for other causes before committing on MR as the cause of sever PAH? Should we not think same analogy in cTGA cases also? One argument was the bowing of intact IVS towards LV changing LV geometry and preparing it. It looked far-fetched to me. Please let me know your takes on it.

PRIMUM PROBLEM

In how many situations do we see severe PAH in an infant with isolated primum defect in a non-Down setting? One of our senior surgeons remarked that he is not surprised with this combination. Is it true? The conventional teaching appears to be against the scenario we faced. In this 7-month-old baby, the baseline Qp/Qs was 0.5! Atleast, I could not recall having faced such situation earlier. Please let us know if you had any such events and how you handled this.

PEDIATRIC CARDIOLOGY PEARLS

71. In dilated cardiomyopathy, the sphericity index, derived from comparing the long-axis left ventricular dimensions in diastole and systole with the chord from the mitral annulus to the apex in diastole and systole, has been used to quantify. The value should be <0.66. If it approaches 1.0, indicating that the chamber is rounded instead of elliptical, a dilated cardiomyopathy is likely (Tani LY, Minich LL, Williams RV, et al. Ventricular remodeling in children with left ventricular dysfunction secondary to various cardiomyopathies. Am J Cardiol in year 2005 page 1157)

72. Cardiomyopathies are defined as diseases of the myocardium associated with cardiac dysfunction (Richardson P, McKenna W, Bristow M, et al. Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation journal in year 1996 page 841)

73. Myocarditis is a process characterized by inflammatory infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischemic damage associated with coronary artery disease. This definition does not take into account the underlying cause (Wynn J, Braunwald E. The cardiomyopathies and myocarditis. In: Braunwald E, ed. Heart disease: A textbook of cardiovascular medicine. Philadelphia: WB Saunders, in year 1997 page 1404)

74. The cardiothoracic ratio on chest radiography is predictive of mortality in patients with dilated cardiomyopathy (Manolio TA, Baughman KL, Rodeheffer R, et al. Prevalence and etiology of idiopathic dilated cardiomyopathy (summary of a National Heart, Lung, and Blood Institute workshop). Am J Cardiol in year 1992 page 1458)

75. In hypertrophic cardiomyopathy, mitral valve systolic anterior motion and outflow obstruction may also develop in childhood, associated with progression of LV hypertrophy in the presence of a developmentally small outflow tract (Panza JA, Maris TJ, Maron BJ. Development and determinants of dynamic obstruction to left ventricular outflow in young patients with hypertrophic cardiomyopathy. Circulation in year 1992 page 1398)

That brings us to the end of another post. For various reasons this post was delayed. Let me try and get them on time in future. Please send your comments, criticisms and confrontations to drkiranvs@gmail.com or put them in the comments box below. I would like to know the need to continue the book review. Also, planning a separate section for Pediatric PGs interested in cardiology. Please let me know your suggestions on structuring the section.

Regards

Kiran

1 comment:

  1. CAN YOU HELP ?? - I AM IN THE UK. MY SECOND CHILD 7YRS AGO WAS DIAGNOSED IN WOMB WITH CTGA, SADLEY THROUIGH LACK OF FOLLOW UP ONCE BORN, HE PASSED AWAY FROM COMPLETE HEART BLOCK AT 6MONTHS OLD. 7 YEARS ON, AND I AM CARRYING MY THIRD CHILD, I AM NOW 25WEEKS AND HAVE FOUND THAT THIS BABY HAS CTGA TOO. I HAVE BEEN CHECKED TO SEE IF THIS IS GENETIC BUT ECG'S HAVE BEEN CLEAR. NOBODY CAN TELL ME WHY THIS IS HAPPENING AGAIN, I HAVE TRIED THE INTERNET ASKED CONSULTANTS NOBODY HAS ANY DETAILED INFORMATION.

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