This is Dr Kiran welcoming you back to the present post of blog. The book review is being received well. Some of the issues written in the learning scenarios of last post had eyebrows of few people rising! But, as my colleague Dr Prem Alva put it, “What’s the purpose of blog if it does not even allow open discussion?” I agree with him. I have retained the post as it stood.
Let us get back to the present post. As usual, we shall see the book review, learn from few patient scenarios and the pearls.
This post, we shall see one of the massive best-sellers of contemporary literature. It is authored by Dr Richard Carlson. It was the number one bestselling book in the USA for two consecutive years. Yet, this is not a theoretical adage for perfection. It was a simple book with about 100 strategies and ideas for avoiding trouble whenever possible! Each idea is briefly elaborated in a short essay or anecdote. It has its basis from an ethereal spiritual law of Hinduism and Buddhism – of taking the path of least resistance whenever and wherever possible for betterment. These strategies have proven their worth for millions across the globe.
There is an interesting story behind the book. One of Dr Carlson’s books had a foreword written by best-selling author, Wayne Dyer. For his next book titled “You can Feel Good”, Dr Carlson requested Dyer to write another foreword. Somehow, it did not happen. But, by mistake, Dr Carlson’s overseas publisher used the previous book’s foreword of Dyer in the new book too! When the copy reached Dr Carlson, he was taken aback. He wrote a lengthy apology to Dyer and spoke of his efforts to get the copies taken off the shelves. In a few weeks time, he received a note from Dyer. It was simple two line letter which read:
“Richard. There are two rules for living in harmony. #1) Don’t sweat the small stuff and #2) It’s all small stuff. Let the quote stand. Love, Wayne.”
That started another super-seller for Dr Carlson!
Good heartedness is what one would appreciate in this book. The present day culture and wants have a crushing demand on our psyche. Lecture from a Guru or a meditation camp on a weekend do not have effects lasting for more than 2 days. What we need is the extension of that feeling for a longer time and possibly for a lifetime! How to do this? This is the question with which Dr Carlson starts. The refreshing approach that “Don’t Sweat the Small Stuff” takes is in not worrying about having bad feelings. “Don’t try to get rid of them, but do try to put them into a larger context” is one of the advices!
Some of the tips that really have amazing effects are:
• Rising early the day, long before the spouse and kids, would entitle oneself to “golden hour.” One can read, meditate, or think about the day in peace and solitude. This single act of becoming an early riser has revolutionized life for many people who practise this religiously!
• Do superachiev ners run through constant emergencies and never relax? On the contrary, Dr Carlson says, frantic thinking and constant movement leach motivation and real success from the lives. He emphasizes that peaceful and loving does not equate oneself to apathy! If inner peace becomes a habit, there is ease in the way one would achieve goals and serve others.
• Do you have the habit of interrupting others or finishing their sentences during conversation? Quit it! This simple measure puts you into lot of peace and happiness with yourself.
• John Lennon had said “Life is what happens when we are busy making other plans.” With attention to the present moment, fear—being associated mostly with an imaginary future—tends not to exist. Tomorrow’s troubles usually sort themselves out. This is a very powerful principle and repeatedly emphasized by people like William Osler and Dale Carnegie.
• If something really worries you a lot at the moment, please ask yourself “Would this matter to me in a year from now?” You may end up laughing at the problem immediately. All the energy that would have gone futile on thinking and getting angry would become more constructive and lively!
• What is the definition of accomplishment? Dr Carlson amazes you by telling that it is not an external thing. Just staying calm and composed during an adversity itself is an accomplishment. He advises to practice and recognise small but significant accomplishments everyday.
• How do you react when someone disapproves you? You may either become very angry and burst out or you may get very emotional and sob silently and get gloomy. Is there another way? Dr Carlson advices us to “respond” to the situation than “react”! He suggests acknowledging the disapproval and re-analyse. The retention of energy is a positive move and lets you take better decision.
• How do you measure your priorities? People who have read Randy Pausch (The Last Lecture) may have some ideas. Dr Carlson does a similar suggestion in his book: Imagining oneself at own funeral! Some relevant questioning at that moment might be - What sort of person was I? Did I do the things I loved and did I really love and cherish those close to me every day? And so on. That allows oneself to cut down the sweat on small things and concentrate on real issues of importance: love and happiness.
The best aspect of the book is its brevity. It is recommended for those who keep saying they don’t have time to read stuff. Feelings are the product of thoughts and by becoming more conscious of own thinking, one can get in a position to change thoughts and therefore feelings.
“Not sweating the small stuff” is simple to follow although many disagree in the first thought. A celebrated psychologist has recognized “Not sweating the small stuff” as a key feature of what he called the self-actualizing person, a person who has given up pettiness for an unusually wide view of the world and life. That is what the book emphasizes in a joyful way.
The beauty of the book is that any page can be opened and read. Though it has nearly 100 strategies all explained in a simple, brief way, practising even a couple of them might be worthwhile and may be life-changing.
Let me know your views on the book if you have read it. If you haven’t yet, I strongly recommend you to lay your hands on one and let me know how you feel after reading it. If you have any additional comments on the book, please post them in the comments section or to my email. I shall post them on your behalf.
With this, let us get back to our interesting learning scenarios.
SPLIT SECOND SOUND AND TETRALOGY
“Is it theoretically possible to get a split second sound in TOF physiology?” was one of the questions asked to me in class. I was taking a class for cardiology diploma students and this question popped up suddenly. I could not recall anytime when I had heard a split S2 in TOF. But, the question is hypothetical here. The logic tells us that any obstruction beyond the valve capable of producing a significant RVOT obstruction should be producing a split S2. Hence, a large VSD with significant bilateral branch pulmonary artery stenoses can theoretically produce the picture of TOF physiology with split S2! If any of the readers has seen such a picture, please enlighten rest of us!
AORTIC DOUBLE EDGE!
How can a dysplastic aortic valve with severe stenosis and moderate regurgitation in a 6-year-old tackled? We had this scenario recently. This dysplastic aortic valve is obviously not suited for ballooning. The difference in the annuli of aortic and pulmonary valves was too big for Ross. Repairing a dysplastic aortic valve is as certain as toss of ten coins at the same time! The fair option would be aortic valve replacement. But, the age was crucial. It is indeed a double edged sword situation. Since the patient was asymptomatic, we thought we could buy some time. How would one approach such scenarios? What is the experience of other institutes? Please let us know if you have handled such scenarios and your experiences on outcome.
OUTING McGOON
The surgeon friendly McGoon ratio may not be the favourite of everyone, but for the lack of anything simpler, it continues to be in use. The logic of measuring abdominal aorta diameter at diaphragm is well explained. However, are there any fallacies to it? We do McGoon ratio and Nakata index for all cath studies that require PA anatomy. The disparity is often striking, especially in VSD with pulmonary atresia. Does the hemodynamic logic applicable to two semilunar valves different from that of one semilunar valve? In other words, does the abdominal aorta get unduly dilated when both the ventricles drain into aorta? What is the observation in other centres? Please let us know.
APICAL VSD AND RV
“In a moderate sized apical VSD, along with LA and LV, even the RV increases in size” was the statement by one of our senior consultants. Is it correct? Just because blood traverses through the body of RV in systole, can the RV get dilated? My understanding is that ventricles get dilated only if they behave like capacitance chambers. In other words, unless the shunt blood stays in a ventricle during diastole, it cannot get dilated. Wherever may the location of VSD be, RV cannot be a capacitance chamber as blood entering into RV via VSD never stays there during diastole. Is there any literature or case study mentioning RV status in apical VSD? Any personal experiences in this regard? Please let us know.
FLOOD OR DROUGHT
Single pulmonary artery is another situation which leads to hair loss in cardiologist and surgeon (due to constant scratching of head!). We had a situation in which 11-year-old had virtual single pulmonary artery physiology. The RPA was about 8 mm and the LPA was hardly 3 mm at narrowest point, becoming 5 mm distally, looked hypoplastic overall. The child saturated 80% at rest. There were high pressure collaterals supplying lungs. One of our surgeons felt the need for a BTT shunt to RPA as possible final palliation. The supposed logic was the growth of PAs and symptomatic improvement. However, does this justify the risk/benefit ratio? There are existing high pressure pulmonary collaterals and tight stenosis of proximal LPA. Wouldn’t the BTT shunt flood right lung and accelerate PVRI there? The LPA is less likely to grow even with the BTT shunt to RPA. I felt that our surgeon had another explanation but could not express it then. I sought his time for further discussion of this scenario. In the meanwhile, what do you think of this scenario? Is the BTT shunt better or worse? Is future drought better than the present flood? Please enumerate your experiences about this condition.
PEDIATRIC CARDIOLOGY PEARLS
81. Nearly one fourth of patients with arch anomalies but without intracardiac defects have 22q11 deletion (McElhinney DB, Clark BJ III, Weinberg PM, et al. Association of chromosome 22q11 deletion with isolated anomalies of aortic arch laterality and branching. Journal of American College of Cardiology in year 2001 page 2114)
82. When PAPVC and ASD coexist, the hemodynamic picture may be similar to that of uncomplicated ASD. The left-to-right shunt may be large. This shunt is the result of anomalous drainage of most of the blood from the anomalously connected lung and of anomalous drainage of half or more of the blood from the normally connected lung via the ASD (Swan HJC, Hetzel PS, Burchell HB, et al. Relative contribution of blood from each lung to the left-to-right shunt in atrial septal defect. Circulation journal in year 1956 page 200)
83. The development of the left innominate vein at the 7th week of gestation usually is followed by the involution of the left SVC (LSVC), which becomes the ligament of Marshall (Marshall J. On the development of the great anterior veins in man and Mammalia. Philosophical Transactions of Royal Society of London in year 1850 page 133)
84. In tricuspid atresia, it is common for the VSD to decrease in size, thereby changing a patient's classification. (Rao PS. Natural history of the ventricular septal defect in tricuspid atresia and its surgical implications. British Heart Journal in year 1977 page 276)
85. In tricuspid atresia, ECG in patients with diminished pulmonary blood flow often shows small R waves with shallow Q waves (Davachi F, Lucas RV Jr, Moller JH. The electrocardiogram and vectorcardiogram in tricuspid atresia. Correlation with pathologic anatomy. Am J Cardiol 1970;25:18)
That brings us to the end of one more post. “Is it necessary to involve controversy to get more people reading your stuff?” is one of the most pertinent questions asked in many quarters. I feel the quality of content has longer lasting punch than the temporary titillation of controversy. Let us just keep up the former than the latter. This blog is meant for dissemination of meaningful knowledge. The contents and questions will always be kept in that way. Any contribution to improve the existing stuff is most welcome. Please use comments box or my email id drkiranvs@gmail.com Thank you all.
Regards
Kiran
ಮಂಗಳವಾರ, ಸೆಪ್ಟೆಂಬರ್ 28, 2010
ಶುಕ್ರವಾರ, ಸೆಪ್ಟೆಂಬರ್ 17, 2010
Dr Kiran welcomes all the readers of this blog. Thanks for the responses I am receiving for book reviews. I have decided to continue the book-reviews till I get another flash! This week, let me introduce another “eye opener”! This would be followed by our regular features: Interesting learning scenarios and Pediatric cardiology pearls. By the way, anyone who has read and appreciated Dr Riesh Sukharamwala’s account in the last post- please reply. He would be encouraged to write more!
Let us get to the book first:
“Do you have Kiyosaki’s book?” asked my Boss one day.
“Yes, Sir. I do. Would you like to read it?”
“Please send it to me.”
When I read Robert Kiyosaki for the first time, only the novelty factor impressed me. However, over a period of time, I think I matured to the contents of book! It is something I would not hesitate recommending to anyone. It is titled “Rich Dad, Poor Dad: What the Rich Teach Their Kids about Money… That the Poor and Middle Class Do Not!”
The best part of the book is that it does not teach anything about market ventures, real-estate, dot com or anything similar. It concentrates on individual discipline and private attitudes towards money. When most of us equate money with wealth, Kiyosaki differs. He teaches us the difference between money and wealth. Money is a result of wealth or real value, and sometimes only a symbol of it. What is real is what has generated the money: a business with revenues greater than costs, a property with rent greater than mortgage, knowledge that earns royalties and so on.
The Rich Dad principle would be, “If you look for money and security, that’s all you’ll get.” You might get “money” but not find the source of money. The fundamental difference between the Rich Dad and Poor Dad is that the Rich Dad knows the difference between an asset and a liability. Anything that generates money—that actually puts it in your pocket—is an asset. Everything that takes money from your pocket without more returns is a liability! The job earnings are returns and not assets. The income coming from assets need not even have you to be around!
Kiyosaki maintains that unless one knows how to read a balance sheet, he is financial illiterate! Financial literacy, he says, is as important as word literacy. “Illiteracy, both in words and numbers, is the foundation of financial struggle.” His Sutra for getting rich is knowledge. Before making any investments, one should educate oneself on all the options and opportunities. “The more you know, the better your decisions will be!” Lack of financial education teamed with the desire for quick riches leads to disaster. “Most people, in their drive to get rich, are trying to build an Empire State Building on a 6-inch slab,” he says. The key to controlling money in his view is by controlling emotions. Becoming rich involves self-discipline and the ability to separate the emotions of fear and greed from a good investment decision.
This book makes the reader think a lot. It forces the reader to reflect not merely about their investments and assets, but about their whole attitude to work and life.
The stock market is always said to be driven by “fear and greed.” Kiyosaki claims that, for most of us, fear is the key influence in our personal economic lives. We are shaped by our attitude to money, and our attitude to money is shaped by our fear. If we could change our attitude to risk and wealth, we could begin to think, act, and live like the rich. But first we must become financially intelligent.
It is strongly advised to get hold of this book for all the simple yet strong principles it offers for enhancing your intelligence!
Please send your comments on the book and criticism on my writing on it!
Let us get back to our regular feature: Interesting learning scenarios
BANDING QUESTION
One of the most fascinating occurrences in pediatric cardiology is congenitally corrected transposition of great arteries (cTGA). Any student of medicine feels extremely fascinated when the anatomy is understood for first time. However, it takes lot many years to understand the lesion. Every child with cTGA teaches a different lesson. We had a 12-year-old with cTGA, intact IVS. The LV was obviously regressed. Cath showed LV pressure of 60mmHg against RV pressure of 120mmHg. There was a voice on PA banding and preparing LV for double switch. Surprisingly, few more people seemed to support this! I have no objective data on till what age such a venture is attempted. What is the maximum age you have come across in which such a surgery was fruitful? Is there a cut-off age till which we can attempt the 2-stage arterial switch? Please send me your opinions and experiences.
REPLACEMENT ISSUES
Continuing with cTGA, is it worth replacing the tricuspid valve in cases of cTGA with severe TR? We accept that the TV and RV are not physiologically fit enough to tolerate systemic pressures. Hence, they fail over a period of time and TR is a part of the natural history of cTGA. Is the problem with the TV or the chamber distal to it which is pumping against the systemic afterload?
THE LEFT PUZZLE
We had a scenario that could not be explained by any of us. This 9-month-old came with a large ASD L to R, moderate VSD L to R and moderate PAH. The surprise in the picture was LA and LV dilatation in the presence of normal sized tricuspid and mitral valves. The RV did reach the apex nicely from subcostal views. We are still wondering how to explain the paradox. The classical teaching is that the sizable proximal shunt always overtakes distal. In this baby with a large ASD, it should invariably RA and RV dominance. How to explain this paradox? Is this seen earlier by any of the readership? Could you offer any explanation for this? I have asked for follow up as the baby was not much symptomatic. Please let me know your experiences and explanations on this issue.
CAT(H) ON THE WALL
Cath studies of borderline values always make a nice “cat(h) on the wall”! The data can be twisted in the most convincing manner depending upon individual moods! We often see the borderline PA pressures in single ventricle physiology either making it for BD Glenn or losing the case based on the individual mood of the day! “The data is collected when patient was continuously on oxygen, hence likely fallacious”, “The numbers are when the patient was sedated and would be more when the patient is walking and talking” are some of the explanations offered for rejecting a case. Similarly, “The PA pressures may come down once we offload the ventricles via BD Glenn”, “Once oxygenated blood starts circulating, the ventricular function is likely to improve” are some of the explanations given for accepting. The problem is: one can argue on either sides of the case. Can the relative non-objectability be replaced by better objective criteria in each case? Is there a way of telling if a child is fit or not-fit for the procedure? How different is the scenario in other places? Let me know your experiences on this critical issue.
ADULT TAPVC
“No TAPVC is inoperable” is the stand of one of our senior surgeons who must have done TAPVC rerouting in thousands of children and significant number of adults. But, objectively, how to p[rove this point? It is very clear that cath study is of no help in deciding operability, as denominator is indeterminable. Is the measurement of RV EDP useful? May be, but by itself, EDP cannot determine operability. Unlike other high Qp situations, pulmonary venous return is not an assessable entity here. Hence, only time can tell whether the decision of operating was appropriate. Fortunately, we do see some of the older patients with TAPVC successfully going through the scalpel and ending up with near normal PA pressures in post op phase. What is the experience of readership? Please inform the others if your views are similar or different.
PEDIATRIC CARDIOLOGY PEARLS:
76. In ASD, the P-R interval may be prolonged, especially in older patients, because of intra-atrial and sometimes H-V conduction delay, resulting in first-degree atrioventricular block (Shiku DJ, Stijns M, Lintermans JP, et al. Influence of age on atrioventricular conduction intervals in children with and without atrial septal defect. Journal of Electrocardiology in year 1982 page 9)
77. The cleft in the anterior mitral leaflet is directed toward the midportion of the ventricular septum, along the anteroinferior rim of the septal defect. In contrast, isolated mitral clefts (not otherwise associated with AVSD) are directed toward the aortic valve annulus (di Segni E, Edwards JE. Cleft anterior leaflet of the mitral valve with intact septa: A study of 20 cases. American Journal of Cardiology in year 1983 page 919)
78. With the perimembranous defect, there can be a variable degree of anterior malalignment between the infundibular septum and the anterior ventricular septum such that the aortic valve appears to override the defect. Such lesions cannot be called tetralogy of Fallot even if there is some RVOT obstruction. (Soto B, Becker AE, Moulaert AJ, et al. Classification of ventricular septal defects. British Heart Journal in year 1980 page 332)
79. In a PDA, due to increased return into the LA, left-to-right shunting through a stretched, incompetent foramen ovale secondary to left atrial dilation is a fairly common association. This should be evaluated correctly and the incidence of coexisting ASD should not be overestimated. (Rudolph AM, Mayer FE, Nadas AS, et al. Patent ductus arteriosus. A clinical and hemodynamic study of patients in the first year of life. AAP Pediatrics journal in year 1958 page 892)
80. Isolated anomalies of minimal significance are more frequent with bicuspid aortic valves (Baroldi G, Scomazzoni G. Coronary circulation in the normal and the pathologic heart. Washington, DC: Office of the Surgeon General, in year 1967)
Good news was the contribution from Dr Ritesh Sukharamwala, a consultant Pediatric Cardiologist from Surat, Gujarat. He was an alumnus of Narayana Hrudayalaya and a member of the team. You can find his early experience as an independent pediatric cardiologist in the previous post. He has promised me atleast one contribution every month from now on. Hope others would follow soon.
That brings us to the end of another post. Please send your comments and criticisms to drkiranvs@gmail.com or put them in the comments box below. I am thankful for the positive responses I am hearing for the book review. Also, as thought previously, planning a separate section for Pediatric PGs interested in cardiology. Please let me know your suggestions on structuring the section.
Regards
Kiran
Let us get to the book first:
“Do you have Kiyosaki’s book?” asked my Boss one day.
“Yes, Sir. I do. Would you like to read it?”
“Please send it to me.”
When I read Robert Kiyosaki for the first time, only the novelty factor impressed me. However, over a period of time, I think I matured to the contents of book! It is something I would not hesitate recommending to anyone. It is titled “Rich Dad, Poor Dad: What the Rich Teach Their Kids about Money… That the Poor and Middle Class Do Not!”
The best part of the book is that it does not teach anything about market ventures, real-estate, dot com or anything similar. It concentrates on individual discipline and private attitudes towards money. When most of us equate money with wealth, Kiyosaki differs. He teaches us the difference between money and wealth. Money is a result of wealth or real value, and sometimes only a symbol of it. What is real is what has generated the money: a business with revenues greater than costs, a property with rent greater than mortgage, knowledge that earns royalties and so on.
The Rich Dad principle would be, “If you look for money and security, that’s all you’ll get.” You might get “money” but not find the source of money. The fundamental difference between the Rich Dad and Poor Dad is that the Rich Dad knows the difference between an asset and a liability. Anything that generates money—that actually puts it in your pocket—is an asset. Everything that takes money from your pocket without more returns is a liability! The job earnings are returns and not assets. The income coming from assets need not even have you to be around!
Kiyosaki maintains that unless one knows how to read a balance sheet, he is financial illiterate! Financial literacy, he says, is as important as word literacy. “Illiteracy, both in words and numbers, is the foundation of financial struggle.” His Sutra for getting rich is knowledge. Before making any investments, one should educate oneself on all the options and opportunities. “The more you know, the better your decisions will be!” Lack of financial education teamed with the desire for quick riches leads to disaster. “Most people, in their drive to get rich, are trying to build an Empire State Building on a 6-inch slab,” he says. The key to controlling money in his view is by controlling emotions. Becoming rich involves self-discipline and the ability to separate the emotions of fear and greed from a good investment decision.
This book makes the reader think a lot. It forces the reader to reflect not merely about their investments and assets, but about their whole attitude to work and life.
The stock market is always said to be driven by “fear and greed.” Kiyosaki claims that, for most of us, fear is the key influence in our personal economic lives. We are shaped by our attitude to money, and our attitude to money is shaped by our fear. If we could change our attitude to risk and wealth, we could begin to think, act, and live like the rich. But first we must become financially intelligent.
It is strongly advised to get hold of this book for all the simple yet strong principles it offers for enhancing your intelligence!
Please send your comments on the book and criticism on my writing on it!
Let us get back to our regular feature: Interesting learning scenarios
BANDING QUESTION
One of the most fascinating occurrences in pediatric cardiology is congenitally corrected transposition of great arteries (cTGA). Any student of medicine feels extremely fascinated when the anatomy is understood for first time. However, it takes lot many years to understand the lesion. Every child with cTGA teaches a different lesson. We had a 12-year-old with cTGA, intact IVS. The LV was obviously regressed. Cath showed LV pressure of 60mmHg against RV pressure of 120mmHg. There was a voice on PA banding and preparing LV for double switch. Surprisingly, few more people seemed to support this! I have no objective data on till what age such a venture is attempted. What is the maximum age you have come across in which such a surgery was fruitful? Is there a cut-off age till which we can attempt the 2-stage arterial switch? Please send me your opinions and experiences.
REPLACEMENT ISSUES
Continuing with cTGA, is it worth replacing the tricuspid valve in cases of cTGA with severe TR? We accept that the TV and RV are not physiologically fit enough to tolerate systemic pressures. Hence, they fail over a period of time and TR is a part of the natural history of cTGA. Is the problem with the TV or the chamber distal to it which is pumping against the systemic afterload?
THE LEFT PUZZLE
We had a scenario that could not be explained by any of us. This 9-month-old came with a large ASD L to R, moderate VSD L to R and moderate PAH. The surprise in the picture was LA and LV dilatation in the presence of normal sized tricuspid and mitral valves. The RV did reach the apex nicely from subcostal views. We are still wondering how to explain the paradox. The classical teaching is that the sizable proximal shunt always overtakes distal. In this baby with a large ASD, it should invariably RA and RV dominance. How to explain this paradox? Is this seen earlier by any of the readership? Could you offer any explanation for this? I have asked for follow up as the baby was not much symptomatic. Please let me know your experiences and explanations on this issue.
CAT(H) ON THE WALL
Cath studies of borderline values always make a nice “cat(h) on the wall”! The data can be twisted in the most convincing manner depending upon individual moods! We often see the borderline PA pressures in single ventricle physiology either making it for BD Glenn or losing the case based on the individual mood of the day! “The data is collected when patient was continuously on oxygen, hence likely fallacious”, “The numbers are when the patient was sedated and would be more when the patient is walking and talking” are some of the explanations offered for rejecting a case. Similarly, “The PA pressures may come down once we offload the ventricles via BD Glenn”, “Once oxygenated blood starts circulating, the ventricular function is likely to improve” are some of the explanations given for accepting. The problem is: one can argue on either sides of the case. Can the relative non-objectability be replaced by better objective criteria in each case? Is there a way of telling if a child is fit or not-fit for the procedure? How different is the scenario in other places? Let me know your experiences on this critical issue.
ADULT TAPVC
“No TAPVC is inoperable” is the stand of one of our senior surgeons who must have done TAPVC rerouting in thousands of children and significant number of adults. But, objectively, how to p[rove this point? It is very clear that cath study is of no help in deciding operability, as denominator is indeterminable. Is the measurement of RV EDP useful? May be, but by itself, EDP cannot determine operability. Unlike other high Qp situations, pulmonary venous return is not an assessable entity here. Hence, only time can tell whether the decision of operating was appropriate. Fortunately, we do see some of the older patients with TAPVC successfully going through the scalpel and ending up with near normal PA pressures in post op phase. What is the experience of readership? Please inform the others if your views are similar or different.
PEDIATRIC CARDIOLOGY PEARLS:
76. In ASD, the P-R interval may be prolonged, especially in older patients, because of intra-atrial and sometimes H-V conduction delay, resulting in first-degree atrioventricular block (Shiku DJ, Stijns M, Lintermans JP, et al. Influence of age on atrioventricular conduction intervals in children with and without atrial septal defect. Journal of Electrocardiology in year 1982 page 9)
77. The cleft in the anterior mitral leaflet is directed toward the midportion of the ventricular septum, along the anteroinferior rim of the septal defect. In contrast, isolated mitral clefts (not otherwise associated with AVSD) are directed toward the aortic valve annulus (di Segni E, Edwards JE. Cleft anterior leaflet of the mitral valve with intact septa: A study of 20 cases. American Journal of Cardiology in year 1983 page 919)
78. With the perimembranous defect, there can be a variable degree of anterior malalignment between the infundibular septum and the anterior ventricular septum such that the aortic valve appears to override the defect. Such lesions cannot be called tetralogy of Fallot even if there is some RVOT obstruction. (Soto B, Becker AE, Moulaert AJ, et al. Classification of ventricular septal defects. British Heart Journal in year 1980 page 332)
79. In a PDA, due to increased return into the LA, left-to-right shunting through a stretched, incompetent foramen ovale secondary to left atrial dilation is a fairly common association. This should be evaluated correctly and the incidence of coexisting ASD should not be overestimated. (Rudolph AM, Mayer FE, Nadas AS, et al. Patent ductus arteriosus. A clinical and hemodynamic study of patients in the first year of life. AAP Pediatrics journal in year 1958 page 892)
80. Isolated anomalies of minimal significance are more frequent with bicuspid aortic valves (Baroldi G, Scomazzoni G. Coronary circulation in the normal and the pathologic heart. Washington, DC: Office of the Surgeon General, in year 1967)
Good news was the contribution from Dr Ritesh Sukharamwala, a consultant Pediatric Cardiologist from Surat, Gujarat. He was an alumnus of Narayana Hrudayalaya and a member of the team. You can find his early experience as an independent pediatric cardiologist in the previous post. He has promised me atleast one contribution every month from now on. Hope others would follow soon.
That brings us to the end of another post. Please send your comments and criticisms to drkiranvs@gmail.com or put them in the comments box below. I am thankful for the positive responses I am hearing for the book review. Also, as thought previously, planning a separate section for Pediatric PGs interested in cardiology. Please let me know your suggestions on structuring the section.
Regards
Kiran
ಮಂಗಳವಾರ, ಸೆಪ್ಟೆಂಬರ್ 14, 2010
At last!
After more than 2 years, I have a contributor for the blog!!
Dr Ritesh Sukharamwala, who trained in our team at Narayana Hrudayalaya from Nov 2006 to July 2009 has shared his experiences as independent Pediatric Cardiologist. Please go through and let us know your opinions:
Following is the complete transcript of his experiences in first person. I have not edited a single word; there was no need for any editing. Everything seems right from heart!
Over to Dr Ritesh:
Where am I standing at the end of 1 year? A freshly passed out pediatric cardiologist
I would life to share my 1 year experience as a pediatric cardiologist in my home town Surat.
After completing my fellowship in Pediatric Cardiology at Narayana Hrudayalaya it was very clear in my mind to settle down in my home town Surat. There were lot of comments and suggestion by senior colleagues stating difficulties of establishing new subspeciality of pediatric cardiology in small town. As a pediatrician during my residency days I have faced lot of problem in treating pediatric cardiac problem. So with a vision of providing tertiary level of pediatric cardiac care in my city I started my journey at CARE hospital Surat. CARE hospital is basically cardiac hospital providing services for adult patients. To begin with, this hospital provided me basic infrastructure in the form of echocardiography machine & OPD.
I started meeting pediatrician in my city and near by areas. To begin with there was lot of apprehension - whether this small city will accept this new subspeciality? Will I get patients? Will I be able to provide quality work? Whether I am capable? Will I be able to do interventions independently?
I started getting 1 or 2 patients a day in my OPD who were primarily referred by pediatricians. There were days where I had not seen a single patient in a day. I also started doing bedside ECHO in outside hospital ICUs.
Everyday was like a new day, learning and applying something new. This was for the first time when I have no backing of my senior. There was always a check echo by senior colleague even in my last days of fellowship. I was making my all patients rely on my reports and there was no second check. I remembered my teacher said” though you have cleared your exam, your exam starts from today”. In my initial few months of my services I got out of inferiority complex and started believing in myself. By this time I was in the second month of my journey. I had a plan to focus more on outdoor work for first six months and then to think of interventional work.
But in second month itself a patient knocked the door for PDA device closure. The time to use other infrastructure i.e. cath lab had come. The patient was admitted for the procedure. My night before procedure was sleepless. At every step I wanted to be double sure. Confirming the diagnosis more and more times and checking the hardware many times. Procedure was done successfully and that was for the first time when I felt that feeling of eternity and happiness of saving somebody’s life. I realized the meaning of job satisfaction. After that I had many diagnostic cath which went uneventfully.
Second challenge came when I had a 2 kg 2 day old preterm with critical aortic stenosis but my confidence level boosted up after its success. It was a true life saving procedure. I mean it is a life saving procedure but I realized it in true sense on that day.
Pediatric cardiology program is incomplete with out a team. I inspired my surgeon to take challenging pediatric cases. I use to go to operating room, gross anatomy was confirmed on table and surgery was done as per plan. We got away with cases like ASD, VSD, PDA & TOF. I also had to play a major role in post operative care especially when my ICU staff was not trained for pediatric critical care. It was now 6 months of my journey and the time have come when I have to think in terms of treating more complex cases which needs trained surgical expertise like arterial switch operation and single ventricle pathway surgery. One of the trained pediatric cardiac surgeons was called for arterial switch operation. Everything went smoothly & child was discharged on 11th POD and doing well on follow up. That day was new landmark in the history of my town Surat when arterial switch operation succeeded. All pediatric procedures were done for the first time in entire South Gujarat and I feel proud of enjoying honour of being the first interventional pediatric cardiologist of South Gujarat.
At the end of one year I am realizing that my journey has in fact started. Today I am seeing around 150 patients in month out of which 2-3 patient gets ready intervention and 3-4 children for surgery. I still have same feeling of apprehension when I do intervention today as every case is a new case and I don’t want to take a chance.
My majority of above said statement depicts my immaturity which I have already realized. However I firmly believe that there is no other way to success when you are alone and not backed up by your senior colleagues. I consider myself lucky to go through this phase which you will never face when you are protected by your seniors. I am trying for progress of pediatric Cardiology branch as a whole rather than individual progress. I am still learning daily and there are lots of things coming forward to learn, I mean life ends but process of learning never ends.
I am looking forward for valuable suggestion and guidance from my senior colleagues and teachers.
Sincerely,
Dr Ritesh Sukharamwala
Pediatric Cardiologist
CARE Hospital –The Heart Institute
Surat.
email: sukharamwalaritesh@yahoo.com
Please reply to the blog comments, or to Dr Ritesh or to drkiranvs@gmail.com
Regards
Kiran
After more than 2 years, I have a contributor for the blog!!
Dr Ritesh Sukharamwala, who trained in our team at Narayana Hrudayalaya from Nov 2006 to July 2009 has shared his experiences as independent Pediatric Cardiologist. Please go through and let us know your opinions:
Following is the complete transcript of his experiences in first person. I have not edited a single word; there was no need for any editing. Everything seems right from heart!
Over to Dr Ritesh:
Where am I standing at the end of 1 year? A freshly passed out pediatric cardiologist
I would life to share my 1 year experience as a pediatric cardiologist in my home town Surat.
After completing my fellowship in Pediatric Cardiology at Narayana Hrudayalaya it was very clear in my mind to settle down in my home town Surat. There were lot of comments and suggestion by senior colleagues stating difficulties of establishing new subspeciality of pediatric cardiology in small town. As a pediatrician during my residency days I have faced lot of problem in treating pediatric cardiac problem. So with a vision of providing tertiary level of pediatric cardiac care in my city I started my journey at CARE hospital Surat. CARE hospital is basically cardiac hospital providing services for adult patients. To begin with, this hospital provided me basic infrastructure in the form of echocardiography machine & OPD.
I started meeting pediatrician in my city and near by areas. To begin with there was lot of apprehension - whether this small city will accept this new subspeciality? Will I get patients? Will I be able to provide quality work? Whether I am capable? Will I be able to do interventions independently?
I started getting 1 or 2 patients a day in my OPD who were primarily referred by pediatricians. There were days where I had not seen a single patient in a day. I also started doing bedside ECHO in outside hospital ICUs.
Everyday was like a new day, learning and applying something new. This was for the first time when I have no backing of my senior. There was always a check echo by senior colleague even in my last days of fellowship. I was making my all patients rely on my reports and there was no second check. I remembered my teacher said” though you have cleared your exam, your exam starts from today”. In my initial few months of my services I got out of inferiority complex and started believing in myself. By this time I was in the second month of my journey. I had a plan to focus more on outdoor work for first six months and then to think of interventional work.
But in second month itself a patient knocked the door for PDA device closure. The time to use other infrastructure i.e. cath lab had come. The patient was admitted for the procedure. My night before procedure was sleepless. At every step I wanted to be double sure. Confirming the diagnosis more and more times and checking the hardware many times. Procedure was done successfully and that was for the first time when I felt that feeling of eternity and happiness of saving somebody’s life. I realized the meaning of job satisfaction. After that I had many diagnostic cath which went uneventfully.
Second challenge came when I had a 2 kg 2 day old preterm with critical aortic stenosis but my confidence level boosted up after its success. It was a true life saving procedure. I mean it is a life saving procedure but I realized it in true sense on that day.
Pediatric cardiology program is incomplete with out a team. I inspired my surgeon to take challenging pediatric cases. I use to go to operating room, gross anatomy was confirmed on table and surgery was done as per plan. We got away with cases like ASD, VSD, PDA & TOF. I also had to play a major role in post operative care especially when my ICU staff was not trained for pediatric critical care. It was now 6 months of my journey and the time have come when I have to think in terms of treating more complex cases which needs trained surgical expertise like arterial switch operation and single ventricle pathway surgery. One of the trained pediatric cardiac surgeons was called for arterial switch operation. Everything went smoothly & child was discharged on 11th POD and doing well on follow up. That day was new landmark in the history of my town Surat when arterial switch operation succeeded. All pediatric procedures were done for the first time in entire South Gujarat and I feel proud of enjoying honour of being the first interventional pediatric cardiologist of South Gujarat.
At the end of one year I am realizing that my journey has in fact started. Today I am seeing around 150 patients in month out of which 2-3 patient gets ready intervention and 3-4 children for surgery. I still have same feeling of apprehension when I do intervention today as every case is a new case and I don’t want to take a chance.
My majority of above said statement depicts my immaturity which I have already realized. However I firmly believe that there is no other way to success when you are alone and not backed up by your senior colleagues. I consider myself lucky to go through this phase which you will never face when you are protected by your seniors. I am trying for progress of pediatric Cardiology branch as a whole rather than individual progress. I am still learning daily and there are lots of things coming forward to learn, I mean life ends but process of learning never ends.
I am looking forward for valuable suggestion and guidance from my senior colleagues and teachers.
Sincerely,
Dr Ritesh Sukharamwala
Pediatric Cardiologist
CARE Hospital –The Heart Institute
Surat.
email: sukharamwalaritesh@yahoo.com
Please reply to the blog comments, or to Dr Ritesh or to drkiranvs@gmail.com
Regards
Kiran
ಬುಧವಾರ, ಸೆಪ್ಟೆಂಬರ್ 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
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
ಗುರುವಾರ, ಆಗಸ್ಟ್ 19, 2010
Dr Kiran welcomes the readership to the new post. In the last few posts, I tried some innovation in the form of anecdotes which carry greater meanings to life. Thanks for all the positive responses to them. In fact, a couple of inspired friends tried their hands on writing some stuff and with minimal editing from my side, they did a fabulous job. Great going!
From this post on, I am rendering a new idea to the readership. I will be introducing few books in next few posts. These are the books that made a great impact on me in the formative years and still rule lot of my thinking process. I had made some systematic notes on such books all these years. I will be presenting one book per post. We shall start with a small introduction to the author, go on to the works and take one classic of the author. We shall see the essence of the classic and if possible, read some excerpts from the book. If the readership has any different strategy in getting introduced to a book, the advice would be most welcoming.
Let me start with the book I admire. In the year 1998, Dr Howard Cutler, a renowned psychiatrist brought out a book titled “The Art of Happiness: A Handbook for Living”. The twist in the tale was the co-author of the book, who probably did not write a single word for the book! Many thought that the name was a gimmick and Dr Cutler just wanted a bigger publicity for his book. However, Dr Cutler maintained that the contents of book essentially belonged to both the authors. The book became a classic by the might of its contents. The role of the co-author was undeniable, for, he was the Holy Dalai Lama.
The essence of the book is simple; it says “happiness is not a luxury but the purpose of our existence”, taking away the mystical component from happiness. Another shackle breaking thing in the book is the concept that there is a definitive way leading towards happiness! It claims that achieving happiness is scientific and not by chance; it needs discipline to do that.
Some of the points emphasized in the book are:
• A basic way to happiness is to cultivate affection and connection with other human beings.
• The real source of happiness is control of your consciousness, which is impossible without a disciplined mind.
• No matter how powerful they seem, negative emotions and states of mind have no foundation in reality.
• Don’t confuse happiness with pleasure. Pleasure is of the senses and can seem like happiness, but lacks meaning. Happiness, in contrast, rests on meaning and is often felt despite negative external conditions. It is stable and persistent. While pleasures are a bonus in life, happiness is mandatory.
• Happiness is something to be developed over time.
• The fundamental nature of human beings is gentleness; people like to be altruistic if they get a chance.
• Compassion is useful. Rather than being sentimental, it is the basis of communicating well between people. Compassion is not “feeling sorry for someone” but a recognition of commonality.
• Distinguish between love based on attachment and love based on compassion.
The essence of the book is its simplicity. It gives off a sense of the lightness to life, despite all the negative things prevailing in the world. We may not understand everything about our existence; it is all the more important to be good to other beings and to leave the world a slightly better place. It should be our objective and one should not astray from it.
Let me know your comments and criticism on the book and its review. If you have any book which you would recommend to the readership, please let me know. I shall try to get that book introduced.
Let us get back to the real world now: The interesting learning scenarios!
EBSTEIN TENSION
One of the most indecisive lesions for a pediatric cardiologist is Ebsteins anomaly. Every surgeon possibly has a different approach to this lesion. But, has anyone seen an Ebsteins anomaly with severe pulmonary hypertension? Looks paradoxical, but I happened to see a report stating this combination! It was fag end of the day and this 6-day-old presented with this echo report. Unable to believe, I had to re-do the echo. To my surprise, I did find severe PAH, but the Ebstein component was missing! The STL origin was normal, but its tip was tethered to the IVS, causing non-coaptation of TV and the resultant severe TR. The lower half of the IVS was swiss cheesed. How to handle such a scenario? I have started the baby on diuretics, ACEI and asked for a surgical opinion. I shall update this issue when the baby returns for follow up.
LESSER CRIME!
What is the least morbid option in cardiac surgery? The witty answer would be not doing the surgery at all! However, this question came up a serious way in one of our meetings. This 6-year-old girl had VSD with pulmonary atresia with small confluent branch PAs and sizeable collaterals. The options would be BT shunts (possibly bilateral) or unifocalization with/without BT shunt. Considering the complexities and the practical problems in approach, the question was “which is the least morbid?” Jokes apart, it was decided to go for the latter option. I shall update the result after the procedure.
FONTAN FOUNTAIN
I can sense why surgeons are not very keen on Fontan completion. It is often said that the patient should earn his Fontan completion. We had a 4-year-old single ventricle Glenned 3 years back with all parameters favoring Fontan completion. He did quite well in the immediate post-op and was nicely extubated. However, in a matter of few days, he has developed desaturation, respiratory distress and his need for oxygen increased. The Fontan fenestration was seen shunting right to left. Added to it, there was significant pleural effusion. To make the matters worse, a saline contrast injected to a peripheral vein showed contrast in the cardiac chambers, indicating the development of pulmonary AV malformations. The last finding could not be easily explained when there was a flow from IVC to PA, indicated by the gradient across the fenestration. Should such children go for a take-down of Fontan or should they be managed conservatively? Please let me know your opinions on this issue.
BAD COMBO
We had a 3-month-old with DORV and remote muscular VSD. This combination is described in the classification, but is rarely seen. The bad part was the other lesions. This baby had normally related great arteries, severe PAH (No PS), restrictive PDA flowing R to L and coarctation of aorta. Baseline saturation in room air was 80%. Obviously, such combination is not suited for 2-pumpo repair. The coarctation would ensure rapid progress of high PVRI. Since the kid was only 3-month-old, we expected some daring surgeries and eventuality. However, our offer of Coarctation repair with PDA ligation with PA banding plus-minus BTT shunt was not taken by surgeon. The option of PA band does not exist when the baseline saturation is less. The addition of BT shunt would reduce the possibility of future single pump. Moreover, the high risk palliation is not a wise option. With all these explanations, the surgery was deferred. What is your opinion? How would you plan something for this? Let me know your takes on this.
SINGLE OR ONE-AND-HALF?
The pulmonary atresia with intact IVS is a tricky situation. Lot of variables may lead to lot of mistakes in decision making. Predicting their outcome is difficult. We had a 1 year 2 month-old boy with this problem. The TR is severe and the RV is muscle bound. RV apex is not visualized on echo. The pulmonary atresia is membranous. The contemplation of single pump was risked by the TR. One of our upcoming surgeons came up with an idea that is worth sharing. He is considering a Brock’s procedure, passing a cannula across the membranous pulmonary valve, slitting the membrane open using a balloon in the OT. This would be a semi-hybrid procedure! We are indeed excited!! I shall update the outcome in next posts. If anyone has done this before, please let us know.
DARING ATTEMPTS
After a long time, our surgeons have started doing adventures things! We did a Norwood stage 1 and the baby is doing very well. It is very encouraging and we should be doing them more from now on. On the other end, we did a REV procedure in a dTGA, VSD, PS when the VSD was deemed non-routable. Our surgeons enlarged the VSD and did a long LV to Aorta patch followed by a REV. It is very commendable and we all pray for good outcomes in these babies. How many centers are actually attempting REV? If you have any experience with it, please share with us.
PEDIATRIC CARDIOLOGY PEARLS
66. In neonatal IE most cases occur in structurally normal hearts. Although relatively uncommon, increasing numbers of cases of neonatal IE have been reported since the 1970s. This reflects the increased use of prosthetic intravascular devices and more frequent insertion of long-term indwelling central venous catheters (Ferrieri P and others: Unique features of infective endocarditis in childhood. Circulation journal in year 2002 page 2115)
67. The pericardial space, lubricated by lymph, normally contains <30 mL of fluid in the adult and considerably less in infants and children (Holt JP. The normal pericardium. Am J Cardiol in year 1970 page 455)
68. Chorea may be the sole presenting manifestation of lupus, this disease should be considered whenever a child presents with chorea (Arisaka O, Obinata K, Sasaki H, et al. Chorea as an initial manifestation of systemic lupus erythematosus: A case report of a 10 year old girl. Clin Pediatr journal in year 1984 page 298)
69. The seasonal variation of Rheumatic Fever in the temperate climates parallels that of Grp A Streptococcus pharyngitis. Both Grp A Streptococcus pharyngitis and Rheumatic Fever are more common during the winter and spring in temperate climates, but there is no consistent seasonal pattern in the tropics. Geographically, Rheumatic Fever occurs in all latitudes and altitudes (Kumar RK, Rammohan R, Narula J, et al. Epidemiology of streptococcal pharyngitis, rheumatic fever, and rheumatic heart disease. In: Narula J, Virmani R, Reddy KS, et al., eds. Rheumatic Fever. Washington, DC: American Registry of Pathology in year 1999 page 41)
70. In Kawasaki disease, generalized microvasculitis occurs throughout the body in the first 10 days of disease. Myocarditis occurs in the first 3 to 4 weeks, with mononuclear cell infiltration and edema within the myocardium and conduction system. Valvulitis may affect the mitral and aortic valves (Gidding SS, Shulman ST, Ilbawi M, et al. Mucocutaneous lymph node syndrome (Kawasaki disease): Delayed aortic and mitral insufficiency secondary to active valvulitis. J Am Coll Cardiol in year 1986 page 894)
With this, we conclude this post. Please send your feedback to drkiranvs@gmail.com Your suggestions are welcome. Please narrate your experiences with the scenarios discussed and post some novel things seen by you hitherto. Please let me know your opinion on the new section.
Regards
Kiran
From this post on, I am rendering a new idea to the readership. I will be introducing few books in next few posts. These are the books that made a great impact on me in the formative years and still rule lot of my thinking process. I had made some systematic notes on such books all these years. I will be presenting one book per post. We shall start with a small introduction to the author, go on to the works and take one classic of the author. We shall see the essence of the classic and if possible, read some excerpts from the book. If the readership has any different strategy in getting introduced to a book, the advice would be most welcoming.
Let me start with the book I admire. In the year 1998, Dr Howard Cutler, a renowned psychiatrist brought out a book titled “The Art of Happiness: A Handbook for Living”. The twist in the tale was the co-author of the book, who probably did not write a single word for the book! Many thought that the name was a gimmick and Dr Cutler just wanted a bigger publicity for his book. However, Dr Cutler maintained that the contents of book essentially belonged to both the authors. The book became a classic by the might of its contents. The role of the co-author was undeniable, for, he was the Holy Dalai Lama.
The essence of the book is simple; it says “happiness is not a luxury but the purpose of our existence”, taking away the mystical component from happiness. Another shackle breaking thing in the book is the concept that there is a definitive way leading towards happiness! It claims that achieving happiness is scientific and not by chance; it needs discipline to do that.
Some of the points emphasized in the book are:
• A basic way to happiness is to cultivate affection and connection with other human beings.
• The real source of happiness is control of your consciousness, which is impossible without a disciplined mind.
• No matter how powerful they seem, negative emotions and states of mind have no foundation in reality.
• Don’t confuse happiness with pleasure. Pleasure is of the senses and can seem like happiness, but lacks meaning. Happiness, in contrast, rests on meaning and is often felt despite negative external conditions. It is stable and persistent. While pleasures are a bonus in life, happiness is mandatory.
• Happiness is something to be developed over time.
• The fundamental nature of human beings is gentleness; people like to be altruistic if they get a chance.
• Compassion is useful. Rather than being sentimental, it is the basis of communicating well between people. Compassion is not “feeling sorry for someone” but a recognition of commonality.
• Distinguish between love based on attachment and love based on compassion.
The essence of the book is its simplicity. It gives off a sense of the lightness to life, despite all the negative things prevailing in the world. We may not understand everything about our existence; it is all the more important to be good to other beings and to leave the world a slightly better place. It should be our objective and one should not astray from it.
Let me know your comments and criticism on the book and its review. If you have any book which you would recommend to the readership, please let me know. I shall try to get that book introduced.
Let us get back to the real world now: The interesting learning scenarios!
EBSTEIN TENSION
One of the most indecisive lesions for a pediatric cardiologist is Ebsteins anomaly. Every surgeon possibly has a different approach to this lesion. But, has anyone seen an Ebsteins anomaly with severe pulmonary hypertension? Looks paradoxical, but I happened to see a report stating this combination! It was fag end of the day and this 6-day-old presented with this echo report. Unable to believe, I had to re-do the echo. To my surprise, I did find severe PAH, but the Ebstein component was missing! The STL origin was normal, but its tip was tethered to the IVS, causing non-coaptation of TV and the resultant severe TR. The lower half of the IVS was swiss cheesed. How to handle such a scenario? I have started the baby on diuretics, ACEI and asked for a surgical opinion. I shall update this issue when the baby returns for follow up.
LESSER CRIME!
What is the least morbid option in cardiac surgery? The witty answer would be not doing the surgery at all! However, this question came up a serious way in one of our meetings. This 6-year-old girl had VSD with pulmonary atresia with small confluent branch PAs and sizeable collaterals. The options would be BT shunts (possibly bilateral) or unifocalization with/without BT shunt. Considering the complexities and the practical problems in approach, the question was “which is the least morbid?” Jokes apart, it was decided to go for the latter option. I shall update the result after the procedure.
FONTAN FOUNTAIN
I can sense why surgeons are not very keen on Fontan completion. It is often said that the patient should earn his Fontan completion. We had a 4-year-old single ventricle Glenned 3 years back with all parameters favoring Fontan completion. He did quite well in the immediate post-op and was nicely extubated. However, in a matter of few days, he has developed desaturation, respiratory distress and his need for oxygen increased. The Fontan fenestration was seen shunting right to left. Added to it, there was significant pleural effusion. To make the matters worse, a saline contrast injected to a peripheral vein showed contrast in the cardiac chambers, indicating the development of pulmonary AV malformations. The last finding could not be easily explained when there was a flow from IVC to PA, indicated by the gradient across the fenestration. Should such children go for a take-down of Fontan or should they be managed conservatively? Please let me know your opinions on this issue.
BAD COMBO
We had a 3-month-old with DORV and remote muscular VSD. This combination is described in the classification, but is rarely seen. The bad part was the other lesions. This baby had normally related great arteries, severe PAH (No PS), restrictive PDA flowing R to L and coarctation of aorta. Baseline saturation in room air was 80%. Obviously, such combination is not suited for 2-pumpo repair. The coarctation would ensure rapid progress of high PVRI. Since the kid was only 3-month-old, we expected some daring surgeries and eventuality. However, our offer of Coarctation repair with PDA ligation with PA banding plus-minus BTT shunt was not taken by surgeon. The option of PA band does not exist when the baseline saturation is less. The addition of BT shunt would reduce the possibility of future single pump. Moreover, the high risk palliation is not a wise option. With all these explanations, the surgery was deferred. What is your opinion? How would you plan something for this? Let me know your takes on this.
SINGLE OR ONE-AND-HALF?
The pulmonary atresia with intact IVS is a tricky situation. Lot of variables may lead to lot of mistakes in decision making. Predicting their outcome is difficult. We had a 1 year 2 month-old boy with this problem. The TR is severe and the RV is muscle bound. RV apex is not visualized on echo. The pulmonary atresia is membranous. The contemplation of single pump was risked by the TR. One of our upcoming surgeons came up with an idea that is worth sharing. He is considering a Brock’s procedure, passing a cannula across the membranous pulmonary valve, slitting the membrane open using a balloon in the OT. This would be a semi-hybrid procedure! We are indeed excited!! I shall update the outcome in next posts. If anyone has done this before, please let us know.
DARING ATTEMPTS
After a long time, our surgeons have started doing adventures things! We did a Norwood stage 1 and the baby is doing very well. It is very encouraging and we should be doing them more from now on. On the other end, we did a REV procedure in a dTGA, VSD, PS when the VSD was deemed non-routable. Our surgeons enlarged the VSD and did a long LV to Aorta patch followed by a REV. It is very commendable and we all pray for good outcomes in these babies. How many centers are actually attempting REV? If you have any experience with it, please share with us.
PEDIATRIC CARDIOLOGY PEARLS
66. In neonatal IE most cases occur in structurally normal hearts. Although relatively uncommon, increasing numbers of cases of neonatal IE have been reported since the 1970s. This reflects the increased use of prosthetic intravascular devices and more frequent insertion of long-term indwelling central venous catheters (Ferrieri P and others: Unique features of infective endocarditis in childhood. Circulation journal in year 2002 page 2115)
67. The pericardial space, lubricated by lymph, normally contains <30 mL of fluid in the adult and considerably less in infants and children (Holt JP. The normal pericardium. Am J Cardiol in year 1970 page 455)
68. Chorea may be the sole presenting manifestation of lupus, this disease should be considered whenever a child presents with chorea (Arisaka O, Obinata K, Sasaki H, et al. Chorea as an initial manifestation of systemic lupus erythematosus: A case report of a 10 year old girl. Clin Pediatr journal in year 1984 page 298)
69. The seasonal variation of Rheumatic Fever in the temperate climates parallels that of Grp A Streptococcus pharyngitis. Both Grp A Streptococcus pharyngitis and Rheumatic Fever are more common during the winter and spring in temperate climates, but there is no consistent seasonal pattern in the tropics. Geographically, Rheumatic Fever occurs in all latitudes and altitudes (Kumar RK, Rammohan R, Narula J, et al. Epidemiology of streptococcal pharyngitis, rheumatic fever, and rheumatic heart disease. In: Narula J, Virmani R, Reddy KS, et al., eds. Rheumatic Fever. Washington, DC: American Registry of Pathology in year 1999 page 41)
70. In Kawasaki disease, generalized microvasculitis occurs throughout the body in the first 10 days of disease. Myocarditis occurs in the first 3 to 4 weeks, with mononuclear cell infiltration and edema within the myocardium and conduction system. Valvulitis may affect the mitral and aortic valves (Gidding SS, Shulman ST, Ilbawi M, et al. Mucocutaneous lymph node syndrome (Kawasaki disease): Delayed aortic and mitral insufficiency secondary to active valvulitis. J Am Coll Cardiol in year 1986 page 894)
With this, we conclude this post. Please send your feedback to drkiranvs@gmail.com Your suggestions are welcome. Please narrate your experiences with the scenarios discussed and post some novel things seen by you hitherto. Please let me know your opinion on the new section.
Regards
Kiran
ಬುಧವಾರ, ಜುಲೈ 28, 2010
Dr Kiran hellos everyone. I had a good response for the previous couple of anecdote written by two friends. We shall see another anecdote now, followed by our regular features: Interesting learning scenarios in Pediatric cardiology and the popular “pediatric cardiology pearls”. The anecdote I have written this time was read few years back. I have expanded it a bit, but have retained the first-person narration of the original.
Please read and send your comments:
During my school days, there was a boy who was adored by everyone. He was not the class topper, he was not a champion sportsman, he was not an orator, he did not have great looks, his father was not the richest man in the community, he did not know any music, and he was, certainly, not a celebrity. Yet, he was liked by everyone. For the simple reason that he was good!
I wanted to know what made him so good that he was liked by all. I could sense that I could trust him; I could believe his words for he never lied. I was fond of him because he seemed to have a very simple and honest solution for every problem!
One day, he invited me to his home. I was curious to know where he lived and how his parents were. I went with him.
It was a very humble house; small, neat and clean. The utility of space was evident. I knew that my house was three times as big, but was pretty cluttered.
“Can I meet your parents?” I asked him.
“Both my parents work. They are not back till 6 PM. My elder brother has gone to tuitions and I am alone as of now”, he replied.
I recalled a joke of 10-year-old who answered the door bell of postman with a cigarette in one hand and a beer bottle in the other. “Is your dad in?” asked the postman. The kid laughed and replied, “You are a dumbo. Would you expect me in the house like this if my father was in?” asked the kid! I would have taken the opportunity of solitude to the hilt. Whereas, my friend appeared to be too good for a normal boy!
“You mean, there is no one to watch you over and still you are so good?” I asked him.
“There are certain principles that we live with in my house. They are not rules. There is no punishment if you break them or no reward if you follow them. But, I have experienced that I win applauds by following them. As for getting naughty, yes we do. But it never reaches a stage of destruction!” he replied.
“What rules…er… principles?” I started wondering now.
“Would you like to see them?” he asked doe eyed.
“See the principles?” I wondered.
“Come”, my friend led me towards a wall. There hung a sheet of parchment with neat writing in lines. Almost everyline had a different handwriting.
I read some of them:
Do unto others as you would have others do unto you
If you open it, close it.
If you turn it on, turn it off.
If you unlock it, lock it up.
If you break it, admit it.
If you can't fix it, call someone who can.
If you borrow it, return it.
If you value it, take care of it.
If you make a mess, clean it up.
If you move it, put it back.
If it belongs to someone else, get permission to use it.
If you don't know how to operate it, leave it alone.
If it's none of your business, don't ask questions.
If it will brighten someone's day, SAY IT!
If what you have to say will hurt somebody, DON'T SAY IT!
If something isn't broken, don't try and fix it.
If you think you know it all, look around and see how little you really know.
I just kept looking at them. None of those lines seemed great. They were all simple instructions, much like what are written in the operating manuals of appliances. In fact they were nothing compared to some of the “good habits” books I had read. But the simplicity did strike.
“What are these? What exactly these lines have to do with the discipline and good behavior?” I asked him with an element of surprise.
“These are the practical principles that we follow! There is no compulsion of following them. As I told you earlier, there are no rewards or punishments attached to them. But the effect of following them is really rewarding. I do follow them very honestly. You can see what I get from everyone!”
“How do you do it?” was my question, still with the tone of surprise.
“Whenever something good strikes any one of us, we discuss the point during our dinner with all family members. The elders in the family refine the content and make it a single line principle. The person who proposed the principle will get to write the line on the sheet in his own handwriting. Once written, we all try to follow it. As you can see, there are different handwritings on the paper. Every morning, we go to the paper, read everyline with maximum concentration that we can. Even though it is a routine and I know most of them byheart, I try to make this morning affair interesting by analyzing how many of them I have followed the previous day and how many I have broken. When there is a chance for rectifying, I do it honestly. Since they are very simple one liners, we tend to remember them for long time. It has not only won me credits, it has also definitely helped in character building.”
I was struck for a while. I took me sometime to appreciate the simplicity yet the power of routine. “It is so simple to be good, but it is so difficult to be simple” was a bollywood quote I had appreciated sometime back. It seemed to manifest in the simple abode of my friend.
The above anecdote is a true life incident I had read, narrated in first person. “Trifles make perfection and perfection is never trifle” was the life motto of Michelangelo. I felt that not only every house but every workplace should also have such a chart of principles that are practical yet simple. Seeing them everyday would be inspiring and seeing the people follow it may end up whipping the “lazy bums” of the department from their inside. Would you like to have one in your home or workplace?
INTERRUPTED PROBLEMS
We saw a 9-month-old with very complex anatomy. There was a PFO shunting left to right, supramitral membrane, large subaortic VSD, complete (100%) DORV, NRGA, large conus with subaortic obstruction, small bicuspid aortic valve (Z score of minus 3), Type B interrupted aortic arch, severe PAH and large PDA continuing as descending aorta. In a cyanosed crying child, the echo took almost an hour to delineate the anatomy. The mere description of components can discourage the surgeon from any management. How to tackle such cases? It is a combination of Shones complex with complete DORV. The small aortic component does not permit too extravagant surgeries. Is there an option? Can we think of DKS in such cases? Arch reconstruction strategy would depend on what we do proximally. Is there an option of a 2-pump repair in such complex anatomies? Please tell me your opinions on this.
EISENMENGER ISSUE
There was an interesting discussion. Our surgeons maintained that the residual VSD of post-TOF patients, howsoever big the VSD might be, does not develop Eisenmengarization! Physiologically, this statement does not make much sense. But the surgeons maintain their stand, as they have not seen a single case of such physiology till now! Is there any physiological explanation for this? Is it because of the paucity of such cases that it is largely unseen? Let me know your views on it.
TO GLENN OR NOT TO
In a patient of cTGA with VSD with conventional repair (VSD closure to convert it to classical cTGA), is there a role of adding a Glenn shunt if PA pressures are acceptable? One of our senior surgeons felt that a role exists. But, logically, this would offload the MLV. The crux of the issue is MRV which is systemic. The MRV preload and afterload would not change. Why should one add a Glenn shunt in such a scenario? If anyone has any more details on this, please start a discussion.
CUT-OFF LIMIT
Is there a limit for the extent of cyanosis in admixture lesion s as against low Qp? We see huge variations in the levels of cyanosis in low Qp situations. Sometimes, even with good admixture, the SO2 would be low in few. We had a patient of cTGA with DORV and non-routable VSD. The child had SO2 of 65% but the Qp/Qs was 3.8:1! How should such instances be treated? Let me know your takes.
MITRAL PUZZLE
How far the PML mobility characterizes the MV involvement in RHD? We often see children with classical history of acute rheumatic fever with significant mitral regurgitation. Many of them have nicely mobile PML. How should we term them? Should we say that they are a combination of Acute rheumatic fever with non-rheumatic MR? How would the management change? Let me know your opinions.
PEDIATRIC CARDIOLOGY PEARLS
61. In cardiac CT scan, when manually injecting a small dose of contrast, the delay from the start of injection to start of scanning is approximated by a circulation time of approximately 12 to 15 seconds. (Siegel MJ. Multiplanar and three-dimensional multi-detector row CT of thoracic vessels and airways in the pediatric population. Radiology. year 2003 page 641)
62. In the cardiac catheterization, in the absence of a shunt, a step-up of >6% at the atrial level, 4% at the ventricular level, and 4% at the great vessel level will occur in <5% of the time. Variations of >9%, 6%, and 6%, respectively (i.e., three times the standard deviation), would be expected no more than 1% of the time, thus would be highly unlikely in the absence of intracardiac shunting. This is the mark of significant step up in cath data. (Freed MD, Miettinen OS, Nadas AS. Oximetric detection of intracardiac left-to-right shunts. Br Heart J in year 1979 page 690)
63. Shorter refractory periods may facilitate the conduction of very closely coupled impulses and could render the newborn atrium more susceptible to intra-atrial re-entry. This may partly explain the occurrence of atrial arrhythmias such as atrial flutter in the otherwise healthy fetus or newborn infant. (Pickoff AS and others. Atrial vulnerability in the immature hearts. Am J Cardiol in year 1985 page 1402)
64. Even in the current era, congenital heart disease is the most common predisposing cause of brain abscess (Goodkin HP, Harper MB, Pomeroy SL. Intracerebral abscess in children: Historical trends at Children's Hospital Boston. Pediatrics in year 2004 page 1765)
65. Kawasaki disease is a panvasculitis. Most of the morbidity and mortality in affected patients is due to coronary artery aneurysms and associated complications. (Fujiwara H, Hamashima Y. Pathology of the heart in Kawasaki disease. Pediatrics in year 1978 page 100)
That brings us to the end of the present post. Please send your inputs to drkiranvs@gmail.com Since some fresh blood is getting infused to NH team, I hope to give you all something fresh!
Regards
Kiran
Please read and send your comments:
During my school days, there was a boy who was adored by everyone. He was not the class topper, he was not a champion sportsman, he was not an orator, he did not have great looks, his father was not the richest man in the community, he did not know any music, and he was, certainly, not a celebrity. Yet, he was liked by everyone. For the simple reason that he was good!
I wanted to know what made him so good that he was liked by all. I could sense that I could trust him; I could believe his words for he never lied. I was fond of him because he seemed to have a very simple and honest solution for every problem!
One day, he invited me to his home. I was curious to know where he lived and how his parents were. I went with him.
It was a very humble house; small, neat and clean. The utility of space was evident. I knew that my house was three times as big, but was pretty cluttered.
“Can I meet your parents?” I asked him.
“Both my parents work. They are not back till 6 PM. My elder brother has gone to tuitions and I am alone as of now”, he replied.
I recalled a joke of 10-year-old who answered the door bell of postman with a cigarette in one hand and a beer bottle in the other. “Is your dad in?” asked the postman. The kid laughed and replied, “You are a dumbo. Would you expect me in the house like this if my father was in?” asked the kid! I would have taken the opportunity of solitude to the hilt. Whereas, my friend appeared to be too good for a normal boy!
“You mean, there is no one to watch you over and still you are so good?” I asked him.
“There are certain principles that we live with in my house. They are not rules. There is no punishment if you break them or no reward if you follow them. But, I have experienced that I win applauds by following them. As for getting naughty, yes we do. But it never reaches a stage of destruction!” he replied.
“What rules…er… principles?” I started wondering now.
“Would you like to see them?” he asked doe eyed.
“See the principles?” I wondered.
“Come”, my friend led me towards a wall. There hung a sheet of parchment with neat writing in lines. Almost everyline had a different handwriting.
I read some of them:
Do unto others as you would have others do unto you
If you open it, close it.
If you turn it on, turn it off.
If you unlock it, lock it up.
If you break it, admit it.
If you can't fix it, call someone who can.
If you borrow it, return it.
If you value it, take care of it.
If you make a mess, clean it up.
If you move it, put it back.
If it belongs to someone else, get permission to use it.
If you don't know how to operate it, leave it alone.
If it's none of your business, don't ask questions.
If it will brighten someone's day, SAY IT!
If what you have to say will hurt somebody, DON'T SAY IT!
If something isn't broken, don't try and fix it.
If you think you know it all, look around and see how little you really know.
I just kept looking at them. None of those lines seemed great. They were all simple instructions, much like what are written in the operating manuals of appliances. In fact they were nothing compared to some of the “good habits” books I had read. But the simplicity did strike.
“What are these? What exactly these lines have to do with the discipline and good behavior?” I asked him with an element of surprise.
“These are the practical principles that we follow! There is no compulsion of following them. As I told you earlier, there are no rewards or punishments attached to them. But the effect of following them is really rewarding. I do follow them very honestly. You can see what I get from everyone!”
“How do you do it?” was my question, still with the tone of surprise.
“Whenever something good strikes any one of us, we discuss the point during our dinner with all family members. The elders in the family refine the content and make it a single line principle. The person who proposed the principle will get to write the line on the sheet in his own handwriting. Once written, we all try to follow it. As you can see, there are different handwritings on the paper. Every morning, we go to the paper, read everyline with maximum concentration that we can. Even though it is a routine and I know most of them byheart, I try to make this morning affair interesting by analyzing how many of them I have followed the previous day and how many I have broken. When there is a chance for rectifying, I do it honestly. Since they are very simple one liners, we tend to remember them for long time. It has not only won me credits, it has also definitely helped in character building.”
I was struck for a while. I took me sometime to appreciate the simplicity yet the power of routine. “It is so simple to be good, but it is so difficult to be simple” was a bollywood quote I had appreciated sometime back. It seemed to manifest in the simple abode of my friend.
The above anecdote is a true life incident I had read, narrated in first person. “Trifles make perfection and perfection is never trifle” was the life motto of Michelangelo. I felt that not only every house but every workplace should also have such a chart of principles that are practical yet simple. Seeing them everyday would be inspiring and seeing the people follow it may end up whipping the “lazy bums” of the department from their inside. Would you like to have one in your home or workplace?
INTERRUPTED PROBLEMS
We saw a 9-month-old with very complex anatomy. There was a PFO shunting left to right, supramitral membrane, large subaortic VSD, complete (100%) DORV, NRGA, large conus with subaortic obstruction, small bicuspid aortic valve (Z score of minus 3), Type B interrupted aortic arch, severe PAH and large PDA continuing as descending aorta. In a cyanosed crying child, the echo took almost an hour to delineate the anatomy. The mere description of components can discourage the surgeon from any management. How to tackle such cases? It is a combination of Shones complex with complete DORV. The small aortic component does not permit too extravagant surgeries. Is there an option? Can we think of DKS in such cases? Arch reconstruction strategy would depend on what we do proximally. Is there an option of a 2-pump repair in such complex anatomies? Please tell me your opinions on this.
EISENMENGER ISSUE
There was an interesting discussion. Our surgeons maintained that the residual VSD of post-TOF patients, howsoever big the VSD might be, does not develop Eisenmengarization! Physiologically, this statement does not make much sense. But the surgeons maintain their stand, as they have not seen a single case of such physiology till now! Is there any physiological explanation for this? Is it because of the paucity of such cases that it is largely unseen? Let me know your views on it.
TO GLENN OR NOT TO
In a patient of cTGA with VSD with conventional repair (VSD closure to convert it to classical cTGA), is there a role of adding a Glenn shunt if PA pressures are acceptable? One of our senior surgeons felt that a role exists. But, logically, this would offload the MLV. The crux of the issue is MRV which is systemic. The MRV preload and afterload would not change. Why should one add a Glenn shunt in such a scenario? If anyone has any more details on this, please start a discussion.
CUT-OFF LIMIT
Is there a limit for the extent of cyanosis in admixture lesion s as against low Qp? We see huge variations in the levels of cyanosis in low Qp situations. Sometimes, even with good admixture, the SO2 would be low in few. We had a patient of cTGA with DORV and non-routable VSD. The child had SO2 of 65% but the Qp/Qs was 3.8:1! How should such instances be treated? Let me know your takes.
MITRAL PUZZLE
How far the PML mobility characterizes the MV involvement in RHD? We often see children with classical history of acute rheumatic fever with significant mitral regurgitation. Many of them have nicely mobile PML. How should we term them? Should we say that they are a combination of Acute rheumatic fever with non-rheumatic MR? How would the management change? Let me know your opinions.
PEDIATRIC CARDIOLOGY PEARLS
61. In cardiac CT scan, when manually injecting a small dose of contrast, the delay from the start of injection to start of scanning is approximated by a circulation time of approximately 12 to 15 seconds. (Siegel MJ. Multiplanar and three-dimensional multi-detector row CT of thoracic vessels and airways in the pediatric population. Radiology. year 2003 page 641)
62. In the cardiac catheterization, in the absence of a shunt, a step-up of >6% at the atrial level, 4% at the ventricular level, and 4% at the great vessel level will occur in <5% of the time. Variations of >9%, 6%, and 6%, respectively (i.e., three times the standard deviation), would be expected no more than 1% of the time, thus would be highly unlikely in the absence of intracardiac shunting. This is the mark of significant step up in cath data. (Freed MD, Miettinen OS, Nadas AS. Oximetric detection of intracardiac left-to-right shunts. Br Heart J in year 1979 page 690)
63. Shorter refractory periods may facilitate the conduction of very closely coupled impulses and could render the newborn atrium more susceptible to intra-atrial re-entry. This may partly explain the occurrence of atrial arrhythmias such as atrial flutter in the otherwise healthy fetus or newborn infant. (Pickoff AS and others. Atrial vulnerability in the immature hearts. Am J Cardiol in year 1985 page 1402)
64. Even in the current era, congenital heart disease is the most common predisposing cause of brain abscess (Goodkin HP, Harper MB, Pomeroy SL. Intracerebral abscess in children: Historical trends at Children's Hospital Boston. Pediatrics in year 2004 page 1765)
65. Kawasaki disease is a panvasculitis. Most of the morbidity and mortality in affected patients is due to coronary artery aneurysms and associated complications. (Fujiwara H, Hamashima Y. Pathology of the heart in Kawasaki disease. Pediatrics in year 1978 page 100)
That brings us to the end of the present post. Please send your inputs to drkiranvs@gmail.com Since some fresh blood is getting infused to NH team, I hope to give you all something fresh!
Regards
Kiran
ಮಂಗಳವಾರ, ಜುಲೈ 27, 2010
This is Dr Kiran helloing everyone. I had a good response for the previous anecdote written by a friend. I am presenting the present one written by another friend. Thanks for the infectious zeal! This will be followed by our regular features: Interesting learning scenarios in Pediatric cardiology and the popular “pediatric cardiology pearls”. First - the anecdote: any resemblance to anyone living or dead is purely coincidental!!
Mrs Ana was enjoying her new dress in the mirror. Her husband, Mr Mike had done the payment after much reluctance. “You must dress your age and profession. You work amongst the public; these are too loud” was his argument, but she would not listen.
Mrs Ana started combing her hair, but the image in the mirror did not! She was surprised. She started waving her hand frantically, but the mirror image stood still. She got afraid and wanted to scream, but the voice did not erupt off her throat.
“Cool down”, the mirror image told her. The reflection in the mirror seemed having its own movements. Mrs Ana had no choice but to listen.
“How are your days going?” the reflection asked her.
Mrs Ana hesitated, but told “Fine”. Surprisingly, the voice had become normal.
“You are spending pretty much time with me nowadays!” said the mirror image.
“Well, you see, I am senior in the office now. My husband has come back from his posting. I have some spare time and I am trying to catch up.”
The reflection did not appear impressed. “How about your colleagues and seniors in the office? Do they have equal spare time?”
“They don’t. They still work like mad. In fact the work has increased. I pressurized the boss to hire few juniors. I clearly told him I cannot work more.”
“How is your typical day?” the mirror still did not look impressed.
“I go at around 10 am. By then, my seniors would have done the apprentices’ training session. I hang around for an hour. Then I go to the office gym. Stay there for an hour and a half. Come back and work for an hour and I go to lunch. After an hour of lunch break, I tell the others that I have to go to bank. Spend another hour hanging around at various places. I come back to the workstation by 3.45PM. By 4, I tell them that I have to attend to my family and leave for the day.”
“Very interesting” said the image sordidly. “How about your seniors?”
“As I told you, they work like mad. They start at around 8.30 AM, train the apprentices, start the work, go on till 2 PM. After the lunch, they continue till 5 or 5.30 PM. Few go on till 7 PM also.”
“How do you escape so easily then?”
“You know my previous boss. She was from my own community. My husband was working outside and my kid was young. So, out of sympathy of being a single mother, she gave lot of relaxations to me. She also paid me extra money as my husband was not earning. Both of us together made one of my colleagues a jackass and made him do all my extra work. We kept telling him that I am taking a pay-cut and he gets relatively more money than me. That idiot believed us and did all my work!! Stupid fellow.”
The image started getting blurred and came back. “You know, legally single mother is the term used for divorced or husband-dead ladies with children, unless they are unmarried and have adopted a child.”
“I do, but my stupid colleague did not” giggled Mrs Ana
“Do you justify what you did was correct? What would you have done if someone else had duped you like this?”
Mrs Ana was stern. “First, what I did was entirely wrong. Second, I would have kicked any person who would have done the same to me. After all this, I think I can still get away because I think I have killed my conscience. But the surprise is, why am I telling all the truth to you that I had hidden inside me all these while?”
The mirror image smiled. “Your first assumption is wrong. I AM your conscience. Second one is right. You can cheat the entire world but you cannot lie to your own conscience. The decision to make me reappear guilt-free or to make me vanish forever is left to you.”
The mirror image faded away leaving an awestruck Mrs Ana.
The above anecdote refers to all the black sheep who wish to outsmart their peers with the help of superiors who misplace the priorities. Work culture and ethics are relatively new terms in the western work-front, but are age-old in the Indian systems. There are numerous anecdotes in our epics and history on how an individual should work holding on to ethics and not cheating the final witness: the one’s own conscience. It is secondary whether such people get punished or get their due for wrong deeds in the outer world. It is probably more important to keep our own conscience free of guilt. The problem is in dealing with such people. They become a blemish and bane on the system. Such liabilities bring down the overall morale and work efficiency. When such characters go unpunished, they either simply spread the infection of indiscipline to others or make the honest workers rebel against the system. Once a critical number of such people are reached, the system collapses. It is for the people at power to decide whether such black sheep should be allowed to exist or perish in the system. Let us know how you deal with the “black-sheep” of your firm.
With this, let us get back to our regular feature: Interesting learning scenarios
A BANDED QUESTION
It is maintained that the best time for PA band in any infant with PAH for future single ventricle pathway is by 1 month. Although many surgeons would like to wait for some more time, the general opinion is for 1 month of age. Are there any studies which support this? What is the natural history of infants who were banded for future SV physiology between 1 month and 6 months of age? We often come across such children. One observation is the disparity in the mean PA pressure and ventricular EDP in such children. We generally get a bit liberal with mean PA pressures and plan a BD Glenn for them with the idea that the pressures may come down with the Glenn shunt. Few advocate tightening of PA further. What is the general consensus on this? Please send in your institution policies.
TAKAYASU DI(E)LEMMAS
It was a learning experience. We saw a 12-year-old girl about 3 months back. She had MVP with mild MR and trivial AR. The LV was disproportionately dilated. We did a detailed clinical examination and did not find any structural anomaly. The anemia was evident. Blood investigations showed anemia with dimorphic blood picture. We advised hematenics and follow up after 3 months to see the response. When she came for follow up, we could clearly see the clinical evidence of Takayasu arteritis. The disease process probably had shown some evidence of its presence, but we could not pick up at the inception. By the time we could pick up, the disease had shown its effects. Is there any way we could have diagnosed the problem at the beginning? Please let me know if you have found any methods.
SPINE Vs CEREBRUM
Continuing with the same issue, how effective are the interventions done in patients with Takayasu arteritis with activity in end stage? Although my seniors are optimistic, I am yet to come across any single kid with end stage Takayasu arteritis intervened and made it to another year. It is true that the morbidity comes down for few months, but the mortality factor does not seem to change much. Considering that isolated balloon dilatation is of limited value and cost of stents is usually not bearable by the poor family, it is largely an ethical question. One junior colleague of mine probably had a better expression: “We spend only spinal cord for managing any medical problem of a patient because we would have burned up our cerebral cortex for thinking the financial and social implications of the problem for the family!” Should there be a consensus for the limited finance set-ups for managing the problems whose outcomes are questionable? No one probably has enough time to think of how the family suffered to arrange the finances to treat a fatal condition with negligible outcome. The family would not have understood either the problem or the treatment, forget the chances of success. In a very high-volume centre, where is the time for one-to-one interaction? Such might be the problems of the third-world, but these are the issues which maintain us in the third-world!
BANDING THE HOMOGRAFT!
This one was a real test. We had a 7-year-old who underwent VSD closure with RV to PA homograft about 2 years back outside. Few small additional muscular VSDs were documented and were probably hoped to get spontaneously closed over time. The child was lost for follow up and presented to us one day with failure. The muscular VSDs appeared sizable. On cath, there was a significant step-up. However, the lesion was typically swiss cheesed and there was no single sizable lesion. Together, the hemodynamic effect was significant. How to handle such scenarios? The VSDs were so small that they could not be closed individually. Since it was a homograft, the option of PA band also did not exist. How to deal with such a scenario? Please let me know your options on this.
TERMINOLOGY
How would you classify tricuspid atresia in the setting of cTGA as per Kuhne’s?! The left sided TV would be atretic and the great arteries would be L malposed. Should we call it type 1 or type 3? Although many classifications are accepted for tricuspid atresia, the most used classification does not involve this scenario. Please let me know your take on it.
PEDIATRIC CARDIOLOGY PEARLS
56. In neonatal IE most cases occur in structurally normal hearts. Although relatively uncommon, increasing numbers of cases of neonatal IE have been reported since the 1970s. This reflects the increased use of prosthetic intravascular devices and more frequent insertion of long-term indwelling central venous catheters. (Ferrieri P, Gewitz MH et al: Unique features of infective endocarditis in childhood. Circulation 2002 page 2115)
57. Genetics in CHD have curious angle of research. Investigators from the Baltimore-Washington Infant Study analyzed the rate of precurrence – which is the number of currently affected relatives at the time of birth. These studies demonstrate substantial rates of familial disease and suggest that CHDs may not be as sporadic as once thought. (Boughman JA, Berg KA, Astemborski JA, et al. Familial risks of congenital heart defect assessed in a population-based epidemiologic study. Am J Med Genet 1987 page 839)
58. Although currently an unproven hypothesis, the potential neurodevelopmental advantage to be derived by the affected neonate who avoids acidemia may, in the long run, prove to be the most important long-term salutary effect of prenatal cardiac diagnosis. (Lavrijsen SW, et al. Severe umbilical cord acidemia and neurological outcome in preterm and full-term neonates. Biol Neonate 2005 page 27)
59. Two kinds of atrial receptors have been described. Type A receptors fire during atrial contraction and respond to changes in atrial pressure, and type B receptors fire during ventricular systole and respond to changes in atrial volume. Type A receptors stimulate and type B receptors inhibit sympathetic activity. These stretch receptors provide feedback to the hypothalamus and inhibit secretion of antidiuretic hormone called vasopressin (Little RC, Little WC. The output of the heart and its control. In: Physiology of the Heart and Circulation. Chicago: Year Book Medical, 1989 page 165)
60. The first reported case of autopsy-proven myocardial contusion was in 1764; it described a boy struck in the chest by a plate! (Akenside M. Account of blow upon heart and its effects. Philos Trans R Soc Lond Biol 1764 page 353)
With that, we come to the end of another post. Please let me know your opinions. Send in your comments and contributions to drkiranvs@gmail.com
Regards
Kiran
Mrs Ana was enjoying her new dress in the mirror. Her husband, Mr Mike had done the payment after much reluctance. “You must dress your age and profession. You work amongst the public; these are too loud” was his argument, but she would not listen.
Mrs Ana started combing her hair, but the image in the mirror did not! She was surprised. She started waving her hand frantically, but the mirror image stood still. She got afraid and wanted to scream, but the voice did not erupt off her throat.
“Cool down”, the mirror image told her. The reflection in the mirror seemed having its own movements. Mrs Ana had no choice but to listen.
“How are your days going?” the reflection asked her.
Mrs Ana hesitated, but told “Fine”. Surprisingly, the voice had become normal.
“You are spending pretty much time with me nowadays!” said the mirror image.
“Well, you see, I am senior in the office now. My husband has come back from his posting. I have some spare time and I am trying to catch up.”
The reflection did not appear impressed. “How about your colleagues and seniors in the office? Do they have equal spare time?”
“They don’t. They still work like mad. In fact the work has increased. I pressurized the boss to hire few juniors. I clearly told him I cannot work more.”
“How is your typical day?” the mirror still did not look impressed.
“I go at around 10 am. By then, my seniors would have done the apprentices’ training session. I hang around for an hour. Then I go to the office gym. Stay there for an hour and a half. Come back and work for an hour and I go to lunch. After an hour of lunch break, I tell the others that I have to go to bank. Spend another hour hanging around at various places. I come back to the workstation by 3.45PM. By 4, I tell them that I have to attend to my family and leave for the day.”
“Very interesting” said the image sordidly. “How about your seniors?”
“As I told you, they work like mad. They start at around 8.30 AM, train the apprentices, start the work, go on till 2 PM. After the lunch, they continue till 5 or 5.30 PM. Few go on till 7 PM also.”
“How do you escape so easily then?”
“You know my previous boss. She was from my own community. My husband was working outside and my kid was young. So, out of sympathy of being a single mother, she gave lot of relaxations to me. She also paid me extra money as my husband was not earning. Both of us together made one of my colleagues a jackass and made him do all my extra work. We kept telling him that I am taking a pay-cut and he gets relatively more money than me. That idiot believed us and did all my work!! Stupid fellow.”
The image started getting blurred and came back. “You know, legally single mother is the term used for divorced or husband-dead ladies with children, unless they are unmarried and have adopted a child.”
“I do, but my stupid colleague did not” giggled Mrs Ana
“Do you justify what you did was correct? What would you have done if someone else had duped you like this?”
Mrs Ana was stern. “First, what I did was entirely wrong. Second, I would have kicked any person who would have done the same to me. After all this, I think I can still get away because I think I have killed my conscience. But the surprise is, why am I telling all the truth to you that I had hidden inside me all these while?”
The mirror image smiled. “Your first assumption is wrong. I AM your conscience. Second one is right. You can cheat the entire world but you cannot lie to your own conscience. The decision to make me reappear guilt-free or to make me vanish forever is left to you.”
The mirror image faded away leaving an awestruck Mrs Ana.
The above anecdote refers to all the black sheep who wish to outsmart their peers with the help of superiors who misplace the priorities. Work culture and ethics are relatively new terms in the western work-front, but are age-old in the Indian systems. There are numerous anecdotes in our epics and history on how an individual should work holding on to ethics and not cheating the final witness: the one’s own conscience. It is secondary whether such people get punished or get their due for wrong deeds in the outer world. It is probably more important to keep our own conscience free of guilt. The problem is in dealing with such people. They become a blemish and bane on the system. Such liabilities bring down the overall morale and work efficiency. When such characters go unpunished, they either simply spread the infection of indiscipline to others or make the honest workers rebel against the system. Once a critical number of such people are reached, the system collapses. It is for the people at power to decide whether such black sheep should be allowed to exist or perish in the system. Let us know how you deal with the “black-sheep” of your firm.
With this, let us get back to our regular feature: Interesting learning scenarios
A BANDED QUESTION
It is maintained that the best time for PA band in any infant with PAH for future single ventricle pathway is by 1 month. Although many surgeons would like to wait for some more time, the general opinion is for 1 month of age. Are there any studies which support this? What is the natural history of infants who were banded for future SV physiology between 1 month and 6 months of age? We often come across such children. One observation is the disparity in the mean PA pressure and ventricular EDP in such children. We generally get a bit liberal with mean PA pressures and plan a BD Glenn for them with the idea that the pressures may come down with the Glenn shunt. Few advocate tightening of PA further. What is the general consensus on this? Please send in your institution policies.
TAKAYASU DI(E)LEMMAS
It was a learning experience. We saw a 12-year-old girl about 3 months back. She had MVP with mild MR and trivial AR. The LV was disproportionately dilated. We did a detailed clinical examination and did not find any structural anomaly. The anemia was evident. Blood investigations showed anemia with dimorphic blood picture. We advised hematenics and follow up after 3 months to see the response. When she came for follow up, we could clearly see the clinical evidence of Takayasu arteritis. The disease process probably had shown some evidence of its presence, but we could not pick up at the inception. By the time we could pick up, the disease had shown its effects. Is there any way we could have diagnosed the problem at the beginning? Please let me know if you have found any methods.
SPINE Vs CEREBRUM
Continuing with the same issue, how effective are the interventions done in patients with Takayasu arteritis with activity in end stage? Although my seniors are optimistic, I am yet to come across any single kid with end stage Takayasu arteritis intervened and made it to another year. It is true that the morbidity comes down for few months, but the mortality factor does not seem to change much. Considering that isolated balloon dilatation is of limited value and cost of stents is usually not bearable by the poor family, it is largely an ethical question. One junior colleague of mine probably had a better expression: “We spend only spinal cord for managing any medical problem of a patient because we would have burned up our cerebral cortex for thinking the financial and social implications of the problem for the family!” Should there be a consensus for the limited finance set-ups for managing the problems whose outcomes are questionable? No one probably has enough time to think of how the family suffered to arrange the finances to treat a fatal condition with negligible outcome. The family would not have understood either the problem or the treatment, forget the chances of success. In a very high-volume centre, where is the time for one-to-one interaction? Such might be the problems of the third-world, but these are the issues which maintain us in the third-world!
BANDING THE HOMOGRAFT!
This one was a real test. We had a 7-year-old who underwent VSD closure with RV to PA homograft about 2 years back outside. Few small additional muscular VSDs were documented and were probably hoped to get spontaneously closed over time. The child was lost for follow up and presented to us one day with failure. The muscular VSDs appeared sizable. On cath, there was a significant step-up. However, the lesion was typically swiss cheesed and there was no single sizable lesion. Together, the hemodynamic effect was significant. How to handle such scenarios? The VSDs were so small that they could not be closed individually. Since it was a homograft, the option of PA band also did not exist. How to deal with such a scenario? Please let me know your options on this.
TERMINOLOGY
How would you classify tricuspid atresia in the setting of cTGA as per Kuhne’s?! The left sided TV would be atretic and the great arteries would be L malposed. Should we call it type 1 or type 3? Although many classifications are accepted for tricuspid atresia, the most used classification does not involve this scenario. Please let me know your take on it.
PEDIATRIC CARDIOLOGY PEARLS
56. In neonatal IE most cases occur in structurally normal hearts. Although relatively uncommon, increasing numbers of cases of neonatal IE have been reported since the 1970s. This reflects the increased use of prosthetic intravascular devices and more frequent insertion of long-term indwelling central venous catheters. (Ferrieri P, Gewitz MH et al: Unique features of infective endocarditis in childhood. Circulation 2002 page 2115)
57. Genetics in CHD have curious angle of research. Investigators from the Baltimore-Washington Infant Study analyzed the rate of precurrence – which is the number of currently affected relatives at the time of birth. These studies demonstrate substantial rates of familial disease and suggest that CHDs may not be as sporadic as once thought. (Boughman JA, Berg KA, Astemborski JA, et al. Familial risks of congenital heart defect assessed in a population-based epidemiologic study. Am J Med Genet 1987 page 839)
58. Although currently an unproven hypothesis, the potential neurodevelopmental advantage to be derived by the affected neonate who avoids acidemia may, in the long run, prove to be the most important long-term salutary effect of prenatal cardiac diagnosis. (Lavrijsen SW, et al. Severe umbilical cord acidemia and neurological outcome in preterm and full-term neonates. Biol Neonate 2005 page 27)
59. Two kinds of atrial receptors have been described. Type A receptors fire during atrial contraction and respond to changes in atrial pressure, and type B receptors fire during ventricular systole and respond to changes in atrial volume. Type A receptors stimulate and type B receptors inhibit sympathetic activity. These stretch receptors provide feedback to the hypothalamus and inhibit secretion of antidiuretic hormone called vasopressin (Little RC, Little WC. The output of the heart and its control. In: Physiology of the Heart and Circulation. Chicago: Year Book Medical, 1989 page 165)
60. The first reported case of autopsy-proven myocardial contusion was in 1764; it described a boy struck in the chest by a plate! (Akenside M. Account of blow upon heart and its effects. Philos Trans R Soc Lond Biol 1764 page 353)
With that, we come to the end of another post. Please let me know your opinions. Send in your comments and contributions to drkiranvs@gmail.com
Regards
Kiran
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