This is Dr Kiran welcoming everyone to the new post. My last post did get me few responses: One of the doctors who read it commented on some of the practical patient management techniques he has been following for past few years. One of which was the use of frozen betadine! He freezes betadine solution in the freezer into small cubes. He uses those cubes to sterilize and prepare the skin before IM injection. The temperature numbs the skin and betadine provides the antisepsis. He says that none of his patients have ever complained of injection pain and no incidence of any injection abscess in the last 25 years! In fact, he claims that he is famous as “Painless injection doctor” in the locality.
“Not everything in medicine needs to be FDA approved” was what Dr Passi had written in his article. It is indeed true. We can innovate; we can change things for better and simple. The above example of using antisepsis is inspiring. I don’t know how many doctors are using the same technique, but I heard this for the first time. Please send me the details of any innovations that you are doing. Let us share them with the readership.
With this, let us start our anecdote. This was sent by a friend and I have retained his own style of narration. Please read this and discuss amongst your colleagues:
Mrs Fragrance was exposed to bright light, but her eyes were comfortable. She did not know where she was, for all that she could see was just bright light.
“Welcome Mrs Fragrance” said a deep, baritone and pleasant voice.
Mrs Fragrance could just hear the voice. The light was so bright that nothing else was seen.
“Where am I? Who are you?” Mrs Fragrance asked in a scared voice.
“You are at the court. This place decides your next journey. It can be the heaven or the hell” said the baritone.
“You mean, I am dead?”
“No conclusions at this place. You are at junction of unknown and uncertainty. Please answer some questions. It will be over soon.”
“OK”, Mrs Fragrance was uncertain.
“You can tell something about yourself.”
“I was working as a school teacher; I taught 4th standard students. I was very pious and God-fearing. I have lived a good life.”
“What subjects were you teaching?” asked the Baritone.
“I was supposed to teach them all subjects – like mathematics, science, history and so on. But everyday, I taught them ‘Jack and Jill’, ‘Twinkle-twinkle’ and ‘Johnny, Johnny’”
“Only those rhymes instead of all the subjects you mentioned to 4th standard students? Don’t they need better quality than that? It never occurred to you that 4th standards do not need ‘Jack and Jill’ anymore?”
“I did my best. I worked very hard to teach them the rhymes because I could not do any better. Coming to all the other harder subjects, I used to make the trainee teachers working in other departments do those difficult jobs.”
“Was it the duty of trainee teachers to do all these?” asked the surprised baritone.
“No; it was not. In fact, it was very hard for them to do my work. Still, I made them do it. I was very close to the head-mistress. I used that influence to get those trainees do my work. Since the trainees were afraid of head-mistress, they used to do it without much resistance.”
“Why did you not hire a junior teacher to do your work?”
“I could have. But, I wanted to show the administration that I was doing all the work. More so, hiring a subordinate would be sharing my income. I wanted all the profit for myself. Since, the head-mistress was close to me, I could do all this. By the time the head-mistress retired, the trainees had no idea that they were actually doing my job and did everything silently thinking that it is their work.”
“You never felt you were performing sub-optimal?” asked the still surprised baritone.
“I always did my best. I spent hours together in teaching ‘Jack and Jill’, ‘Twinkle-twinkle’ and ‘Johnny, Johnny’ to all the 4th standard students over years. You know how sharp these kids are. They refused to learn those old rhymes and few even demanded learning other subjects. I scolded them nicely and forced them to learn what I knew the best. But, some of my colleagues had objection. They felt that my teaching is inferior and referred few kids to other teachers. But, I brought this to the notice of head-mistress and penalized those stupid colleagues.”
“Mrs. Fragrance,” said the baritone. “Let me get it correct. You were supposed to teach normal 4th standard students and all that you taught them was ‘Jack and Jill’, ‘Twinkle-twinkle’ and ‘Johnny, Johnny’. You made poor trainee teachers who did not even belong to your department do all the hard work that was supposedly yours. You used the influence of your head-mistress in the entire wrong doing. Throughout your life, you have never kept the standards. Still, you convinced the management that you are doing all the work. You made all the money without even hiring an able subordinate. Some unlucky trainees were always there to do your work at the cost of their learning. You still think that you were hard working and deserved all the good things that happened to you all this time. Am I right?”
“Yes” said Mrs Fragrance. “Even though many in my own department used to joke, I was very honest in teaching ‘Jack and Jill’, ‘Twinkle-twinkle’ and ‘Johnny, Johnny’ to all the higher class students. I think I have done my job the best way. More so, I always attended churches. I used to apply leave or just scoot out of the job during working hours to attend the prayers and as many places of worship as possible. I must have attended more churches than any other person in my city! I was always pious and God-fearing.”
“Who would see your regular school work on all those days when you attended the places of worship?”
“The trainees. I used my influence with the head-mistress to make the trainees do my regular work. In fact, in my absence, they used to do all my work and the management was not even aware of my absence. I was paid even for my absence. Good terms with head-mistress are very important.”
“Final question, Mrs Fragrance” the baritone said. “Do you think you deserve heaven or hell?”
“Definitely heaven. I have sincerely taught nursery rhymes to 4th standard students with best of my ability. I have attended all possible places of worship, even at the cost of my own work and by applying as many legal and illegal leaves as possible. My head-mistress always felt that I was very good. I should not go anywhere other than heaven.”
The baritone started laughing. The laugh grew so loud that it filled the place more than the light. Mrs Fragrance started feeling a bit uncomfortable and …….
……she opened her eyes to the reality.
The above anecdote is written by one of my close friends who got inspired by the previous anecdotes I have been posting in this blog. He is a dedicated pediatrician working in a government hospital. He was expressing his concern about the poor quality of people working with him and how they were misutilising the system by the aid of their contacts with higher up officials. I encouraged him to write a story and he did. It is his first attempt and he seems to have done a good job! The point is, these underperformers exist in every system. Most of such people make themselves a liability for others. They are tolerated either due to fear of their contacts, for respect of harmony in workplace, by exploiting junior people to compensate for their laziness. Such black sheep shamelessly celebrate their mediocrity to pain the rest. One of the highly revered vice-chancellors of Bangalore University, Dr HN told once: “There are 2 classes of people; those who work and those who take the credit for the work! The battle in the second category is fierce. One would do very well in the first category.” Is there any example of how such people were set right? If anyone knows the tactics, please enlighten our readership!
With that, let us get back to the regular feature: Interesting learning scenarios:
A TETHERED QUESTION
We saw a 5-year-old with tethered STL of tricuspid valve. The origin appeared to be from the crux, but the STL effectively started off from 18mm from crux. Till that point, it was finely tethered, which could be made out on a high resolution with zooming. Surprisingly, the ATL was sail like. In a case of isolated tethered TV, does ATL also get involved? Is the ATL involvement a corroborative evidence of Ebstein’s anomaly? Please let me know your ideas about it.
VOLUMES, VOLUMES
It is always maintained that the saturations are not the criterion for BD Glenn shunt. The criterion should be the volume reduction. Hence, even when the baby with single ventricle physiology is saturating more than 90%, it may still be prudent to go ahead with BD Glenn even at the cost of some desaturation. If this is the case, why is SO2 taken as a criterion for Fontan completion? In India atleast, there is lot of resistance for Fontan completion. It is always maintained that the patient should earn Fontan completion than it is being given. SO2 plays a major role in pushing the surgeon for Fontan completion. Should we not have same criteria for BD Glenn and Fontan completion? Are the complexity and the presumed Risk/Benefit ratio the hitch for Fontan completion? Are we still at the learning curve for Fontan? Let me have your opinions on this issue.
COLLATERALS IN EISENMENGARIZATION
We had an interesting scenario for discussion. A middle aged male came with TGA, VSD, PAH. He was Eisenmengarized by opinion and natural history. However, his presenting complaint was hemoptysis. He had bouts of blood being coughed out. Cath study showed multiple collaterals. The pertinent question was: Is collateral formation possible in Eisenmengarised patient? The opinions were divided. Few were categorical that the collateral and Eisenmenger do not go together. Few had an opinion that not all the lobules of lung are equally Eisenmengered and those which are affected less might have developed the collaterals. Few felt that the pathology was different from Eisenmenger and should be evaluated, as proving Eisenmenger in this anatomy was not possible. Cardiac CT led to more complexity, as it gave a DD of sequestration too! However, sticking to the basic question, please send me your ideas on the combination of Eisenmenger and collateral formation. What is your opinion? Do you have a separate analogy or do you agree with one of the explanations offered by our team? Please let me know.
TWO POSSIBILITIES
What do you think is the suitable cut off age for a two-stage arterial switch surgery in those infants who come a bit late? We had a 2-month-old with dTGA, PFO and regressed LV. The option of 2 stage arterial switch is always there. Our surgical team is divided in opinion. One senior surgeon believes that the 2 stage arterial switch is a futile exercise and has not shown benefit in long run. He feels that the Senning palliation would be much superior to the hurried 2 stage ASO. The other senior surgeon has opposite opinion and prefers 2 stage ASO to Senning anytime. What is the opinion of the readership? Please let me know how you have been handling such scenarios.
CORONARIES FOR RESCUE
It is a rare thing for the pediatric cardiologist to chase the coronaries fervently. Barring the cases of tetralogy, TGA, Pre-Ross assessment, ALCAPA, Kawasaki and few more, the coronaries are not the area of interest. It so happened that coronaries came to the rescue. We saw a baby with VSD with two great vessels, one of which was hypoplastic. The orientation of posterior great vessel was towards left. The anterior vessel was hypoplastic with a gradient of 70mmHg. The arch vessels could not be visualized. The PA confluence was absent. We could not see the LPA. Supply to the right lung appeared to be from few AP collaterals. The arch appeared to be right sided with a right PDA. Overall, the picture of anatomy distal to semilunar valves was totally unclear. The differentiation of PA from aorta was largely dependent on the coronaries. We ended up chasing the coronaries to determine the great vessels, keeping the possibility of ALCAPA aside! If you were made to chase the coronaries as fervently as we did, please let me know the reason.
PEDIATRIC CARDIOLOGY PEARLS
51. The echocardiographic findings in boys with Duchenne muscular dystrophy correlate with the autopsy findings of posterior epicardial thinning leading to ultimate dilated cardiomyopathy. Studies have showed thinner left ventricular posterior walls, especially behind the posterior mitral valve leaflet, diastolic dysfunction, contraction abnormalities that progressed inferiorly, and temporally progressive wall thinning. (Goldberg SJ, Feldman L, Reinecke C, et al. Echocardiographic determination of contraction and relaxation measurements of the left ventricular wall in normal subjects and patients with muscular dystrophy. Circulation 1980 page 1061)
52. High-dose IVIG has been shown in many clinical trials to reduce the incidence of coronary aneurysms to <5% when administered for 7 to 10 days of the disease onset. (Newburger JW, Takahashi M, Beiser AS, et al. A single intravenous infusion of gamma globulin as compared with four infusions in the treatment of acute Kawasaki syndrome. N Engl J Med 1991 page 1633)
53. Administration of antibiotics during an episode of RF does not alter the course or severity of cardiac involvement. (Tompkins DG, Boxerbaum B, Liebman J. Long-term prognosis of rheumatic fever patients receiving regular intramuscular benzathine penicillin. Circulation 1972 page 543)
54. The most common cardiac manifestation of Juvenile Rheumatoid Arthritis is pericarditis. (Gedalia A, Giannini EH, Brewer EJ, et al. Prevalence of pericardial effusion by echocardiography in juvenile rheumatoid arthritis. J Rheumatol 1993 page 206)
55. Pericardial effusion has been reported in as many as 25% of patients infected with the HIV virus; however, large effusions are rare. (Starc TJ, Lipschultz SE, Kaplan S, et al. Cardiac complications in children with human immunodeficiency virus infection. Pediatrics 1999 page 14)
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.
Regards
Kiran
ಶನಿವಾರ, ಜುಲೈ 17, 2010
ಶುಕ್ರವಾರ, ಜುಲೈ 9, 2010
Dr Kiran welcoming everyone to the present post
This time, I am not writing any story or scenario.
I happened to read something about the creativity and medical education recently and got pained a lot.
Just sharing my feelings with the readership. Please comment. Use the comments box or my email drkiranvs@gmail.com
Please go through and discuss:
MEDICAL FEST A.L.A. IIT FESTS
“Give them any challenge and they are ready to do it” was the compliment given by my erstwhile Boss. She was talking of the IT professionals she has hired for her new IT venture. The glow and pride in her eyes was very evident. “They are too good. There is something in them that is not in….” the continuity was lost as if something stuck and topic was deliberately shifted to something else. I did not miss the point. I could complete the half done sentence. We are trying to dodge the unpleasant and that is not the way life goes.
Yes, it is true that the creative energies of everyone in the world is appreciated other than doctors. In the recent issue of Indian Pediatrics, Dr Gauri Rao Passi had rightly pointed one thing. He was talking of the IIT fest and all the new ideas that got a material form and displayed with pride in the fest. It stood as the testimony of the creative and lateral thinking of the bright student community of future engineers. In entire lifetime, can anyone recall a similar medical fest? All the non-academic happenings of medical college are limited to a cultural event with Anthaksharis ruling the roost.
Where exactly the things went wrong? Till 12th std, all the students of science stream go through the same process of learning. By and large, best of these brains enter the medical field. (It was atleast true till the IT boom) After that? We see the engineering students creating their own satellite launched by ISRO, we see the law students representing the country in international law fests, we see the architecture students winning applauds in international forums for their creative designs and so on. What about medical students? The maximum I can recall any medical student achieving is a prize in an essay writing competition. What happened to those “Best of brains”?
Have you ever been encouraged to do some lateral thinking during your basic MBBS training? Were you ever confident of uttering a novel idea that might have come to your mind? Did you anytime feel some lacuna in the medical curriculum and wanted to desperately modify something? How many times could you do all these in a state of fearlessness?
There are lots of reasons for a decline in the creative thinking in medical student community. Lot of it is realized only on a retrospect. The teachers who teach the basic medical sciences are usually discarded ones. Most of them chose to stick to basic sciences because they did not get a clinical subject for their post-graduation. Their frustration is usually evident. I have seen PGs of basic sciences who tried yearly PG entrance exam throughout their 3 year PG course in the hope of getting a “better subject”. They never concentrated enough on their own subject during the most important formative years of their post-graduation. How would you expect such people to become good and inspiring teachers for the younger lot?
In the paramedical field, the good brains usually have a “good” attachment! A really good pathologist or microbiologist would concentrate more on developing their lab practice than teaching. But, the relative numbers of “better” people are certainly higher than in basic sciences.
By the time a student of MBBS reached the final year, the phobia of exams would surround to such an extent that it is blasphemous to think of anything other than the text book. Although really inspiring teachers may exist, the vision of a final year medical student fails to acknowledge it. For most of the students, a mediocre teacher who can consistently rant out the “Exam questions” or “Viva questions” is a bigger hero than the person who can teach with a systematic and scientific methodology.
In the entire period of MBBS, almost every student finds it difficult to accommodate to the consistently changing subjects, curriculum, teaching, preparation for didactic sessions, written and photocopied “notes” and so on. There is practically no one to encourage the creative thinking. By the time students reach a teacher with a creative bent, their mould would not let them move out of the self/system created boundaries.
Examination in the Indian medical education is no less than a horror. It is time for the students to recall how good or bad they were! It is time for the examiners to take revenge or reward the loyalty. Money, influence, good behavior, non-controversial nature etc find a larger place than the actual talent of the candidate. Passing in the final exam is such a big relief even for a consistent hard worker who knew their stuff well. By this time, their lesser intelligent friend in any non-medical professional field would have got his degree and a handsome 6-digit salary and a vehicle.
MBBS marks the end of a beginning. The actual ordeal starts from now. People with enough money can buy any subject of their choice in a private medical college. What was earlier in lakhs has reached crores now. People with influence can get direct seats from the biggies. Next best would be getting question papers of entrance exams for a price. The nexus is strong and powerful and in India, it takes a CBI enquiry to break the code! The other way is to move through your caste. If anyone can prove that they belong to the caste that government considers as backward, irrespective of any other factor, position or assets, the PG seat belongs to them for free. I have personally seen PG students who obtained their seat by reservation coming to the hospital in a Mercedes. Added to this, the nexus of fake caste certificates is probably impossible for even CBI to crack!!
However, the lesser mortals with no money or influence or reservations will have to go through the hard way. They have to take a “break” of couple of years in prime of their life after MBBS to “prepare” for the PG entrance exams. In this period, one has to sustain on the income of their parents or should do very low paying jobs of a “duty doctor”, which is actually a glorified clerkship in a private hospital. They fill exam forms of almost all entrance exams of the country, travel to the exam centre by a third class sleeper coach (which the Indian railways call second class), stay in cheapest of places to save money, eat roadside as they cannot afford high prices of restaurants and write exams for a handful of PG seats. The competition would be something like 700 doctors for each PG seat! With every successive year’s failure, the potential competition increases, as a new batch of MBBS pass outs would have arrived.
With all these difficulties, few get successful in acquiring a PG seat. Most of the doctors would not achieve the subject they always liked and loved. They end up in such a state that they would take the course which they detested from their core! Still, the life should go on. How long can you feed yourself with the parental earnings? How long would you keep answering the relatives who were jealous of your academic success few years back, but are very happy with you now that you are struggling and their otherwise low-performer son is earning 5-digits a month in a call centre or an IT company? It is time to prove. Success comes with hard work in any field. The PG subject you are studying does not matter as long as you are hard working!!
Right? Yeah! Life is smooth once you have got a PG seat? Yeah! Lot of things change in just 3 months. Bright MBBS doctors are made to feel that they are actually duffers. The first years get to do a peon’s job. They run around to collect the lab investigation reports, chest radiography films, arrange the glass vials for blood samples, store the blood and urine culture bottles in their cupboards for emergency use, make a note of all new instructions given by the bosses, request the proud class III and IV workers for shifting the patients to investigation rooms and so on. “Look at the cobweb in that corner of the ward. You people don’t work!” is the remark that I have personally got from my consultant during rounds in my first year of post graduation course.
Thesis is a source of pain for most of the PG students. Not only the process of conceiving and delivering it is tedious, bearing the idiosyncrasies of the “guide” is hellish. For the people who believe in reincarnation, all the good deeds done in the previous birth manifests as a good PG guide and vice-versa! I had the opportunity of seeing the brutalities in first hand. I know some of my colleagues, who were used by the “guide” to get vegetables for the house, drop his kids to the school, make the PG drop guide’s niece in scooter to her work place and get her back in the evening every day, wash his car and get it serviced, book his air tickets at the cost of PG and so on. It is not necessary to say that all the academic work of the guide is actually done by the PG, whether it is preparing slides for a class or writing a chapter for the text book or publishing a study. Should I mention that the PG gets no credit or authorship or acknowledgement for the work? Worse are the cases that I have heard, in which the female PGs have undergone more inhumane treatment and exploitation. With all this, the moment of getting the thesis signed by the “guide” goes through many more phases of torture and is a relieving moment at the end of it.
Where is the creative energy that was bestowed to everyone? Why our medical education system does systematically suppresses the creative thinking? Why is a person who attempts to talk out of the box is treated as a joker? Why do we behave as if we should not think outside the textbooks? The archival system of teaching medicine, inept or inert teachers, lack of opportunity for expressions, fear of getting jeered by the peer group and so many other issues end up in suppressing the ideas and creativity of every medical student. Our conventional upbringing does not allow most of us to rebel against the set norms.
I discussed this issue with some of the peers. “You cannot crib that someone’s wife is more beautiful”, “We are dealing with human lives; we cannot afford to experiment”, “Mere talk is waste; who is going to find a solution?” “All that you feel is right. But the remedy does not lie in the hands of a single person”, “You are burning from inside; you need vipasyana meditation to cool yourself” were some of the answers I got.
Why do we think of an improbable end point and stop a beginning? Who is asking anyone to radically change the treatments? There are so many innovations that can occur in teaching, learning, patient examination techniques, diagnostics, assessment pattern and so on. Why not involve student community in these? Just to suggest, why can’t we dedicate one hour every week for listening to the students? Why not a session for them to talk in an open forum to present their ideas on innovation? If someone is shy of presenting himself on the podium, why not keep a box in which he can drop his idea in writing, which can go through a set of understanding and sympathetic senior doctors? In every institute, there are few extra-ordinary and respected, out-of-the-box thinking doctors. Why not they form a group and encourage the student community in catering a creative angle to thinking? Once we dare to change a bit, we can think of changing this ignoble way of conducting our curriculum and assessment patterns.
There might be lot many ways of inculcating the innovation and creativity of the budding doctors during their formative years. “I was treated badly by my guide and now it is my turn to be bad with my students” is the hallmark of a wretched brain. How can such people make good doctors when they are not even good human beings? Isn’t there a need for changing this system somewhere? Till we think of solving these issues, we cannot think of medical fests with new ideas coming from “best of the brains” in the community.
Regards
Kiran
This time, I am not writing any story or scenario.
I happened to read something about the creativity and medical education recently and got pained a lot.
Just sharing my feelings with the readership. Please comment. Use the comments box or my email drkiranvs@gmail.com
Please go through and discuss:
MEDICAL FEST A.L.A. IIT FESTS
“Give them any challenge and they are ready to do it” was the compliment given by my erstwhile Boss. She was talking of the IT professionals she has hired for her new IT venture. The glow and pride in her eyes was very evident. “They are too good. There is something in them that is not in….” the continuity was lost as if something stuck and topic was deliberately shifted to something else. I did not miss the point. I could complete the half done sentence. We are trying to dodge the unpleasant and that is not the way life goes.
Yes, it is true that the creative energies of everyone in the world is appreciated other than doctors. In the recent issue of Indian Pediatrics, Dr Gauri Rao Passi had rightly pointed one thing. He was talking of the IIT fest and all the new ideas that got a material form and displayed with pride in the fest. It stood as the testimony of the creative and lateral thinking of the bright student community of future engineers. In entire lifetime, can anyone recall a similar medical fest? All the non-academic happenings of medical college are limited to a cultural event with Anthaksharis ruling the roost.
Where exactly the things went wrong? Till 12th std, all the students of science stream go through the same process of learning. By and large, best of these brains enter the medical field. (It was atleast true till the IT boom) After that? We see the engineering students creating their own satellite launched by ISRO, we see the law students representing the country in international law fests, we see the architecture students winning applauds in international forums for their creative designs and so on. What about medical students? The maximum I can recall any medical student achieving is a prize in an essay writing competition. What happened to those “Best of brains”?
Have you ever been encouraged to do some lateral thinking during your basic MBBS training? Were you ever confident of uttering a novel idea that might have come to your mind? Did you anytime feel some lacuna in the medical curriculum and wanted to desperately modify something? How many times could you do all these in a state of fearlessness?
There are lots of reasons for a decline in the creative thinking in medical student community. Lot of it is realized only on a retrospect. The teachers who teach the basic medical sciences are usually discarded ones. Most of them chose to stick to basic sciences because they did not get a clinical subject for their post-graduation. Their frustration is usually evident. I have seen PGs of basic sciences who tried yearly PG entrance exam throughout their 3 year PG course in the hope of getting a “better subject”. They never concentrated enough on their own subject during the most important formative years of their post-graduation. How would you expect such people to become good and inspiring teachers for the younger lot?
In the paramedical field, the good brains usually have a “good” attachment! A really good pathologist or microbiologist would concentrate more on developing their lab practice than teaching. But, the relative numbers of “better” people are certainly higher than in basic sciences.
By the time a student of MBBS reached the final year, the phobia of exams would surround to such an extent that it is blasphemous to think of anything other than the text book. Although really inspiring teachers may exist, the vision of a final year medical student fails to acknowledge it. For most of the students, a mediocre teacher who can consistently rant out the “Exam questions” or “Viva questions” is a bigger hero than the person who can teach with a systematic and scientific methodology.
In the entire period of MBBS, almost every student finds it difficult to accommodate to the consistently changing subjects, curriculum, teaching, preparation for didactic sessions, written and photocopied “notes” and so on. There is practically no one to encourage the creative thinking. By the time students reach a teacher with a creative bent, their mould would not let them move out of the self/system created boundaries.
Examination in the Indian medical education is no less than a horror. It is time for the students to recall how good or bad they were! It is time for the examiners to take revenge or reward the loyalty. Money, influence, good behavior, non-controversial nature etc find a larger place than the actual talent of the candidate. Passing in the final exam is such a big relief even for a consistent hard worker who knew their stuff well. By this time, their lesser intelligent friend in any non-medical professional field would have got his degree and a handsome 6-digit salary and a vehicle.
MBBS marks the end of a beginning. The actual ordeal starts from now. People with enough money can buy any subject of their choice in a private medical college. What was earlier in lakhs has reached crores now. People with influence can get direct seats from the biggies. Next best would be getting question papers of entrance exams for a price. The nexus is strong and powerful and in India, it takes a CBI enquiry to break the code! The other way is to move through your caste. If anyone can prove that they belong to the caste that government considers as backward, irrespective of any other factor, position or assets, the PG seat belongs to them for free. I have personally seen PG students who obtained their seat by reservation coming to the hospital in a Mercedes. Added to this, the nexus of fake caste certificates is probably impossible for even CBI to crack!!
However, the lesser mortals with no money or influence or reservations will have to go through the hard way. They have to take a “break” of couple of years in prime of their life after MBBS to “prepare” for the PG entrance exams. In this period, one has to sustain on the income of their parents or should do very low paying jobs of a “duty doctor”, which is actually a glorified clerkship in a private hospital. They fill exam forms of almost all entrance exams of the country, travel to the exam centre by a third class sleeper coach (which the Indian railways call second class), stay in cheapest of places to save money, eat roadside as they cannot afford high prices of restaurants and write exams for a handful of PG seats. The competition would be something like 700 doctors for each PG seat! With every successive year’s failure, the potential competition increases, as a new batch of MBBS pass outs would have arrived.
With all these difficulties, few get successful in acquiring a PG seat. Most of the doctors would not achieve the subject they always liked and loved. They end up in such a state that they would take the course which they detested from their core! Still, the life should go on. How long can you feed yourself with the parental earnings? How long would you keep answering the relatives who were jealous of your academic success few years back, but are very happy with you now that you are struggling and their otherwise low-performer son is earning 5-digits a month in a call centre or an IT company? It is time to prove. Success comes with hard work in any field. The PG subject you are studying does not matter as long as you are hard working!!
Right? Yeah! Life is smooth once you have got a PG seat? Yeah! Lot of things change in just 3 months. Bright MBBS doctors are made to feel that they are actually duffers. The first years get to do a peon’s job. They run around to collect the lab investigation reports, chest radiography films, arrange the glass vials for blood samples, store the blood and urine culture bottles in their cupboards for emergency use, make a note of all new instructions given by the bosses, request the proud class III and IV workers for shifting the patients to investigation rooms and so on. “Look at the cobweb in that corner of the ward. You people don’t work!” is the remark that I have personally got from my consultant during rounds in my first year of post graduation course.
Thesis is a source of pain for most of the PG students. Not only the process of conceiving and delivering it is tedious, bearing the idiosyncrasies of the “guide” is hellish. For the people who believe in reincarnation, all the good deeds done in the previous birth manifests as a good PG guide and vice-versa! I had the opportunity of seeing the brutalities in first hand. I know some of my colleagues, who were used by the “guide” to get vegetables for the house, drop his kids to the school, make the PG drop guide’s niece in scooter to her work place and get her back in the evening every day, wash his car and get it serviced, book his air tickets at the cost of PG and so on. It is not necessary to say that all the academic work of the guide is actually done by the PG, whether it is preparing slides for a class or writing a chapter for the text book or publishing a study. Should I mention that the PG gets no credit or authorship or acknowledgement for the work? Worse are the cases that I have heard, in which the female PGs have undergone more inhumane treatment and exploitation. With all this, the moment of getting the thesis signed by the “guide” goes through many more phases of torture and is a relieving moment at the end of it.
Where is the creative energy that was bestowed to everyone? Why our medical education system does systematically suppresses the creative thinking? Why is a person who attempts to talk out of the box is treated as a joker? Why do we behave as if we should not think outside the textbooks? The archival system of teaching medicine, inept or inert teachers, lack of opportunity for expressions, fear of getting jeered by the peer group and so many other issues end up in suppressing the ideas and creativity of every medical student. Our conventional upbringing does not allow most of us to rebel against the set norms.
I discussed this issue with some of the peers. “You cannot crib that someone’s wife is more beautiful”, “We are dealing with human lives; we cannot afford to experiment”, “Mere talk is waste; who is going to find a solution?” “All that you feel is right. But the remedy does not lie in the hands of a single person”, “You are burning from inside; you need vipasyana meditation to cool yourself” were some of the answers I got.
Why do we think of an improbable end point and stop a beginning? Who is asking anyone to radically change the treatments? There are so many innovations that can occur in teaching, learning, patient examination techniques, diagnostics, assessment pattern and so on. Why not involve student community in these? Just to suggest, why can’t we dedicate one hour every week for listening to the students? Why not a session for them to talk in an open forum to present their ideas on innovation? If someone is shy of presenting himself on the podium, why not keep a box in which he can drop his idea in writing, which can go through a set of understanding and sympathetic senior doctors? In every institute, there are few extra-ordinary and respected, out-of-the-box thinking doctors. Why not they form a group and encourage the student community in catering a creative angle to thinking? Once we dare to change a bit, we can think of changing this ignoble way of conducting our curriculum and assessment patterns.
There might be lot many ways of inculcating the innovation and creativity of the budding doctors during their formative years. “I was treated badly by my guide and now it is my turn to be bad with my students” is the hallmark of a wretched brain. How can such people make good doctors when they are not even good human beings? Isn’t there a need for changing this system somewhere? Till we think of solving these issues, we cannot think of medical fests with new ideas coming from “best of the brains” in the community.
Regards
Kiran
ಸೋಮವಾರ, ಜುಲೈ 5, 2010
This is Dr Kiran welcoming everyone to the new post of the blog. As we have seen, the primary objective of this blog is dissemination of genuine interest in Pediatric cardiology to all those who have got smitten by this charming bug! I had the opportunity of writing a lot of historical details about the subject and drugs used in this field. For the past few weeks, I have been writing a few short anecdotes which may touch the readers somewhere and may bring back some memories. None of these stories are my own. Most of them are heard, read or sent by the friends. It may seem personal if there is lot of relevance, but that is purely coincidental! With this disclaimer, I am moving on to the following anecdote which was sent by a friend. He did not specify if it is his own. But, the quality of story was worth sharing. Please go through:
Ram was 14 years old. His adolescence was more visible on his recent “don’t care” attitude. He was fond of science classes in the school and was quite good at it. He would often tease his father with the question, “Dad, what is relativity?” His accountant father was probably unaware of who Einstein was! Father used to just smile and keep quiet.
A new circus company had campaigned in their town. Ram wanted to see the circus. It was almost the month-end and his dad did not have spare cash for the new expense. Somehow, after taking a hand-lone from a colleague in the office, the father-son duo went for the show.
They were standing in the queue. A parallel lane was buying tickets from another counter. There was one group in the parallel lane. It was a big group with eight children, all under the age of 12. Ram felt that they didn't have much money. Their clothes were frayed but clean, and the children were well-behaved all of them standing in line, two-by-two holding hands in back of the man who had brought the kids. They were jabbering about the clowns, elephants and other acts they would see that evening. Ram, who had gone to a circus a couple of years back, could sense those kids had never been to the circus before. That evening looked like a highlight of those young lives.
Ram and his dad were behind a couple of people in the line when the children’s group reached the counter. “One full and eight half tickets, please” the man said. The lady in the counter told the amount. The man opened few notes of currency from his pocket and counted. His face fell sad. He counted the money again. “How much did you say the amount was?” he asked the counter lady again. He was turning pale with the answer.
Ram and his father were witnessing the scene. Suddenly, Ram’s dad pulled up a note of Rs 100, dropped it on ground and told the man in the opposite lane: “Sir, you have dropped this note. It fell from your pocket.”
The man looked at Ram’s father. His eyes were filling with tears. He meekly accepted the note and bought the tickets. He came towards Ram, held the hands of his father and told in a choked voice, “I don’t know how to thank you. These are the children from the neighboring orphanage. What the donors pay is just enough for food and clothes. They were dreaming day and night about the circus. As their caretaker, I could not resist bringing them here. I got some of my money and asked for some from my friends. Still, I fell short of some. Bless you, Sir; can’t repay your kindness.”
When Ram reached the counter, they did not have enough money for the tickets. They just walked away from the counter. After few yards, Ram’s dad held hands of his son. “Can we just postpone our programme by a week?” he asked Ram.
“No problems, dad”, Ram said. “Three things, actually. First, I can wait for a week. Second, I can do without too; I have seen the circus earlier. Lastly, today you have taught me what relativity is!” Ram said with a glee in his face.
Ram had found a new meaning for life that day. Moreover, he decided never to tease his father again.
The above anecdote is quite touching, especially for people who empathise. The community of Doctors probably has highest chances for empathy. One of the doctor friends, who does community service told me about her experience with patients wherein she had to make decision for them imagining herself in their shoes! It is a tough experience. The relativity of the issue probably depends on how many tough situation we have passed through in our life. There is the story of a man who was cursing God for not having footwear till he saw a man without legs! The cursing suddenly got transformed to praise. The quantum paradigm shift in this instance is evident. Life is relative and the meek ones need to know this well before they decide on something drastic. Understanding who is right is probably not as important as what is right. This is the biggest aspect of effective leadership, management, parenting, teaching and coaching. It's amazing how much we can accomplish if we simply focus on leaving everyone we meet in better shape than we found them.
With this, let us get back to our regular feature: Interesting learning scenarios
RIGHT PARACHUTE
We can all recall a number of parachute mitral valves. When the papillary muscle of left ventricle is alone, the entire chordae end up getting inserted to the same site and the physical picture is of a parachute with the pointing end at pap muscle and the balloon at the annulus. This is possible for the mitral valve where the site of insertion is well defined. How about the tricuspid valve which sends its chordate over a wider area? We saw a 9-month-old with all the tricuspid chordae getting attached to a single pap muscle. On searching the literature, we found the existence of such an entity. Anderson et al had reported this in a setting of TGA and Aziz et al for TOF. In our case, it was a large VSD and a small ASD. If anyone has any data on this entity, please let us know.
ATRIAL OUTLETS
Another interesting variant of tricuspid valve was seen by us. We have seen a double orifice mitral valve. However, a double orifice tricuspid valve is a rare variant. We had such a scenario in a 6-month-old wherein the TV had two openings on either side of interventricular septum. This was associated with a large inlet VSD and a small RV. The entire MV and one opening of TV were to the MLV and the other opening of TV was to the small MRV. It was an eventual single pump repair. The literature shows the existence of this condition without any other heart lesions. If you can recall any instance of noticing such an anatomical variant, please put up your experience.
PARTIALLY TRANSITIONAL
What would you term a Transitional AV canal defect in which the VSD has closed by a septal pouch? What is the terminology to be used? It is taught that the inlet VSD does not close. However, we have often seen a small inlet VSD of transitional AV canal defect closing spontaneously over a period of time and becoming a partial AV canal defect. Should we continue to call it transitional or change to partial? Tell me your views.
RIMS AND LOCATION
Of late, we have been largely successful in eliminating the need of Transesophageal echocardiography for ASD device closures. Our transthoracic echos have been found sufficient for ASD devices. In this process, we often find that the IVC rims being unsteady. Many times, the defect is not visible at all when the IVC is opened in the subcostal saggital view or in the short axis view. In such cases, we have found a mixed success rate. Is there is fool-proof method in the TTE for this problem? How many centres have actually dropped the TEE for ASD device closures? What are the experiences in those places? Please let us know.
SIDE TO SIDE!
Continuing the problems with devices, we have seen few muscular VSDs which look perfectly OK for device closures during echo evaluation. However, on the table, the LV side of the defect would be much larger than the RV side. Not only crossing becomes a problem, the size of the device to be used is also an issue. Since the muscular VSD devices are symmetrical, the LV side of the device may be too small for the defect and the RV side may be correspondingly big. Our experience with the VSD devices is not as extensive as our PDA and ASD devices. How are the other centres managing this issue? Please let us know if there is a way.
PEDIATRIC CARDIOLOGY PEARLS:
46. Sildenafil seems to be beneficial in the management of Primary pulmonary hypertension. Acute vasoreactivity studies in PAH patients suggest that sildenafil may have greater acute hemodynamic effects than inhaled nitric oxide and may further reduce pulmonary vascular resistance. (Michelakis E, Tymchak W, Lien D, et al. Oral sildenafil compared with inhaled nitric oxide in PAH. Circulation. year 2002 page 2398)
47. AHA guidelines on IE prophylaxis extend to HCM. Bacterial endocarditis appears to be virtually confined to patients with the obstructive form of HCM, with a prevalence of <1%. Vegetations most commonly involve the anterior mitral leaflet or septal endocardium at the site of mitral valve - septal contact and less commonly the aortic valve. ( Spirito P, Rapezzi C, Bellone P, et al. Infective endocarditis in hypertrophic cardiomyopathy. A good review is done by authors. Circulation. year 1999 Page 2132)
48. Levosimendan is a calcium-sensitizing agent that has been evaluated in adults with acute decompensated heart failure and in patients with chronic heart failure. One pharmacokinetic study has been performed in children with congenital heart disease. There is no increase in myocardial oxygen consumption or arrhythmias. (Turanlahti M, Boldt T, Palkama T, et al. levosimendan in pediatric patients evaluated for cardiac surgery. Pediatr Crit Care Med. year 2004 page 457)
49. In cases of myocarditis with congestive heart failure, digitalis may be used and has effected dramatic improvement in many instances. However, during periods of acute inflammation, the myocardium may be hypersensitive to digitalis, so rapid administration to achieve therapeutic levels should be avoided. (Parrillo JE. Myocarditis: Good review article on treatment. J Heart Lung Transplant. year 1998 page 941)
50. In Pediatric restrictive cardiomyopathy, beta-blocker therapy was suggested to blunt rapid heart rates in their patient population in whom significant ST-segment depression was noted at higher heart rates. However, tolerating the therapy is the chief caveat. (Rivenes SM, Kearney DL, Smith EO, et al. Sudden death and cardiovascular collapse in children with restrictive cardiomyopathy. Circulation. year 2000 page 876)
With that, we come to the end of another post. Please send your views, opinions, criticisms either by the comments box or by email to drkiranvs@gmail.com I shall post them on your behalf. I am preparing the list of books about which I can talk in next few posts. Till then, I shall continue with the anecdotes. If you have any interesting short stories to share, please mail them to me. Your contribution would be acknowledged.
Regards
Kiran
Ram was 14 years old. His adolescence was more visible on his recent “don’t care” attitude. He was fond of science classes in the school and was quite good at it. He would often tease his father with the question, “Dad, what is relativity?” His accountant father was probably unaware of who Einstein was! Father used to just smile and keep quiet.
A new circus company had campaigned in their town. Ram wanted to see the circus. It was almost the month-end and his dad did not have spare cash for the new expense. Somehow, after taking a hand-lone from a colleague in the office, the father-son duo went for the show.
They were standing in the queue. A parallel lane was buying tickets from another counter. There was one group in the parallel lane. It was a big group with eight children, all under the age of 12. Ram felt that they didn't have much money. Their clothes were frayed but clean, and the children were well-behaved all of them standing in line, two-by-two holding hands in back of the man who had brought the kids. They were jabbering about the clowns, elephants and other acts they would see that evening. Ram, who had gone to a circus a couple of years back, could sense those kids had never been to the circus before. That evening looked like a highlight of those young lives.
Ram and his dad were behind a couple of people in the line when the children’s group reached the counter. “One full and eight half tickets, please” the man said. The lady in the counter told the amount. The man opened few notes of currency from his pocket and counted. His face fell sad. He counted the money again. “How much did you say the amount was?” he asked the counter lady again. He was turning pale with the answer.
Ram and his father were witnessing the scene. Suddenly, Ram’s dad pulled up a note of Rs 100, dropped it on ground and told the man in the opposite lane: “Sir, you have dropped this note. It fell from your pocket.”
The man looked at Ram’s father. His eyes were filling with tears. He meekly accepted the note and bought the tickets. He came towards Ram, held the hands of his father and told in a choked voice, “I don’t know how to thank you. These are the children from the neighboring orphanage. What the donors pay is just enough for food and clothes. They were dreaming day and night about the circus. As their caretaker, I could not resist bringing them here. I got some of my money and asked for some from my friends. Still, I fell short of some. Bless you, Sir; can’t repay your kindness.”
When Ram reached the counter, they did not have enough money for the tickets. They just walked away from the counter. After few yards, Ram’s dad held hands of his son. “Can we just postpone our programme by a week?” he asked Ram.
“No problems, dad”, Ram said. “Three things, actually. First, I can wait for a week. Second, I can do without too; I have seen the circus earlier. Lastly, today you have taught me what relativity is!” Ram said with a glee in his face.
Ram had found a new meaning for life that day. Moreover, he decided never to tease his father again.
The above anecdote is quite touching, especially for people who empathise. The community of Doctors probably has highest chances for empathy. One of the doctor friends, who does community service told me about her experience with patients wherein she had to make decision for them imagining herself in their shoes! It is a tough experience. The relativity of the issue probably depends on how many tough situation we have passed through in our life. There is the story of a man who was cursing God for not having footwear till he saw a man without legs! The cursing suddenly got transformed to praise. The quantum paradigm shift in this instance is evident. Life is relative and the meek ones need to know this well before they decide on something drastic. Understanding who is right is probably not as important as what is right. This is the biggest aspect of effective leadership, management, parenting, teaching and coaching. It's amazing how much we can accomplish if we simply focus on leaving everyone we meet in better shape than we found them.
With this, let us get back to our regular feature: Interesting learning scenarios
RIGHT PARACHUTE
We can all recall a number of parachute mitral valves. When the papillary muscle of left ventricle is alone, the entire chordae end up getting inserted to the same site and the physical picture is of a parachute with the pointing end at pap muscle and the balloon at the annulus. This is possible for the mitral valve where the site of insertion is well defined. How about the tricuspid valve which sends its chordate over a wider area? We saw a 9-month-old with all the tricuspid chordae getting attached to a single pap muscle. On searching the literature, we found the existence of such an entity. Anderson et al had reported this in a setting of TGA and Aziz et al for TOF. In our case, it was a large VSD and a small ASD. If anyone has any data on this entity, please let us know.
ATRIAL OUTLETS
Another interesting variant of tricuspid valve was seen by us. We have seen a double orifice mitral valve. However, a double orifice tricuspid valve is a rare variant. We had such a scenario in a 6-month-old wherein the TV had two openings on either side of interventricular septum. This was associated with a large inlet VSD and a small RV. The entire MV and one opening of TV were to the MLV and the other opening of TV was to the small MRV. It was an eventual single pump repair. The literature shows the existence of this condition without any other heart lesions. If you can recall any instance of noticing such an anatomical variant, please put up your experience.
PARTIALLY TRANSITIONAL
What would you term a Transitional AV canal defect in which the VSD has closed by a septal pouch? What is the terminology to be used? It is taught that the inlet VSD does not close. However, we have often seen a small inlet VSD of transitional AV canal defect closing spontaneously over a period of time and becoming a partial AV canal defect. Should we continue to call it transitional or change to partial? Tell me your views.
RIMS AND LOCATION
Of late, we have been largely successful in eliminating the need of Transesophageal echocardiography for ASD device closures. Our transthoracic echos have been found sufficient for ASD devices. In this process, we often find that the IVC rims being unsteady. Many times, the defect is not visible at all when the IVC is opened in the subcostal saggital view or in the short axis view. In such cases, we have found a mixed success rate. Is there is fool-proof method in the TTE for this problem? How many centres have actually dropped the TEE for ASD device closures? What are the experiences in those places? Please let us know.
SIDE TO SIDE!
Continuing the problems with devices, we have seen few muscular VSDs which look perfectly OK for device closures during echo evaluation. However, on the table, the LV side of the defect would be much larger than the RV side. Not only crossing becomes a problem, the size of the device to be used is also an issue. Since the muscular VSD devices are symmetrical, the LV side of the device may be too small for the defect and the RV side may be correspondingly big. Our experience with the VSD devices is not as extensive as our PDA and ASD devices. How are the other centres managing this issue? Please let us know if there is a way.
PEDIATRIC CARDIOLOGY PEARLS:
46. Sildenafil seems to be beneficial in the management of Primary pulmonary hypertension. Acute vasoreactivity studies in PAH patients suggest that sildenafil may have greater acute hemodynamic effects than inhaled nitric oxide and may further reduce pulmonary vascular resistance. (Michelakis E, Tymchak W, Lien D, et al. Oral sildenafil compared with inhaled nitric oxide in PAH. Circulation. year 2002 page 2398)
47. AHA guidelines on IE prophylaxis extend to HCM. Bacterial endocarditis appears to be virtually confined to patients with the obstructive form of HCM, with a prevalence of <1%. Vegetations most commonly involve the anterior mitral leaflet or septal endocardium at the site of mitral valve - septal contact and less commonly the aortic valve. ( Spirito P, Rapezzi C, Bellone P, et al. Infective endocarditis in hypertrophic cardiomyopathy. A good review is done by authors. Circulation. year 1999 Page 2132)
48. Levosimendan is a calcium-sensitizing agent that has been evaluated in adults with acute decompensated heart failure and in patients with chronic heart failure. One pharmacokinetic study has been performed in children with congenital heart disease. There is no increase in myocardial oxygen consumption or arrhythmias. (Turanlahti M, Boldt T, Palkama T, et al. levosimendan in pediatric patients evaluated for cardiac surgery. Pediatr Crit Care Med. year 2004 page 457)
49. In cases of myocarditis with congestive heart failure, digitalis may be used and has effected dramatic improvement in many instances. However, during periods of acute inflammation, the myocardium may be hypersensitive to digitalis, so rapid administration to achieve therapeutic levels should be avoided. (Parrillo JE. Myocarditis: Good review article on treatment. J Heart Lung Transplant. year 1998 page 941)
50. In Pediatric restrictive cardiomyopathy, beta-blocker therapy was suggested to blunt rapid heart rates in their patient population in whom significant ST-segment depression was noted at higher heart rates. However, tolerating the therapy is the chief caveat. (Rivenes SM, Kearney DL, Smith EO, et al. Sudden death and cardiovascular collapse in children with restrictive cardiomyopathy. Circulation. year 2000 page 876)
With that, we come to the end of another post. Please send your views, opinions, criticisms either by the comments box or by email to drkiranvs@gmail.com I shall post them on your behalf. I am preparing the list of books about which I can talk in next few posts. Till then, I shall continue with the anecdotes. If you have any interesting short stories to share, please mail them to me. Your contribution would be acknowledged.
Regards
Kiran
ಶುಕ್ರವಾರ, ಜುಲೈ 2, 2010
Hello everyone, this is Dr Kiran welcoming you to the new post. The objective of the blog is to develop an interest in Pediatric cardiology for curious. We learn few interesting facts and discuss few scenarios on practical issues. As previous, let us start with an anecdote which carries a greater meaning in life. The following anecdote is what everyone goes through in life. Please quote your views on it.
Mr Ray was a worried man. His peace was disturbed due to some problems at his office. He was not willing to discuss it with anyone, for he was afraid people may trifle his problems and start talking of their own. He was of the opinion that no one else could understand the significance, quality or gravity of his problem.
His wife, Mrs Ray could not tolerate the downhill condition of her husband. They had a common cousin who was a motivational speaker and well known “agony-uncle”. She sought his assistance and the man agreed to casually visit the Rays for a non-formal session.
Mr Ray did not know of these arrangements. He welcomed the cousin and both of them started talking. Mrs Ray took this opportunity to re-inform that the cousin was a well known advisor and specialized in solving problems in the work environment.
Mr Ray got interested to know the qualification. He hinted that he had a problem in his office. The cousin acknowledged the hint and told, “Would you like to discuss the problem with me? I can try and help it if you don’t mind.”
Mr Ray took the opportunity. His frustration had been piling up for a while. He thought of shooting it off.
“I don’t know if my problem sounds silly. But, it is killing from inside. I am a very principled man who sticks to discipline. If somebody breaks it, I get very frustrated. More so if I have no control on the person doing it. It multiplies if I get victimized in the process of someone else’s indiscipline”, Mr Ray ranted out.
“You cannot be abstract if you want a solution. Get me the facts straight”, his cousin told with a smiling but straight face.
“I have a colleague”, Mr Ray started. “I don’t want to name him. He was an apprentice when I joined, but he got promoted to the same position as mine in few months of my joining. He did not have the qualification for the post, but the Boss took special interest. Probably because they are from same community.”
The cousin nodded. He knew the rule: Do not break the chain of thought!
“It does not bother me. After all, they manipulated the rules of the firm. In a private firm, the rules are flexible if the Bosses agree. What bothers me is the attitude of the person I do not want to name.”
His cousin interrupted. “Let us call him ‘Nameless’. That will solve the problem of expression.”
“OK”, Mr Ray continued. “Nameless is an opportunistic and lazy person. He quoted his family problems and was scooting off from work. Later, he started quoting the health problems. After sometime, he took off for acquiring new training and qualification. Even now when he has got promoted to a higher position, he continues to do the same. His problems seem to be perpetual and he poses as if no one else in the world has any problems. He wants everyone to share the burden of his problems and there is absolutely no help from his side when the other people have problems”, Mr Ray was increasing his tone of anger and was getting breathless while saying all these.
His cousin was simply nodding. He also took some notes in a piece of paper as Mr Ray spoke.
“The biggest problem is on me. I have to bear all the unfinished work of Nameless. He simply gets up and goes home at his will, well ahead of the closing time of office. I have to stay back extra time to complete his incomplete business. When there is some extra work few days, he simply orders the peon to get all the files and leaves by the time files arrive. All those files get dumped on my table. Of course, the other colleagues also chip in, but I have to take the maximum brunt. I have complained to higher authorities many times, but somehow, they are very sympathetic towards him. They kept telling me that since Nameless does not work full-time, they are cutting a portion of his pay. My earlier Boss who was of the same community as Nameless was so moved by all the pathos uttered by Nameless, that he always gave an out-of-the-turn bonus for him! I recently found out that there was never a pay-cut either for him and my Boss used to present a white lie in front of me to keep me silent. Since then, my anger is burning me from inside.”
His cousin’s face did not show any emotion; neither he gestured any noises of sympathy. He kept jotting up something occasionally.
Mr Ray took a gulp of water. His catharsis was evident. His tone was returning back to normal slowly.
“The problem continues even today. Nameless hardly does any work and gets paid the same amount of salary as I do. Nobody cares on how his work gets transferred to others for completion. For the sake of the office pride, we silently bear the burden and finish the work. My burden is heavier nowadays and I cannot even say a word. I often feel like doing the same thing what Nameless does. I am seriously thinking of going scot-free. I will also do half jobs and put the rest on someone else. Anyway, when my boss is tolerating him, he will have no other option other than tolerating me too.”
Mr Ray took another gulp of water and kept silent.
“Any other people in your office? Any other person with similar nature as Nameless?” his cousin asked Mr Ray.
“There are lots working in my office, but as of now, only Nameless is the exception. Others are hard working. Few, in fact, keep very high standards in work. Few people are really inspirational.”
“Can I tell you a small story?” his cousin asked.
“Sure”, Mr Ray said.
“What I quote are from the Vedas - the divine Hindu scriptures. There is mention of a bird called Vyoma, whose sole aim is to reach the sun. It keeps ascending. It lays its egg en-route its journey. The egg keeps dropping all the way, but since the mother bird was at a very high altitude, the egg has to travel a long distance to reach the earth. Still on its journey down in the sky, the egg hatches and the baby bird is delivered. The baby bird starts of its ascent immediately and starts moving towards the sun. The mother bird continues its journey to sun till it burns off in the way due to the heat. As the Sun is described as a ball of fire and the bird also catches fire and burns out, they become essentially one. Do you find any message in this story?”
Mr Ray was silent. Obviously, it was above his head.
His cousin continued: “The story, as any other story from Vedas, is symbolic of life. It should not be taken in literal sense. The sole pursuit of life is to reach the excellence. It should be so powerful that your progeny picks it up as an inborn, innate nature. No external influence should affect the journey. You should rise so high that what other people talk of you should not even fall into your ears. For, people who stop their journey to talk are simply wasting their life. People with a high objective in life have only one way.”
Mr Ray was not convinced. “Is this advice practical?”
“Of course, yes” his cousin continued. “It depends on where you keep your vision. You can either be the anecdotal Vyoma bird to keep you vision high or you can be a vulture, which keeps flying high but always has its vision fixed on the dead bodies lying on the earth. Here, you are always watching Nameless and getting the vision of a vulture which probably befits the Nameless; not you. Why not keep the vision of some other person in office whom you admire? Why not simulate him? Why not try and get the standards that the other person has achieved? Why not excel and set a standard for others? Why not do the inevitable extra work as a learning experience and gain more out of it? Why should you ever think of going the way Nameless has gone? Would you tolerate yourself if you become what you detest?”
It was hard-hitting for Mr Ray. He was expecting sympathy. What he got was more than what he sought.
“So, how do you think I should rectify the mistakes in the office? Is it not my duty to set it right? Is it not correct to demand my rights for equality and peace of mind?” he asked meekly.
“As a matter of fact, it is not your duty” his cousin said curtly. “You have done your best by bringing it to the notice of your superiors. What they do is not your business. Yes, we all go through phases of injustice in life. It is true that Nameless does not deserve what he is getting. But it happens to almost everyone and almost everywhere. It is neither unique nor rare. If you keep thinking and cribbing about it, you are getting stalled in your journey towards excellence. You are wasting your time by underachieving your potential. You are a creative man. You can be of greater pertinence to the world. Only that you have to think in the correct direction.”
Mr Ray was speechless. He took sometime to digest what he heard. Slowly, he got up from his chair, shook hands with his cousin and said, “I may not agree with all that you said, but seems to make sense in a way. I shall try to implement and let you know the results”.
This anecdote is symbolic of what happens in everyone’s life. In every working place, a certain percentage of people are found who live a parasitic life on others. We used to call it 80:20 principle in the government run hospital I worked earlier. Overall, 20% of honest staff did 80% of all the work, but those 80% staff was struggling hard to get all the credit for the good work not done by them. The scenario may not be much different in any private set up either. There are always people who make a living by sycophancy; they just need a gullible boss! There are people who think being smart is better than being honest. There are people who allow their conscience to collect their full salary without working for it. There are people who are first to attend the meetings with higher authorities and take lead in presenting data for which they have not even contributed. There are people who believe in getting their work done by others by any hook or crook. Such people may present as witty, jovial, smart, wise-cracking and popular with everyone except for their colleagues who actually end up doing the pending work of such characters. But all those apparently smart qualities are largely to hide their lazy self. It is a frustrating experience to be colleagues of such kind. The above anecdote shares one way of dealing with such people. Such breed is so common that each one of us can recall such a character in our working place. How are your experiences in dealing with such people? How do you make yourself compatible in such situations? Please share your experiences with other readers. It is really good to have some solace from every possible corner!
With this, let us get back to our regular feature: Interesting learning scenarios.
SMALL INTO LARGE: POSSIBLE?
We had one year old girl with Tricuspid atresia IIB with disproportionate branch PAs. The LPA was far smaller than the RPA. This baby also had bilateral SVCs with LSVC far bigger than the RSVC. Cath data showed suitability for Glenn shunt. Now the problem was attaching the big LSVC to small LPA! We have seen BTT shunts that cannot exceed the size of the native ipsilateral PA. Is the rule applicable to Glenn too? Is it possible to attach a 10mm SVC to a 5mm PA? How are the dynamics different? The surgical team had a split opinion on this. Please let me know your take on it.
IMPROVEMENT IS PROGRESSIVE AND VICE-VERSA!
This one was learning experience. We had a two-year-old single ventricle- DILV. Cath data for Glenn suitability showed a mean PA pressure of 18mmHg. It was above the comfort level of our surgical team. We were about to negate the possibility of surgery when one of our senior surgeons (who is otherwise very conservative) opted to do the Glenn in this baby. It was a matter of surprise and we wanted to know the basis for his opinion. He explained in very simple terms that Glenn will take off about 30% of his systemic venous input into the heart and about 15% of total cardiac output in this baby. So, post-op, the PA pressures are likely to come down by about 15%, bringing it into comfort zone! It was an eye-opener for mathematically challenged people like some of us! But the logic appeared very appealing. The offloading concept of ventricles is the basis for Glenn shunt. When the criteria are made, is this mathematical calculation already incorporated? That is, do we fix a mean PA standard after making correction for the post-op reduction or not? I could not find an answer. If anyone knows this, please let me know.
LOCATION LOGISTICS
I had brought up this question earlier. In Ebstein’s anomaly if there is a communication between LV and atrialised RV, can we call it a VSD?! One more facet came up this time. It was a 6-year-old girl with Ebstein’s anomaly with the communication between LV and atrialised RV low down and had an aneurysm of STL projecting up and partially covering the defect! Can we call this “restriction of VSD”? Here, neither the term VSD nor the direction of STL limiting the flow is semantically confirmed! Can STL send the aneurysm towards the direction of RA and be still called by the same name? Let me know your ideas on it.
HOW EARLY IS EARLY?
It is tough to picture the cause/effect relationship in retrospect. We had a 2-day-old newborn with Tetralogy – absent pulmonic valve complex. It came with respiratory distress. On echo, the branch PAs were dilated. The chest radiograph showed pneumothorax on the right. The condition deteriorated in a couple of days and the neonate was intubated and electively ventilated. The repeat chest radiograph showed a pneumonic patch with no evidence of pneumothorax this time. The question is: Can absent pulmonic valve complex produce respiratory symptoms so early? Is it beneficial to get a cardiopulmonary CT scan? What is your experience of early presentations in such entities? Please let me know your take on this.
CAUSE – EFFECT
We had a 7-month-old with heart pushed to right. Echo revealed TOF with small RPA. The return from right sided pulmonary veins was minimal. Chest radiograph showed a totally collapsed right lung. CT chest done outside was reported as hypoplastic left lung. Is the lung status acquired or congenital? Is the small RPA the cause of right lung hypoplasia or vice-versa? Is there any way of determining the cause-effect relationship? Please let me know your opinion on this issue.
PEDIATRIC CARDIOLOGY PEARLS:
41. Reporting echocardiography in a systematic manner conveys meaning for management. As per the norm, right-sided and left-sided structures at each level are evaluated according to their morphology, their relative positions, their connections to proximal and distal segments, and the presence and location of shunts, obstructions, and valvular regurgitation. (Edwards WD. Congenital heart disease. In: Schoen FJ, ed. Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia: WB Saunders, 1989:281-367)
42. The only prospective control trial of Carvedilol use in children with heart failure was published by Shaddy et al in 2007. The trial showed an improvement in children less than 24 months on echo parameters. However, on composite end points of study, there was no significant benefit. (JAMA, 2007, page 1171)
43. Shepard et al in 1991 reported that 1 in 40 patients with tuberous sclerosis may die as a direct result of cardiac rhabdomyomas. (Mayo Clin Proc 1991;66:792-796)
44. When cardiac myxomas obstruct the semilunar valves, patients experience symptoms while bending forward or lying down, with relief of symptoms when standing. (Robertson R. Primary cardiac tumours: Surgical treatment. Am J Surg 1957;94:183-193)
45. Rheumatic mitral stenosis severe enough to result in symptomatic heart failure may occur in the first two decades of life in developing countries. (Agarwal BL. Juvenile mitral stenosis in developing countries: Problems and challenge. J Assoc Physicians India 1986;34:141-144)
With that, we come to the conclusion of one more post. I am really interested to know if there are any readers of this blog other than me! Please send your inputs via the comments section or to my email id drkiranvs@gmail.com The purpose of this blog is to make it interactive. Hope someday it happens!
Regards
Kiran
Mr Ray was a worried man. His peace was disturbed due to some problems at his office. He was not willing to discuss it with anyone, for he was afraid people may trifle his problems and start talking of their own. He was of the opinion that no one else could understand the significance, quality or gravity of his problem.
His wife, Mrs Ray could not tolerate the downhill condition of her husband. They had a common cousin who was a motivational speaker and well known “agony-uncle”. She sought his assistance and the man agreed to casually visit the Rays for a non-formal session.
Mr Ray did not know of these arrangements. He welcomed the cousin and both of them started talking. Mrs Ray took this opportunity to re-inform that the cousin was a well known advisor and specialized in solving problems in the work environment.
Mr Ray got interested to know the qualification. He hinted that he had a problem in his office. The cousin acknowledged the hint and told, “Would you like to discuss the problem with me? I can try and help it if you don’t mind.”
Mr Ray took the opportunity. His frustration had been piling up for a while. He thought of shooting it off.
“I don’t know if my problem sounds silly. But, it is killing from inside. I am a very principled man who sticks to discipline. If somebody breaks it, I get very frustrated. More so if I have no control on the person doing it. It multiplies if I get victimized in the process of someone else’s indiscipline”, Mr Ray ranted out.
“You cannot be abstract if you want a solution. Get me the facts straight”, his cousin told with a smiling but straight face.
“I have a colleague”, Mr Ray started. “I don’t want to name him. He was an apprentice when I joined, but he got promoted to the same position as mine in few months of my joining. He did not have the qualification for the post, but the Boss took special interest. Probably because they are from same community.”
The cousin nodded. He knew the rule: Do not break the chain of thought!
“It does not bother me. After all, they manipulated the rules of the firm. In a private firm, the rules are flexible if the Bosses agree. What bothers me is the attitude of the person I do not want to name.”
His cousin interrupted. “Let us call him ‘Nameless’. That will solve the problem of expression.”
“OK”, Mr Ray continued. “Nameless is an opportunistic and lazy person. He quoted his family problems and was scooting off from work. Later, he started quoting the health problems. After sometime, he took off for acquiring new training and qualification. Even now when he has got promoted to a higher position, he continues to do the same. His problems seem to be perpetual and he poses as if no one else in the world has any problems. He wants everyone to share the burden of his problems and there is absolutely no help from his side when the other people have problems”, Mr Ray was increasing his tone of anger and was getting breathless while saying all these.
His cousin was simply nodding. He also took some notes in a piece of paper as Mr Ray spoke.
“The biggest problem is on me. I have to bear all the unfinished work of Nameless. He simply gets up and goes home at his will, well ahead of the closing time of office. I have to stay back extra time to complete his incomplete business. When there is some extra work few days, he simply orders the peon to get all the files and leaves by the time files arrive. All those files get dumped on my table. Of course, the other colleagues also chip in, but I have to take the maximum brunt. I have complained to higher authorities many times, but somehow, they are very sympathetic towards him. They kept telling me that since Nameless does not work full-time, they are cutting a portion of his pay. My earlier Boss who was of the same community as Nameless was so moved by all the pathos uttered by Nameless, that he always gave an out-of-the-turn bonus for him! I recently found out that there was never a pay-cut either for him and my Boss used to present a white lie in front of me to keep me silent. Since then, my anger is burning me from inside.”
His cousin’s face did not show any emotion; neither he gestured any noises of sympathy. He kept jotting up something occasionally.
Mr Ray took a gulp of water. His catharsis was evident. His tone was returning back to normal slowly.
“The problem continues even today. Nameless hardly does any work and gets paid the same amount of salary as I do. Nobody cares on how his work gets transferred to others for completion. For the sake of the office pride, we silently bear the burden and finish the work. My burden is heavier nowadays and I cannot even say a word. I often feel like doing the same thing what Nameless does. I am seriously thinking of going scot-free. I will also do half jobs and put the rest on someone else. Anyway, when my boss is tolerating him, he will have no other option other than tolerating me too.”
Mr Ray took another gulp of water and kept silent.
“Any other people in your office? Any other person with similar nature as Nameless?” his cousin asked Mr Ray.
“There are lots working in my office, but as of now, only Nameless is the exception. Others are hard working. Few, in fact, keep very high standards in work. Few people are really inspirational.”
“Can I tell you a small story?” his cousin asked.
“Sure”, Mr Ray said.
“What I quote are from the Vedas - the divine Hindu scriptures. There is mention of a bird called Vyoma, whose sole aim is to reach the sun. It keeps ascending. It lays its egg en-route its journey. The egg keeps dropping all the way, but since the mother bird was at a very high altitude, the egg has to travel a long distance to reach the earth. Still on its journey down in the sky, the egg hatches and the baby bird is delivered. The baby bird starts of its ascent immediately and starts moving towards the sun. The mother bird continues its journey to sun till it burns off in the way due to the heat. As the Sun is described as a ball of fire and the bird also catches fire and burns out, they become essentially one. Do you find any message in this story?”
Mr Ray was silent. Obviously, it was above his head.
His cousin continued: “The story, as any other story from Vedas, is symbolic of life. It should not be taken in literal sense. The sole pursuit of life is to reach the excellence. It should be so powerful that your progeny picks it up as an inborn, innate nature. No external influence should affect the journey. You should rise so high that what other people talk of you should not even fall into your ears. For, people who stop their journey to talk are simply wasting their life. People with a high objective in life have only one way.”
Mr Ray was not convinced. “Is this advice practical?”
“Of course, yes” his cousin continued. “It depends on where you keep your vision. You can either be the anecdotal Vyoma bird to keep you vision high or you can be a vulture, which keeps flying high but always has its vision fixed on the dead bodies lying on the earth. Here, you are always watching Nameless and getting the vision of a vulture which probably befits the Nameless; not you. Why not keep the vision of some other person in office whom you admire? Why not simulate him? Why not try and get the standards that the other person has achieved? Why not excel and set a standard for others? Why not do the inevitable extra work as a learning experience and gain more out of it? Why should you ever think of going the way Nameless has gone? Would you tolerate yourself if you become what you detest?”
It was hard-hitting for Mr Ray. He was expecting sympathy. What he got was more than what he sought.
“So, how do you think I should rectify the mistakes in the office? Is it not my duty to set it right? Is it not correct to demand my rights for equality and peace of mind?” he asked meekly.
“As a matter of fact, it is not your duty” his cousin said curtly. “You have done your best by bringing it to the notice of your superiors. What they do is not your business. Yes, we all go through phases of injustice in life. It is true that Nameless does not deserve what he is getting. But it happens to almost everyone and almost everywhere. It is neither unique nor rare. If you keep thinking and cribbing about it, you are getting stalled in your journey towards excellence. You are wasting your time by underachieving your potential. You are a creative man. You can be of greater pertinence to the world. Only that you have to think in the correct direction.”
Mr Ray was speechless. He took sometime to digest what he heard. Slowly, he got up from his chair, shook hands with his cousin and said, “I may not agree with all that you said, but seems to make sense in a way. I shall try to implement and let you know the results”.
This anecdote is symbolic of what happens in everyone’s life. In every working place, a certain percentage of people are found who live a parasitic life on others. We used to call it 80:20 principle in the government run hospital I worked earlier. Overall, 20% of honest staff did 80% of all the work, but those 80% staff was struggling hard to get all the credit for the good work not done by them. The scenario may not be much different in any private set up either. There are always people who make a living by sycophancy; they just need a gullible boss! There are people who think being smart is better than being honest. There are people who allow their conscience to collect their full salary without working for it. There are people who are first to attend the meetings with higher authorities and take lead in presenting data for which they have not even contributed. There are people who believe in getting their work done by others by any hook or crook. Such people may present as witty, jovial, smart, wise-cracking and popular with everyone except for their colleagues who actually end up doing the pending work of such characters. But all those apparently smart qualities are largely to hide their lazy self. It is a frustrating experience to be colleagues of such kind. The above anecdote shares one way of dealing with such people. Such breed is so common that each one of us can recall such a character in our working place. How are your experiences in dealing with such people? How do you make yourself compatible in such situations? Please share your experiences with other readers. It is really good to have some solace from every possible corner!
With this, let us get back to our regular feature: Interesting learning scenarios.
SMALL INTO LARGE: POSSIBLE?
We had one year old girl with Tricuspid atresia IIB with disproportionate branch PAs. The LPA was far smaller than the RPA. This baby also had bilateral SVCs with LSVC far bigger than the RSVC. Cath data showed suitability for Glenn shunt. Now the problem was attaching the big LSVC to small LPA! We have seen BTT shunts that cannot exceed the size of the native ipsilateral PA. Is the rule applicable to Glenn too? Is it possible to attach a 10mm SVC to a 5mm PA? How are the dynamics different? The surgical team had a split opinion on this. Please let me know your take on it.
IMPROVEMENT IS PROGRESSIVE AND VICE-VERSA!
This one was learning experience. We had a two-year-old single ventricle- DILV. Cath data for Glenn suitability showed a mean PA pressure of 18mmHg. It was above the comfort level of our surgical team. We were about to negate the possibility of surgery when one of our senior surgeons (who is otherwise very conservative) opted to do the Glenn in this baby. It was a matter of surprise and we wanted to know the basis for his opinion. He explained in very simple terms that Glenn will take off about 30% of his systemic venous input into the heart and about 15% of total cardiac output in this baby. So, post-op, the PA pressures are likely to come down by about 15%, bringing it into comfort zone! It was an eye-opener for mathematically challenged people like some of us! But the logic appeared very appealing. The offloading concept of ventricles is the basis for Glenn shunt. When the criteria are made, is this mathematical calculation already incorporated? That is, do we fix a mean PA standard after making correction for the post-op reduction or not? I could not find an answer. If anyone knows this, please let me know.
LOCATION LOGISTICS
I had brought up this question earlier. In Ebstein’s anomaly if there is a communication between LV and atrialised RV, can we call it a VSD?! One more facet came up this time. It was a 6-year-old girl with Ebstein’s anomaly with the communication between LV and atrialised RV low down and had an aneurysm of STL projecting up and partially covering the defect! Can we call this “restriction of VSD”? Here, neither the term VSD nor the direction of STL limiting the flow is semantically confirmed! Can STL send the aneurysm towards the direction of RA and be still called by the same name? Let me know your ideas on it.
HOW EARLY IS EARLY?
It is tough to picture the cause/effect relationship in retrospect. We had a 2-day-old newborn with Tetralogy – absent pulmonic valve complex. It came with respiratory distress. On echo, the branch PAs were dilated. The chest radiograph showed pneumothorax on the right. The condition deteriorated in a couple of days and the neonate was intubated and electively ventilated. The repeat chest radiograph showed a pneumonic patch with no evidence of pneumothorax this time. The question is: Can absent pulmonic valve complex produce respiratory symptoms so early? Is it beneficial to get a cardiopulmonary CT scan? What is your experience of early presentations in such entities? Please let me know your take on this.
CAUSE – EFFECT
We had a 7-month-old with heart pushed to right. Echo revealed TOF with small RPA. The return from right sided pulmonary veins was minimal. Chest radiograph showed a totally collapsed right lung. CT chest done outside was reported as hypoplastic left lung. Is the lung status acquired or congenital? Is the small RPA the cause of right lung hypoplasia or vice-versa? Is there any way of determining the cause-effect relationship? Please let me know your opinion on this issue.
PEDIATRIC CARDIOLOGY PEARLS:
41. Reporting echocardiography in a systematic manner conveys meaning for management. As per the norm, right-sided and left-sided structures at each level are evaluated according to their morphology, their relative positions, their connections to proximal and distal segments, and the presence and location of shunts, obstructions, and valvular regurgitation. (Edwards WD. Congenital heart disease. In: Schoen FJ, ed. Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia: WB Saunders, 1989:281-367)
42. The only prospective control trial of Carvedilol use in children with heart failure was published by Shaddy et al in 2007. The trial showed an improvement in children less than 24 months on echo parameters. However, on composite end points of study, there was no significant benefit. (JAMA, 2007, page 1171)
43. Shepard et al in 1991 reported that 1 in 40 patients with tuberous sclerosis may die as a direct result of cardiac rhabdomyomas. (Mayo Clin Proc 1991;66:792-796)
44. When cardiac myxomas obstruct the semilunar valves, patients experience symptoms while bending forward or lying down, with relief of symptoms when standing. (Robertson R. Primary cardiac tumours: Surgical treatment. Am J Surg 1957;94:183-193)
45. Rheumatic mitral stenosis severe enough to result in symptomatic heart failure may occur in the first two decades of life in developing countries. (Agarwal BL. Juvenile mitral stenosis in developing countries: Problems and challenge. J Assoc Physicians India 1986;34:141-144)
With that, we come to the conclusion of one more post. I am really interested to know if there are any readers of this blog other than me! Please send your inputs via the comments section or to my email id drkiranvs@gmail.com The purpose of this blog is to make it interactive. Hope someday it happens!
Regards
Kiran
ಶನಿವಾರ, ಜೂನ್ 26, 2010
Hello everyone, Dr Kiran’s welcome to all for the new post. The objective of the blog is to develop a dissemination of Pediatric cardiology for everyone interested. We learn few interesting facts and discuss few scenarios on practical issues.
Before we start our anecdote, let me congratulate our Fellowship students: Dr Sripadh Upadhya and Dr Vishal Changela, who finally had their exams last week! They have performed very well and are sure to pass out with flying colours. Dr Changela is a very honest and sincere worker. He has amazing patience while he teaches someone and often called “teacher material”! Dr Upadhya is likely to join the NH team. Good luck for the future of both these fellows.
Also, let me take this opportunity to welcome Dr Dhanya as our new fellowship student under RGUHS. Good luck for her stay and career.
With that, let us start with an anecdote as we have been doing in past few posts. The present anecdote was sent to me by mail by a friend. It is told in many management classes and motivation seminars. Enjoy:
An offbeat lecturer who was known for his eccentric ideas came to the class. He was supposed to take the class for the final year degree students. He carried a couple of bags with him.
He wished the class and opened his bags. The students were interested on what he would do without starting the regular class.
He got a glass jar out and kept it on the table. He started pouring glass marbles into it till the brim.
“Is this glass jar full?” he asked the class. “Yes, sir” came the reply.
“Is it?” the lecturer said. He carefully placed few more marbles on the pile till it started falling.
“Now, is it full?” he questioned again.
“Yes, sir” was the reply, more emphatic this time.
“Let us see” the lecturer said and brought out some fine pieces of stone and started putting into the glass jar. The stone pieces percolated down and settled in the spaces between the marbles.
“Now, what is your opinion?” he asked.
“The jar now seems to be full, sir” came the reply.
“Let us see”, the lecturer said. He took his bag and took out some fine sand. He poured the sand carefully over the jar. The sand occupied the spaces between the stone. The lecturer looked at the class.
The class went silent. Nobody wanted to commit.
“I know what you are thinking. The jar now is full. Is there anything I can fit in?” the lecturer pulled out a bottle of water and started pouring it into the jar, which seamlessly got accommodated!
“I have just demonstrated how the perception changes in life”, the lecturer began. “Our perceptions of ‘full’ and ‘fill’ are very relative. First time, adding one more marble would have dropped it out. But we had forgotten the spaces in between. So, ‘full’ was by the perception of marbles, not for space in the jar.”
The class was listening.
“Our life may seem quite filling with the job we do” lecturer continued, “but there is always scope for few more things. It need not be as major as our primary profession. It can be an activity, a hobby, a service for someone or anything. If the jar in this example was your life, the marbles would be your profession. As you saw, the jar was full with marbles, but was still empty. Life would not be a fulfilling experience unless you fill it with something more than your profession.”
The silence of the class was broken by a loud applause.
The above anecdote is self explanatory. I have seen people who keep complaining about lack of time for pursuing anything other than their job. However, they would nicely discuss a recent cricket match, a new movie, some odd soap series in the television and so on. Ask them about their reading habit, the answer would be a sharp ‘where is the time?’ Not that they do not find time, but they do not recognize it. Probably, reading does not feature in their list of priorities. I know how hard my present boss works. He is in the hospital by the time we reach and keeps going on even when we leave. I find it surprising how he manages time to read a lot. He seems to have read quite lot of contemporary literature. When I was in a book festival, I called him to ask if he wanted any book. He could easily tell me 3-4 books which he liked to read. Some of them were part of a series of which he had the initial volumes and had read them already. It is really commendable and not many actually know of this quality of his. It may be prudent to take a cue from this anecdote and try something new, which would be a fulfilling experience in life.
With this, let us get back to our regular feature, interesting learning scenarios:
OPERABILITY REGURGITATES!!
In a given scenario of operability decisions in echo for cases with severe PAH, the chamber dilatation and pulmonary venous return play the vital roles. For example, in a case of large VSD with bidirectional shunt on echo, we look at pulmonary venous return and LA/LV enlargement to ascertain the operability. We happened to see a child recently which put us into confusion. The child had multiple muscular VSDs which shunted bidirectional. There was severe TR with flow reversal in IVC. Hence, there was RA/RV dilatation. As the TR was severe, the forward flow across the pulmonary valve was probably compromised. This may result in low pulmonary venous return. That compromises both components of operability in echo. Is there any study on how a severe TR compromise Qp in cases VSD? Is the hypothesis of low pulmonary venous return in severe TR correct? Please let me know your take on it.
ONE MORE; ONE LESS
How frequent are the combination lesions with TAPVC? As a feature, we have seen TAPVC being a part of heterotaxy isomerisms. But when the TAPVC is the primary lesion, presence of defects other than a mandatory ASD are not very frequent. I have initially mentioned of a TAPVC with intact IAS, but a large VSD. We found TAPVC with severe coarctation of aorta recently. It was difficult to diagnose to begin with, as the flow across aortic valve itself is less in TAPVC. The likelihood of underestimating coarctation is very high. However, this child had a very clear 2-D picture and gradients diagnostic of coarctation. The combination of high Qp with obstruction to Qs is not very common. The same was confirmed in the operating room. Please let us know your experiences of such atypical combinations.
DUAL DIFFICULTIES
One more variant of TAPVC was seen on the same day as the previous scenario. A 6-month-old came with features of increased Qp. We found a dilated coronary sinus and the common confluence of pulmonary veins entering the CS. We prepared the report of cardiac TAPVC. But, the routine suprasternal view picked up something more. We could see another channel with the colour Doppler showing the flow towards the probe. We started tracing the origin of flow and it went into the common confluence. We reconfirmed the presence of dilated CS and the entry of common confluence into it. It was an instance with the common confluence of pulmonary veins communicating with more than one exit channel. In our case, it was communicating with CS and via ascending vertical vein into the SVC and RA. The combination is very well described, but not frequently seen. It reconfirmed the sayings that our seniors repeatedly told us: Always see all the possible pathways of exit in a TAPVC. If our complacence permitted us to stop at the level of CS, we would have lost an important finding of surgical implication. Let us know your experiences of TAPVCs with dual drainages.
WHY SHOULD NOT WE?!
Several logical explanations are put up on why a small PDA be closed. The risk of endocarditis and the ease of device closure top the list. In the same logic, why should we spare a small muscular VSD? The VSDs described as “maladie de Roger” are the small mid muscular VSDs with high gradient, often with a thrill but no volume overload of left heart. Such lesions have risk of endocarditis, but are too much for open heart surgical risk. Extending the logic of small PDAs, the risk can be eliminated with the device closure of such VSDs. With the learning curve for muscular VSD device closures getting sustained in many centers, why should our guidelines be changed for the favor of device closure of such lesions? Give your opinion on this issue.
THE QUEST FOR CORONARIES
One of the popular viva questions in pediatric cardiology involves coronaries. “Where all in pediatric cardiology do you need to chase the coronaries?” Usual expected answers are TGA, TOF, Kawasaki, ALCAPA, VSD with intact IVS, coronary fistulae, coronary collaterals and ruptured sinus of Valsalva. We had a situation in which none of the above featured and yet, our chase for coronaries was essential! It was a 7-month-old child weighing 3 kg with aortic atresia, VSD, normal sized ventricles, large AP window feeding the ascending aorta, type B arch interruption and the PDA continuing into descending aorta! “Why not a truncus” was the logical question. The answer was in coronaries. We could not see proximal aorta at all. The coronaries were visualized, but their origen was elusive. We could not connect the origin of coronaries with the single great vessel that arose from RV. This finding was against the diagnosis of trunk, which by definition should give rise to systemic, pulmonary and coronary circulations. We have asked for a CT scan, but are not really sure if CT can pick up the origin of coronary. The child looked operable on echo. But the plan may be tedious. Translocating the coronaries, routing LV to common vessel, closing the AP window on the pulmonary side, creating RV to PA homograft, correction of type B interruption and PDA closure!! The procedure may take an entire day in the OR for the braveheart surgeon. We are awaiting the cardiac CT report. I shall keep you informed on the progress. Please let us know if any such diagnostic puzzles were encountered involving the coronaries in your experience.
PEDIATRIC CARDIOLOGY PEARLS
36. In pulmonic stenosis, the pulmonary ejection click corresponds to the time when the doming pulmonary valve reaches its open position. The more severe the stenosis, the earlier in systole the click occurs, until it merges with the first heart sound and becomes inaudible. The intensity of the click varies with respiration, decreasing during inspiration and increasing during expiration. These findings enable a confident physical diagnosis. (Vogelpoel L, Schrire V. Circulation journal 1960 page 55)
37. In VSD with Pulmonary atresia, the pulmonary circulation is dependent on PDA or aortopulmonary collaterals. Ductal and collateral sources may coexist in the same patient but only rarely coexist in the same lung. (Liao PK, Edwards WD, Julsrud PR, et al. Journal of American College of Cardiology 1985 page1343)
38. The risk of tetralogy of Fallot increases in the siblings of an affected child. Nora and Nora have suggested sibling recurrence risk of 2.5% if one sibling was affected, and 8% if two or more siblings were affected (Nora JJ, Nora AH. American Journal of Medical Genetics 1988 page 137)
39. In truncus arteriosus, the truncal valve was tricuspid in 277 (69%), quadricuspid in 86 (22%), bicuspid in 35 (9%), pentacuspid in 1 (0.3%), and unicommissural in 1 (0.3%). (Fuglestad S, Puga F, Danielson G. American Journal of Cardiovascular Pathology 1988 page 39)
40. The original classification of Tricuspid Atresia by Kuhne in 1906 was impractical, yet survived as not many were bothered! Once the treatment modalities started, there was a need to refurbish the classification. The present modification of the classification of Tricuspid Atresia as types 1,2 and 3 and subtypes A, B and C was given by Rajesh Tandon and JE Edwards in 1974. (Tandon R, Edwards JE. Journal of Thoracic and Cardiovascular Surgery 1974 page 530)
This brings us to the end of one more post. I am planning to introduce few books of interest for the medical personnel outside their subject. Let me know your take on this plan. Use the comment box for your ideas and suggestions. Use my email id if you find any problem in using the comments box. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed.
Regards
Kiran
Before we start our anecdote, let me congratulate our Fellowship students: Dr Sripadh Upadhya and Dr Vishal Changela, who finally had their exams last week! They have performed very well and are sure to pass out with flying colours. Dr Changela is a very honest and sincere worker. He has amazing patience while he teaches someone and often called “teacher material”! Dr Upadhya is likely to join the NH team. Good luck for the future of both these fellows.
Also, let me take this opportunity to welcome Dr Dhanya as our new fellowship student under RGUHS. Good luck for her stay and career.
With that, let us start with an anecdote as we have been doing in past few posts. The present anecdote was sent to me by mail by a friend. It is told in many management classes and motivation seminars. Enjoy:
An offbeat lecturer who was known for his eccentric ideas came to the class. He was supposed to take the class for the final year degree students. He carried a couple of bags with him.
He wished the class and opened his bags. The students were interested on what he would do without starting the regular class.
He got a glass jar out and kept it on the table. He started pouring glass marbles into it till the brim.
“Is this glass jar full?” he asked the class. “Yes, sir” came the reply.
“Is it?” the lecturer said. He carefully placed few more marbles on the pile till it started falling.
“Now, is it full?” he questioned again.
“Yes, sir” was the reply, more emphatic this time.
“Let us see” the lecturer said and brought out some fine pieces of stone and started putting into the glass jar. The stone pieces percolated down and settled in the spaces between the marbles.
“Now, what is your opinion?” he asked.
“The jar now seems to be full, sir” came the reply.
“Let us see”, the lecturer said. He took his bag and took out some fine sand. He poured the sand carefully over the jar. The sand occupied the spaces between the stone. The lecturer looked at the class.
The class went silent. Nobody wanted to commit.
“I know what you are thinking. The jar now is full. Is there anything I can fit in?” the lecturer pulled out a bottle of water and started pouring it into the jar, which seamlessly got accommodated!
“I have just demonstrated how the perception changes in life”, the lecturer began. “Our perceptions of ‘full’ and ‘fill’ are very relative. First time, adding one more marble would have dropped it out. But we had forgotten the spaces in between. So, ‘full’ was by the perception of marbles, not for space in the jar.”
The class was listening.
“Our life may seem quite filling with the job we do” lecturer continued, “but there is always scope for few more things. It need not be as major as our primary profession. It can be an activity, a hobby, a service for someone or anything. If the jar in this example was your life, the marbles would be your profession. As you saw, the jar was full with marbles, but was still empty. Life would not be a fulfilling experience unless you fill it with something more than your profession.”
The silence of the class was broken by a loud applause.
The above anecdote is self explanatory. I have seen people who keep complaining about lack of time for pursuing anything other than their job. However, they would nicely discuss a recent cricket match, a new movie, some odd soap series in the television and so on. Ask them about their reading habit, the answer would be a sharp ‘where is the time?’ Not that they do not find time, but they do not recognize it. Probably, reading does not feature in their list of priorities. I know how hard my present boss works. He is in the hospital by the time we reach and keeps going on even when we leave. I find it surprising how he manages time to read a lot. He seems to have read quite lot of contemporary literature. When I was in a book festival, I called him to ask if he wanted any book. He could easily tell me 3-4 books which he liked to read. Some of them were part of a series of which he had the initial volumes and had read them already. It is really commendable and not many actually know of this quality of his. It may be prudent to take a cue from this anecdote and try something new, which would be a fulfilling experience in life.
With this, let us get back to our regular feature, interesting learning scenarios:
OPERABILITY REGURGITATES!!
In a given scenario of operability decisions in echo for cases with severe PAH, the chamber dilatation and pulmonary venous return play the vital roles. For example, in a case of large VSD with bidirectional shunt on echo, we look at pulmonary venous return and LA/LV enlargement to ascertain the operability. We happened to see a child recently which put us into confusion. The child had multiple muscular VSDs which shunted bidirectional. There was severe TR with flow reversal in IVC. Hence, there was RA/RV dilatation. As the TR was severe, the forward flow across the pulmonary valve was probably compromised. This may result in low pulmonary venous return. That compromises both components of operability in echo. Is there any study on how a severe TR compromise Qp in cases VSD? Is the hypothesis of low pulmonary venous return in severe TR correct? Please let me know your take on it.
ONE MORE; ONE LESS
How frequent are the combination lesions with TAPVC? As a feature, we have seen TAPVC being a part of heterotaxy isomerisms. But when the TAPVC is the primary lesion, presence of defects other than a mandatory ASD are not very frequent. I have initially mentioned of a TAPVC with intact IAS, but a large VSD. We found TAPVC with severe coarctation of aorta recently. It was difficult to diagnose to begin with, as the flow across aortic valve itself is less in TAPVC. The likelihood of underestimating coarctation is very high. However, this child had a very clear 2-D picture and gradients diagnostic of coarctation. The combination of high Qp with obstruction to Qs is not very common. The same was confirmed in the operating room. Please let us know your experiences of such atypical combinations.
DUAL DIFFICULTIES
One more variant of TAPVC was seen on the same day as the previous scenario. A 6-month-old came with features of increased Qp. We found a dilated coronary sinus and the common confluence of pulmonary veins entering the CS. We prepared the report of cardiac TAPVC. But, the routine suprasternal view picked up something more. We could see another channel with the colour Doppler showing the flow towards the probe. We started tracing the origin of flow and it went into the common confluence. We reconfirmed the presence of dilated CS and the entry of common confluence into it. It was an instance with the common confluence of pulmonary veins communicating with more than one exit channel. In our case, it was communicating with CS and via ascending vertical vein into the SVC and RA. The combination is very well described, but not frequently seen. It reconfirmed the sayings that our seniors repeatedly told us: Always see all the possible pathways of exit in a TAPVC. If our complacence permitted us to stop at the level of CS, we would have lost an important finding of surgical implication. Let us know your experiences of TAPVCs with dual drainages.
WHY SHOULD NOT WE?!
Several logical explanations are put up on why a small PDA be closed. The risk of endocarditis and the ease of device closure top the list. In the same logic, why should we spare a small muscular VSD? The VSDs described as “maladie de Roger” are the small mid muscular VSDs with high gradient, often with a thrill but no volume overload of left heart. Such lesions have risk of endocarditis, but are too much for open heart surgical risk. Extending the logic of small PDAs, the risk can be eliminated with the device closure of such VSDs. With the learning curve for muscular VSD device closures getting sustained in many centers, why should our guidelines be changed for the favor of device closure of such lesions? Give your opinion on this issue.
THE QUEST FOR CORONARIES
One of the popular viva questions in pediatric cardiology involves coronaries. “Where all in pediatric cardiology do you need to chase the coronaries?” Usual expected answers are TGA, TOF, Kawasaki, ALCAPA, VSD with intact IVS, coronary fistulae, coronary collaterals and ruptured sinus of Valsalva. We had a situation in which none of the above featured and yet, our chase for coronaries was essential! It was a 7-month-old child weighing 3 kg with aortic atresia, VSD, normal sized ventricles, large AP window feeding the ascending aorta, type B arch interruption and the PDA continuing into descending aorta! “Why not a truncus” was the logical question. The answer was in coronaries. We could not see proximal aorta at all. The coronaries were visualized, but their origen was elusive. We could not connect the origin of coronaries with the single great vessel that arose from RV. This finding was against the diagnosis of trunk, which by definition should give rise to systemic, pulmonary and coronary circulations. We have asked for a CT scan, but are not really sure if CT can pick up the origin of coronary. The child looked operable on echo. But the plan may be tedious. Translocating the coronaries, routing LV to common vessel, closing the AP window on the pulmonary side, creating RV to PA homograft, correction of type B interruption and PDA closure!! The procedure may take an entire day in the OR for the braveheart surgeon. We are awaiting the cardiac CT report. I shall keep you informed on the progress. Please let us know if any such diagnostic puzzles were encountered involving the coronaries in your experience.
PEDIATRIC CARDIOLOGY PEARLS
36. In pulmonic stenosis, the pulmonary ejection click corresponds to the time when the doming pulmonary valve reaches its open position. The more severe the stenosis, the earlier in systole the click occurs, until it merges with the first heart sound and becomes inaudible. The intensity of the click varies with respiration, decreasing during inspiration and increasing during expiration. These findings enable a confident physical diagnosis. (Vogelpoel L, Schrire V. Circulation journal 1960 page 55)
37. In VSD with Pulmonary atresia, the pulmonary circulation is dependent on PDA or aortopulmonary collaterals. Ductal and collateral sources may coexist in the same patient but only rarely coexist in the same lung. (Liao PK, Edwards WD, Julsrud PR, et al. Journal of American College of Cardiology 1985 page1343)
38. The risk of tetralogy of Fallot increases in the siblings of an affected child. Nora and Nora have suggested sibling recurrence risk of 2.5% if one sibling was affected, and 8% if two or more siblings were affected (Nora JJ, Nora AH. American Journal of Medical Genetics 1988 page 137)
39. In truncus arteriosus, the truncal valve was tricuspid in 277 (69%), quadricuspid in 86 (22%), bicuspid in 35 (9%), pentacuspid in 1 (0.3%), and unicommissural in 1 (0.3%). (Fuglestad S, Puga F, Danielson G. American Journal of Cardiovascular Pathology 1988 page 39)
40. The original classification of Tricuspid Atresia by Kuhne in 1906 was impractical, yet survived as not many were bothered! Once the treatment modalities started, there was a need to refurbish the classification. The present modification of the classification of Tricuspid Atresia as types 1,2 and 3 and subtypes A, B and C was given by Rajesh Tandon and JE Edwards in 1974. (Tandon R, Edwards JE. Journal of Thoracic and Cardiovascular Surgery 1974 page 530)
This brings us to the end of one more post. I am planning to introduce few books of interest for the medical personnel outside their subject. Let me know your take on this plan. Use the comment box for your ideas and suggestions. Use my email id if you find any problem in using the comments box. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed.
Regards
Kiran
ಭಾನುವಾರ, ಜೂನ್ 20, 2010
Dr Kiran welcomes everyone to the new post. The objective of the blog is to develop a meaning dissemination of Pediatric cardiology for everyone with a taste for this phenomenal subject. We learn few interesting facts and discuss few scenarios on practical issues. Before that, let me start with an anecdote. As a part of my interest in medical history, I came across this extraordinary piece of courage and conviction which I felt like sharing. Please go through this and discuss.
Tylenol is the brand name for paracetamol, which is a household name in USA. It is one of the most popular over-the-counter medications and a household name. It was manufactured and marketed by Johnson and Johnson. In contrast to the tablets from of present day, it was available in capsule form 3 decades back.
In 1982, something terrible happened. Eight people who used the Tylenol capsules died. A psychopath claimed that he had put cyanide in some of the capsules. No further information was available as which batches were affected and how many such capsules were likely contaminated.
If you are the boss of a company who has something like 31 million bottles of the drug in the market at that moment with few possible contaminated capsules (claimed and not proven), how would you react?
Random sample testing? Financial assistance to the deceased? Legal battle on proving the non-involvement of the company? Animal testing? Methods to educate the public on ways to find out the non-contamination? Denial? Prove that the deaths are not related to Tylenol? Bribe the officials to get a clean chit? Bury the issue? Some more skeletons in the cabinet? What else?
Mr James Burke, the CEO of J&J at that time was a smart man and a smarter businessman. He could have done anything mentioned above or even more. But what he “did” was amazing.
He opted for full cooperation with the media immediately. He personally appeared on one TV program after another to take responsibility and keep people up to date on the situation. He ordered withdrawal of all the 31 million bottles of Tylenol from the market! He offered to replace the possibly contaminated capsules by Tablets, whose packing was fool-proof. On behalf of the company he accepted responsibility and made it sure to everyone that J&J had not actually done anything wrong, but still is taking the measures for damage control.
It cost J&J a whooping $100 million! More for the replacement in the form of tablets. For the mistake not committed by them.
What J&J gained out of this could not be measured by money. Its way of handling the situation and the decisions taken won applauds from media. "What Johnson & Johnson executives have done is communicate the message that the company is candid, contrite and compassionate, committed to solving the murders and protecting the public," noted the Washington Post.
But what J&J had lost was not just money. It had to recreate the trust. It is not easy when a big thing falls. And Tylenol was the biggest J&J had. It invested heavily in the restoration job. Its share was estimated to be around 37% in the market."It will take time, it will take money, and it will be very difficult; but we consider it a moral imperative, as well as good business, to restore Tylenol to its preeminent position," said James Burke.
It was the responsible handling of the situation that probably saved the day for J&J. It was too big a catastrophe for easy recovery. J&J made it only because its CEO stuck to the ethics, forgetting the money. The Tylenol crisis brought values of J&J into sharp relief. Instead of bringing in a contingency plan, the company carried on by expressing the principles and values. The public could see the transparency of effort, magnitude of the exercise and more importantly, a principled leadership.
Very shortly, public had placed Tylenol on its top position. Its market value enhanced. People could see why they need to trust the brand. Moreover, they were not ready to disown a company which had social responsibility of the magnitude they displayed.
Today, the market share of Tylenol is much larger than what it used to be. Just to end the anecdote, it did not take J&J more than 2 years to recover their financial losses. What they gained out of the display of honesty was priceless.
It takes good principles and strong base of ethics to be a leader. There are bosses so thimble that they cannot even reprimand an undisciplined subordinate! If a problem is brought to their notice, the first thing they do is to demoralize the whistle-blower! They find the whistle-blowers to be a big nuisance. Good or bad, the show must go on with minimal tension for them. Internal nexus with people of cheap morals for ulterior motives by others in the company does not bother them. Honesty need not be honoured; indiscipline need not be punished; cheating someone of their rights need not be corrected – all for own peace of mind. The definition of success in the present day corporate culture depends on how many controversies the leader avoids. After all, avoiding resolving a problem or denying the existence of a problem is much simpler than solving it. Why put your hand into a troublesome beehive when the the affected person is not you?!
Contrasting such scenarios of the present day is what makes James Burke a magnanimous character. He accepted the problem instead of brushing it aside despite his company did not really have anything to do with the actions of a psychopath; the entire thing had happened outside the production and despatch. He instilled a discipline amongst his staff by setting up a crisis management team. He identified the key people who needed to be involved, and limited the number of spokespersons. Most important of all, he took the lead and worked hard in executing the morals. The whistle blowers were honoured. No lazy bum was spared. Profits and losses did not matter in front of ethics. He did not let any internal nexus or outsider encash the situation to their profit. The cash flow would have suffered as the brand was the biggest they had. He accepted it. He sought a lion’s share of trouble by being in the air and media, taking questions, justifying the stand of his company to public and so on. If we can name any one person with maximum loss of sleep and peace in this fiasco, it was the leader, James Burke.
It is just to see what prevails in the end. The loose characters in corporate history who “ruled” with a single objective have perished shortly. It is the people with courage and ethics whose names are remembered today. It is for anyone to choose what they want to be.
Type Tylenol and James Burke in Google. Read the amazing story with many other details when you are free.
With this, let us get back to our regular feature: Interesting leaning scenarios:
DOUBLE LEFT: OK; DOUBLE RIGHT: TOO!
We happened to see a child with a double orifice tricuspid valve. I do not remember to have seen this before. This particular child had one orifice communicating with RV and the other with LV! A large VSD was associated. An ASD had decompressed the RA, so the flow gradient was not found across the TV orifices. Overall, the hemodynamic effects of the lesion were effaced due to coexisting lesions. If such a lesion is seen by you earlier, please let us know how it was and how it behaved.
TOO EARLY OR TOO LATE?
We often come across such situations. We had a 7-month-old first timer who presented with a large PDA. The operability was unclear in the clinical evaluation and echo. On cath, the pulmonary and systemic pressures were identical and Qp/Qs was 0.9:1. Calculated PVRI was 7.3. Is the condition due to failure of primary pressures to fall or rapid development of PVRI? Both possibilities will have opposite ends of management. Should we do something or leave? Would a trial of sildenafil help? Someone suggested a partial ligation of PDA. It will control the Qp in former case if the primary pressures drop. Otherwise, it will act as a pop-off and help the overall survival. It sounded practical, but is it accepted? Please let me know your experiences of handling such situations.
UNACCOUNTABLE
Few children come with diastolic challenges. The picture remains unclear even with the last investigation we can think of. One such had come to us one year back with left ventricular failure. She had a subaortic membrane with moderate gradient across LVOT. Medical management did not get along. She was operated on and the membrane was resected. With a ferocious post-operative battle by team of our intensivists, she could be discharged. She did not come back for follow up for one year and recently, returned with biventricular failure. There was no subaortic membrane this time, but the LVOT gradient was severe. Being refractive to medical therapy, we catheterized her to get a better delineation of anatomy. The EDPs were very high (30-45 mmHg). Her LVOT gradient was 70 mmHg. We projected a high risk and asked surgical team to take a call. They wanted to go in and take the risk of “act of commission”. However, she could not take make it to OT; died a day prior to proposed surgery. The scenario was depressing. We wanted to get a pathological and histochemical diagnosis, but the family was not for it. If such scenarios are seen earlier, please enlighten us on the possible lines of management.
DEVIL AND DEEP BLUE SEA
It is difficult to take a stand in some of the situations. We had a 22-year-old with TOF and diminutive RPA. About 9 years back, he had undergone a BTT shunt. He came back now with history of exercise intolerance and increasing cyanosis. We could not see the BTT shunt on echo. We expected the shunt to have got blocked. On cath, we found a different scene. The RPA had grown a little to about 6 mm. The LPA was big. The left lung had received a good quantity of blood from BTT shunt for the past 9 years and had become hypertensive. The PVRI of left lung was very high. This had lead to the tardiness of BTT shunt. Management was the issue now. Doing nothing Vs doing another palliation. Since the patient was symptomatic, some felt that another shunt should be created to RPA. However, the risk of another procedure, high risk palliation, proposed benefit and other factors took precedence and the patient was decided on medical management. What is the opinion of readership? How would you go about in such cases?
COLOUR FACTOR
An interesting discussion happened between two of the senior consultants of our team recently. The cardiologist quoted a “big man from the west” of having avoided transannular patching in Tetralogies. The statistics and the outcome presented in the data were impressive. However, our surgeon was not impressed. He quoted the anatomical variations of the Hispanic populations versus oriental populations. He said that the Asian anatomy demands transannular patching where as the western may not. These statements open up the possibility for epidemiological research. If anyone knows any further data on this, please let us know.
PEDIATRIC CARDIOLOGY PEARLS
31. In CCTGA, Complete heart block may be as high as 10% at initial presentation and the incidence is cumulative as the age progresses (Bharati S, McCue CM, Tingelstad JB, et al. American Journal of Cardiology 1978 page147)
32. Although the incidence of congenital bicuspid aortic valve is as high as 1.3 to 2% of general population, only 2% of patients with congenitally abnormal aortic valve will experience significant stenosis or regurgitation by adolescence (Bonowro, Carabello B, de Leon AC Jr, et al Journal of American College of Cardiology 1998 page148)
33. Although anterior leaflet of the mitral valve appears to be bigger, it is not so. The posterior mitral leaflet is longer at its base and shorter in its basal-to-apical length than the anterior leaflet. Hence, both the leaflets have approximately the same area (Ranganathan M, Lam JHC, Wigle ED, et al. Circulation journal 1970 page 459)
34. In the mitral valve, congenital cleft is directed anteriorly toward the outflow septum or aortic root in contrast to the cleft in atrioventricular septal defect, which is directed towards the interventricular septum (Smallhorn J, de Leval M, Stark J, et al. British Heart Journal 1982 page 109)
35. A correlation has been found between the anatomy of mitral valve and the central nervous system, more in the behavioural aspects. The subendocardial surface on the atrial aspect of the middle portion of the mitral valve is rich in nerve endings, including afferent nerves; mechanical stimuli from this area caused by abnormal mitral valve coaptation may cause abnormal autonomic nerve feedback between the central nervous system and mitral valve nervous system. Floppy Mitral Valve innervation patterns with distinct nerve terminals provide a neural basis for brain - heart interactions, augmented by mechanical stimuli from the prolapsing Floppy Mitral Valve (Boudoulas H, Schaal SF, Wooley CF. Floppy mitral valve/mitral valve prolapse: Cardiac arrhythmias. In: Vardas PE, ed. Cardiac Arrhythmias, Pacing, and Electrophysiology. London: Kluwer Academic Publishers, 1998: page 95)
This brings us to the end of one more post. I have been answering any comments in the same comment box. So, please go through the comment box if you have posted any idea. I have been sending emails to all the known followers since last couple of times informing about the update. Since we do not have a visitor counter, I will not know of your visit if you do not comment. Use the comment box for your ideas and suggestions. Use my email id if you find any problem in using the comments box. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed.
Regards
Kiran
Tylenol is the brand name for paracetamol, which is a household name in USA. It is one of the most popular over-the-counter medications and a household name. It was manufactured and marketed by Johnson and Johnson. In contrast to the tablets from of present day, it was available in capsule form 3 decades back.
In 1982, something terrible happened. Eight people who used the Tylenol capsules died. A psychopath claimed that he had put cyanide in some of the capsules. No further information was available as which batches were affected and how many such capsules were likely contaminated.
If you are the boss of a company who has something like 31 million bottles of the drug in the market at that moment with few possible contaminated capsules (claimed and not proven), how would you react?
Random sample testing? Financial assistance to the deceased? Legal battle on proving the non-involvement of the company? Animal testing? Methods to educate the public on ways to find out the non-contamination? Denial? Prove that the deaths are not related to Tylenol? Bribe the officials to get a clean chit? Bury the issue? Some more skeletons in the cabinet? What else?
Mr James Burke, the CEO of J&J at that time was a smart man and a smarter businessman. He could have done anything mentioned above or even more. But what he “did” was amazing.
He opted for full cooperation with the media immediately. He personally appeared on one TV program after another to take responsibility and keep people up to date on the situation. He ordered withdrawal of all the 31 million bottles of Tylenol from the market! He offered to replace the possibly contaminated capsules by Tablets, whose packing was fool-proof. On behalf of the company he accepted responsibility and made it sure to everyone that J&J had not actually done anything wrong, but still is taking the measures for damage control.
It cost J&J a whooping $100 million! More for the replacement in the form of tablets. For the mistake not committed by them.
What J&J gained out of this could not be measured by money. Its way of handling the situation and the decisions taken won applauds from media. "What Johnson & Johnson executives have done is communicate the message that the company is candid, contrite and compassionate, committed to solving the murders and protecting the public," noted the Washington Post.
But what J&J had lost was not just money. It had to recreate the trust. It is not easy when a big thing falls. And Tylenol was the biggest J&J had. It invested heavily in the restoration job. Its share was estimated to be around 37% in the market."It will take time, it will take money, and it will be very difficult; but we consider it a moral imperative, as well as good business, to restore Tylenol to its preeminent position," said James Burke.
It was the responsible handling of the situation that probably saved the day for J&J. It was too big a catastrophe for easy recovery. J&J made it only because its CEO stuck to the ethics, forgetting the money. The Tylenol crisis brought values of J&J into sharp relief. Instead of bringing in a contingency plan, the company carried on by expressing the principles and values. The public could see the transparency of effort, magnitude of the exercise and more importantly, a principled leadership.
Very shortly, public had placed Tylenol on its top position. Its market value enhanced. People could see why they need to trust the brand. Moreover, they were not ready to disown a company which had social responsibility of the magnitude they displayed.
Today, the market share of Tylenol is much larger than what it used to be. Just to end the anecdote, it did not take J&J more than 2 years to recover their financial losses. What they gained out of the display of honesty was priceless.
It takes good principles and strong base of ethics to be a leader. There are bosses so thimble that they cannot even reprimand an undisciplined subordinate! If a problem is brought to their notice, the first thing they do is to demoralize the whistle-blower! They find the whistle-blowers to be a big nuisance. Good or bad, the show must go on with minimal tension for them. Internal nexus with people of cheap morals for ulterior motives by others in the company does not bother them. Honesty need not be honoured; indiscipline need not be punished; cheating someone of their rights need not be corrected – all for own peace of mind. The definition of success in the present day corporate culture depends on how many controversies the leader avoids. After all, avoiding resolving a problem or denying the existence of a problem is much simpler than solving it. Why put your hand into a troublesome beehive when the the affected person is not you?!
Contrasting such scenarios of the present day is what makes James Burke a magnanimous character. He accepted the problem instead of brushing it aside despite his company did not really have anything to do with the actions of a psychopath; the entire thing had happened outside the production and despatch. He instilled a discipline amongst his staff by setting up a crisis management team. He identified the key people who needed to be involved, and limited the number of spokespersons. Most important of all, he took the lead and worked hard in executing the morals. The whistle blowers were honoured. No lazy bum was spared. Profits and losses did not matter in front of ethics. He did not let any internal nexus or outsider encash the situation to their profit. The cash flow would have suffered as the brand was the biggest they had. He accepted it. He sought a lion’s share of trouble by being in the air and media, taking questions, justifying the stand of his company to public and so on. If we can name any one person with maximum loss of sleep and peace in this fiasco, it was the leader, James Burke.
It is just to see what prevails in the end. The loose characters in corporate history who “ruled” with a single objective have perished shortly. It is the people with courage and ethics whose names are remembered today. It is for anyone to choose what they want to be.
Type Tylenol and James Burke in Google. Read the amazing story with many other details when you are free.
With this, let us get back to our regular feature: Interesting leaning scenarios:
DOUBLE LEFT: OK; DOUBLE RIGHT: TOO!
We happened to see a child with a double orifice tricuspid valve. I do not remember to have seen this before. This particular child had one orifice communicating with RV and the other with LV! A large VSD was associated. An ASD had decompressed the RA, so the flow gradient was not found across the TV orifices. Overall, the hemodynamic effects of the lesion were effaced due to coexisting lesions. If such a lesion is seen by you earlier, please let us know how it was and how it behaved.
TOO EARLY OR TOO LATE?
We often come across such situations. We had a 7-month-old first timer who presented with a large PDA. The operability was unclear in the clinical evaluation and echo. On cath, the pulmonary and systemic pressures were identical and Qp/Qs was 0.9:1. Calculated PVRI was 7.3. Is the condition due to failure of primary pressures to fall or rapid development of PVRI? Both possibilities will have opposite ends of management. Should we do something or leave? Would a trial of sildenafil help? Someone suggested a partial ligation of PDA. It will control the Qp in former case if the primary pressures drop. Otherwise, it will act as a pop-off and help the overall survival. It sounded practical, but is it accepted? Please let me know your experiences of handling such situations.
UNACCOUNTABLE
Few children come with diastolic challenges. The picture remains unclear even with the last investigation we can think of. One such had come to us one year back with left ventricular failure. She had a subaortic membrane with moderate gradient across LVOT. Medical management did not get along. She was operated on and the membrane was resected. With a ferocious post-operative battle by team of our intensivists, she could be discharged. She did not come back for follow up for one year and recently, returned with biventricular failure. There was no subaortic membrane this time, but the LVOT gradient was severe. Being refractive to medical therapy, we catheterized her to get a better delineation of anatomy. The EDPs were very high (30-45 mmHg). Her LVOT gradient was 70 mmHg. We projected a high risk and asked surgical team to take a call. They wanted to go in and take the risk of “act of commission”. However, she could not take make it to OT; died a day prior to proposed surgery. The scenario was depressing. We wanted to get a pathological and histochemical diagnosis, but the family was not for it. If such scenarios are seen earlier, please enlighten us on the possible lines of management.
DEVIL AND DEEP BLUE SEA
It is difficult to take a stand in some of the situations. We had a 22-year-old with TOF and diminutive RPA. About 9 years back, he had undergone a BTT shunt. He came back now with history of exercise intolerance and increasing cyanosis. We could not see the BTT shunt on echo. We expected the shunt to have got blocked. On cath, we found a different scene. The RPA had grown a little to about 6 mm. The LPA was big. The left lung had received a good quantity of blood from BTT shunt for the past 9 years and had become hypertensive. The PVRI of left lung was very high. This had lead to the tardiness of BTT shunt. Management was the issue now. Doing nothing Vs doing another palliation. Since the patient was symptomatic, some felt that another shunt should be created to RPA. However, the risk of another procedure, high risk palliation, proposed benefit and other factors took precedence and the patient was decided on medical management. What is the opinion of readership? How would you go about in such cases?
COLOUR FACTOR
An interesting discussion happened between two of the senior consultants of our team recently. The cardiologist quoted a “big man from the west” of having avoided transannular patching in Tetralogies. The statistics and the outcome presented in the data were impressive. However, our surgeon was not impressed. He quoted the anatomical variations of the Hispanic populations versus oriental populations. He said that the Asian anatomy demands transannular patching where as the western may not. These statements open up the possibility for epidemiological research. If anyone knows any further data on this, please let us know.
PEDIATRIC CARDIOLOGY PEARLS
31. In CCTGA, Complete heart block may be as high as 10% at initial presentation and the incidence is cumulative as the age progresses (Bharati S, McCue CM, Tingelstad JB, et al. American Journal of Cardiology 1978 page147)
32. Although the incidence of congenital bicuspid aortic valve is as high as 1.3 to 2% of general population, only 2% of patients with congenitally abnormal aortic valve will experience significant stenosis or regurgitation by adolescence (Bonowro, Carabello B, de Leon AC Jr, et al Journal of American College of Cardiology 1998 page148)
33. Although anterior leaflet of the mitral valve appears to be bigger, it is not so. The posterior mitral leaflet is longer at its base and shorter in its basal-to-apical length than the anterior leaflet. Hence, both the leaflets have approximately the same area (Ranganathan M, Lam JHC, Wigle ED, et al. Circulation journal 1970 page 459)
34. In the mitral valve, congenital cleft is directed anteriorly toward the outflow septum or aortic root in contrast to the cleft in atrioventricular septal defect, which is directed towards the interventricular septum (Smallhorn J, de Leval M, Stark J, et al. British Heart Journal 1982 page 109)
35. A correlation has been found between the anatomy of mitral valve and the central nervous system, more in the behavioural aspects. The subendocardial surface on the atrial aspect of the middle portion of the mitral valve is rich in nerve endings, including afferent nerves; mechanical stimuli from this area caused by abnormal mitral valve coaptation may cause abnormal autonomic nerve feedback between the central nervous system and mitral valve nervous system. Floppy Mitral Valve innervation patterns with distinct nerve terminals provide a neural basis for brain - heart interactions, augmented by mechanical stimuli from the prolapsing Floppy Mitral Valve (Boudoulas H, Schaal SF, Wooley CF. Floppy mitral valve/mitral valve prolapse: Cardiac arrhythmias. In: Vardas PE, ed. Cardiac Arrhythmias, Pacing, and Electrophysiology. London: Kluwer Academic Publishers, 1998: page 95)
This brings us to the end of one more post. I have been answering any comments in the same comment box. So, please go through the comment box if you have posted any idea. I have been sending emails to all the known followers since last couple of times informing about the update. Since we do not have a visitor counter, I will not know of your visit if you do not comment. Use the comment box for your ideas and suggestions. Use my email id if you find any problem in using the comments box. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed.
Regards
Kiran
ಶನಿವಾರ, ಜೂನ್ 12, 2010
This is Dr Kiran welcoming everyone to the new post. The objective of the blog is to develop a meaning dissemination of Pediatric cardiology for all enthusiastics. We learn few interesting facts and discuss few scenarios on practical issues. Before that, let me start with an anecdote. This small story got reprinted in a prominent daily. It brought out my old memories of fascination when I had read it few years back. Just see how you feel about it!
A couple of decades back in a small town lived a man famous for his intelligence. He was well read and respected. People used to come to him for discussing their problems. He would give them the advice, free of cost. In a way, he was popular as a wise man.
For obvious reasons, certain people in the town disliked him. They wanted to demean him. Since they would not be any match for him on a direct confrontation, they were seeking surrogate opportunities.
One day, someone told the man, “The local politician has been spreading the word that your son is an idiot. Do something”.
The man was surprised. His son was in 4th standard and far from idiocy! He was a clever boy, even though he never topped the class.
The man thought of getting the facts straight. He called his son to chamber and asked, “Do you know the local politician?”
“Yes”, the son answered with a twinkle in his eyes.
“He was saying something bad about you. Any tussle between you?”
“Oh, ignore him, Dad. He is not a smart man”
The man was surprised. The comment was too much for a boy of nine.
“You must not use such terms for elders. I have come to know that the man thinks you are an idiot. But I know that you are not. What makes him think so?”
The boy grinned. “The politician fellow has no good business. He sits with few of his friends everyday in the porch in front of his house. I have to go the same way to reach the school. On seeing, he calls me near him, keeps a 5 rupee coin in one palm and one rupee coin in the other. He asks me to pick up one coin. Once I pick up the coin, he laughs loudly and tells his friends: “Did I not tell you?” asks me to keep the coin for myself. Later all of them laugh again. This happens every day.”
The man was interested. “And what coin do you pick up?”
“Obviously, the one rupee coin”
The man was surprised. “I think you know that 5 is more than one?”
“Of course Dad, I know”
“Still you pick up the one rupee coin?”
The boy looked at his dad in surprise. He excused himself and left the room. He came back within a minute with a glass jar in his hand. The jar was three-fourth full of one-rupee coins.
“What is this?” the man demanded.
“This is to show who the idiot is!” the son laughed.
The man was still unsure whether he understood the situation correctly. “Explain” he told his son.
“It is wits versus stupidity. The moment I pick up the five-rupee coin, this joke would end. The politician has no other business than proving me wrong. I oblige. This will continue as long as I keep picking up the single rupee coin. I want to keep the game alive. Now, I want you to tell me whether 5 rupee coin is worth more or this jar.”
The man was taken aback. His son looked the smartest kid on the world to him at that moment.
The mere feeling that we are better or smarter than others sounds clichéd. The joke is usually on us when we deliberately seek to outsmart others. I recently came across a man who had manipulated the system so effectively that he has his cake and has been eating it too. Only because he makes the people around him feel superior. Every place has such smart people. We often find juniors outsmarting the egoistic seniors, class IV outsmarting their bosses and so on. Whether the act is cheating or outsmarting or manipulating depends on where we stand. If our perspective is of the boy in the story, then we are outsmarting. If it is of the politician, we are getting manipulated! The hunter and the hunted need not be permanent. The places can change. The anecdote is only serves a reminder for better introspection before we attempt to demean the others. Never sure who the victim is!
With this, we shall get back to the regular feature: Interesting clinical scenarios.
SMALL Vs BIG RV
We came across a toddler with TOF physiology with small Tricuspid valve annulus. The resultant RV was suboptimal in size. The decision was for a one-and-a-half ventricle correction. Since pulmonary annulus was small, the decision was to get a transannular patch done. How does such a physiology affect RV and Glenn shunt? Can the free PR be detrimental for RV function? Can the TAP take away the purpose of Glenn shunt in reducing RV preload? Even if RV sustains the load, can the increased preload of RV increase the eventual PA pressures and cause Glenn shunt to fail? If anyone has seen this combo working, please let us know the expected dynamics of post op status.
MASS(IVE) DECISION
A 10-year-old boy was admitted to our ICU with rapidly deteriorating LV function. He came in clear LVF. After the basic resuscitation, we did his echo. The LA and LV were dilated and LV EF was about 20%. Behind the LA, a dense, homogenous mass was visualised. The mass was compressing on the LA, deforming its contours. Moderate MR was seen. One of our colleagues noted a thickened mitral valve with restricted mobility of posterior leaflet. Some pericardial effusion added to confusion. Since the mass did not appear to have much effect on the ventricles and the history was acute, he suspected the diagnosis to be rheumatic, with associated mass. To add on, ASLO titres were positive, ESR and CRP were high. There was no clinical history suggestive of rheumatic fever. Still, the patient was started on steroids in suspicion of indolent rheumatic carditis in failure suggestive of rheumatic activity, along with supportive measures and antibiotics. The patient made a very good recovery on this, with EF increasing to 50% in 48 hours of therapy. We got a CT scan, which showed a homogenous mass behind the heart. The Hounsfield unit measurements favoured the diagnosis of lipoma. With the improvement of EF, repeat echo showed a normal motion of mitral valve, taking away the suspicion of RHD! We have stopped steroids and observing the child, with rest of the supportive treatments on. There are some pertinent questions to be answered. How did a slowly growing lipoma produce the mass effect all of a sudden? If no other super-added disease process is adding on, how do we explain the rapid deterioration in this boy? What post-operative histology can explain all the sequence of events? We are yet to get the surgery done for him due to infection. Once we get further answers, I shall brief you. But the rarity of the case is interesting. Lipomas in the mediastinum are not very frequent. That too, massive ones are very rare. We got just one case report in the literature. If any new waves of thought occur, please post them.
IMMUNE DECISION
How good are the screening tests for primary immune deficiency in a country like India? With such a massive population and rampant consanguinity, our numbers in primary immune deficiency must be enormous. However, no medical student with substantial number of years in paediatrics can recall many such children. Comparatively, our database on HIV is better, thanks to awareness and availability of diagnostic modalities. We had a 9-month-old with vegetations on both AV valves and aortic valve. The child had a significant history of abscess formation with IM injections. Our primary suspicion was immune deficiency. But, primary screening for that turned out to be negative. HIV screening in child and both parents was negative. We involved our hemato-oncologist into the picture, but the scenario did not become any clearer. Assays of immuneglobulins are just one part of the diagnosis. How about the complement function, leukocyte functional assay, receptor level abnormalities and others? Our fellows vehemently chased the diagnosis, but we are financially stressed. We did not want to burden the parents over massive expenditure on investigations. Has anyone come across cases like this anytime? How did you go about the diagnosis? Also of interest is the methodology to be followed in India if a suspected case of primary immune deficiency comes when the immune globulins are of normal levels. Please let us know your viewpoints on it.
UNGUARDED EBSTEINS
What is the DD for Ebsteins anomaly!? The question sounds a bit tough, as there can hardly be any. The picture of Ebsteins is so clear that even partially trained fetal echocardiographers vouch by the diagnosis. We had a baby with such an eventuality. It was reported as Ebsteins from outside. What we found surprised us. It was a case of unguarded tricuspid valve! The leaflets were in the right place with no displacement. But, none of them coapted with each other, leaving an unguarded opening to allow a free to-and-fro movement of the blood. The RA was enlarged and the moderator band looked thick and mobile, giving an impression of displaced STL. Is this condition common? It is possible to have missed this condition for Ebstiens. Please let me know if you have seen such entity earlier.
AGELESS REGURGITATION!
How would the pulmonary regurgitation behave with age in setting of absent pulmonic valve? We had a 24-year-old with TOF and absent pulmonic valve! His PR was minimal, but the PAs were huge. The latter findings suggest that the PR must have been there and significant. How to explain the minimal PR that we find now? No one could recall any patient of this age with such findings. Does the free/severe PR improve with age in absent pulmonic valve syndrome? If anyone has come across such a scenario, please let us know.
PEDIATRIC CARDIOLOGY PEARLS:
26. There is a sub-variant of Partial AV canal defect called Transitional type. In the transitional form of partial AVSD, there is aneurysmal replacement of a portion of the inlet ventricular septum, leaving a minimal VSD with a tricuspid pouch which usually obstructs any major shunting at the ventricular level. (Seward JB, Tajik AJ, Edwards WD, et al. Congenital heart disease. In: Two-Dimensional Echocardiographic Atlas. Vol. 1. New York: Springer-Verlag, 1987)
27. In 1973, when echocardiographic evaluation was not a part of diagnosis, it was suggested that the diameter of the ventricular septal defect compared to the diameter of the ascending aorta could be used in determining the prognosis. When the ratio was ≥ 0.8, this defect was considered large, was unlikely to spontaneously close, and the infant would have a large pulmonary blood flow and pulmonary artery hypertension. Although the determinants are changed with the advents of Echocardiography, few still consider this point as a significant one. (Rowe RD. In: Barratt- Boyes BG, Neutze JM, Harris EA, eds. Heart Disease in Infancy. Diagnosis and Surgical Treatment. Proceedings of the Second International Symposium. Edinburgh: Churchill Livingstone, 1973 page 121)
28. In Atrial Septal defect, Eisenmenger reaction was found to be 7% in the first decade, 8% in the second decade, 10% in the third decade, and 11% in the fourth decade and beyond. (Cherian G, Uthaman CB, Durairaj M et al. Pulmonary hypertension in isolated secundum atrial septal defect: high frequency in young patients. American Heart Journal 1983 page 954)
29. The commonest congenital heart disease with right aortic arch is common arterial trunk (popularly called Truncus arteriosus) (Anderson RH, Thiene G. European Journal of Cardiothorac Surgery 1989 page 481)
30. In d-TGA newborns, increased numbers and size of pancreatic islet cells, and increased weight of the adrenal cortex are found. These findings in the pancreas and adrenal cortex are similar to those seen in infants of diabetic mothers and support the contention that the higher-than-usual glucose concentration in the descending aorta during fetal development may play a role (Naeye RL. Archives of Pathology 1966 page 412)
This brings us to the end of one more post. I had sent the emails to all the known followers last time. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed. Also, send your feedbacks by email or via the comments section.
Regards
KIran
A couple of decades back in a small town lived a man famous for his intelligence. He was well read and respected. People used to come to him for discussing their problems. He would give them the advice, free of cost. In a way, he was popular as a wise man.
For obvious reasons, certain people in the town disliked him. They wanted to demean him. Since they would not be any match for him on a direct confrontation, they were seeking surrogate opportunities.
One day, someone told the man, “The local politician has been spreading the word that your son is an idiot. Do something”.
The man was surprised. His son was in 4th standard and far from idiocy! He was a clever boy, even though he never topped the class.
The man thought of getting the facts straight. He called his son to chamber and asked, “Do you know the local politician?”
“Yes”, the son answered with a twinkle in his eyes.
“He was saying something bad about you. Any tussle between you?”
“Oh, ignore him, Dad. He is not a smart man”
The man was surprised. The comment was too much for a boy of nine.
“You must not use such terms for elders. I have come to know that the man thinks you are an idiot. But I know that you are not. What makes him think so?”
The boy grinned. “The politician fellow has no good business. He sits with few of his friends everyday in the porch in front of his house. I have to go the same way to reach the school. On seeing, he calls me near him, keeps a 5 rupee coin in one palm and one rupee coin in the other. He asks me to pick up one coin. Once I pick up the coin, he laughs loudly and tells his friends: “Did I not tell you?” asks me to keep the coin for myself. Later all of them laugh again. This happens every day.”
The man was interested. “And what coin do you pick up?”
“Obviously, the one rupee coin”
The man was surprised. “I think you know that 5 is more than one?”
“Of course Dad, I know”
“Still you pick up the one rupee coin?”
The boy looked at his dad in surprise. He excused himself and left the room. He came back within a minute with a glass jar in his hand. The jar was three-fourth full of one-rupee coins.
“What is this?” the man demanded.
“This is to show who the idiot is!” the son laughed.
The man was still unsure whether he understood the situation correctly. “Explain” he told his son.
“It is wits versus stupidity. The moment I pick up the five-rupee coin, this joke would end. The politician has no other business than proving me wrong. I oblige. This will continue as long as I keep picking up the single rupee coin. I want to keep the game alive. Now, I want you to tell me whether 5 rupee coin is worth more or this jar.”
The man was taken aback. His son looked the smartest kid on the world to him at that moment.
The mere feeling that we are better or smarter than others sounds clichéd. The joke is usually on us when we deliberately seek to outsmart others. I recently came across a man who had manipulated the system so effectively that he has his cake and has been eating it too. Only because he makes the people around him feel superior. Every place has such smart people. We often find juniors outsmarting the egoistic seniors, class IV outsmarting their bosses and so on. Whether the act is cheating or outsmarting or manipulating depends on where we stand. If our perspective is of the boy in the story, then we are outsmarting. If it is of the politician, we are getting manipulated! The hunter and the hunted need not be permanent. The places can change. The anecdote is only serves a reminder for better introspection before we attempt to demean the others. Never sure who the victim is!
With this, we shall get back to the regular feature: Interesting clinical scenarios.
SMALL Vs BIG RV
We came across a toddler with TOF physiology with small Tricuspid valve annulus. The resultant RV was suboptimal in size. The decision was for a one-and-a-half ventricle correction. Since pulmonary annulus was small, the decision was to get a transannular patch done. How does such a physiology affect RV and Glenn shunt? Can the free PR be detrimental for RV function? Can the TAP take away the purpose of Glenn shunt in reducing RV preload? Even if RV sustains the load, can the increased preload of RV increase the eventual PA pressures and cause Glenn shunt to fail? If anyone has seen this combo working, please let us know the expected dynamics of post op status.
MASS(IVE) DECISION
A 10-year-old boy was admitted to our ICU with rapidly deteriorating LV function. He came in clear LVF. After the basic resuscitation, we did his echo. The LA and LV were dilated and LV EF was about 20%. Behind the LA, a dense, homogenous mass was visualised. The mass was compressing on the LA, deforming its contours. Moderate MR was seen. One of our colleagues noted a thickened mitral valve with restricted mobility of posterior leaflet. Some pericardial effusion added to confusion. Since the mass did not appear to have much effect on the ventricles and the history was acute, he suspected the diagnosis to be rheumatic, with associated mass. To add on, ASLO titres were positive, ESR and CRP were high. There was no clinical history suggestive of rheumatic fever. Still, the patient was started on steroids in suspicion of indolent rheumatic carditis in failure suggestive of rheumatic activity, along with supportive measures and antibiotics. The patient made a very good recovery on this, with EF increasing to 50% in 48 hours of therapy. We got a CT scan, which showed a homogenous mass behind the heart. The Hounsfield unit measurements favoured the diagnosis of lipoma. With the improvement of EF, repeat echo showed a normal motion of mitral valve, taking away the suspicion of RHD! We have stopped steroids and observing the child, with rest of the supportive treatments on. There are some pertinent questions to be answered. How did a slowly growing lipoma produce the mass effect all of a sudden? If no other super-added disease process is adding on, how do we explain the rapid deterioration in this boy? What post-operative histology can explain all the sequence of events? We are yet to get the surgery done for him due to infection. Once we get further answers, I shall brief you. But the rarity of the case is interesting. Lipomas in the mediastinum are not very frequent. That too, massive ones are very rare. We got just one case report in the literature. If any new waves of thought occur, please post them.
IMMUNE DECISION
How good are the screening tests for primary immune deficiency in a country like India? With such a massive population and rampant consanguinity, our numbers in primary immune deficiency must be enormous. However, no medical student with substantial number of years in paediatrics can recall many such children. Comparatively, our database on HIV is better, thanks to awareness and availability of diagnostic modalities. We had a 9-month-old with vegetations on both AV valves and aortic valve. The child had a significant history of abscess formation with IM injections. Our primary suspicion was immune deficiency. But, primary screening for that turned out to be negative. HIV screening in child and both parents was negative. We involved our hemato-oncologist into the picture, but the scenario did not become any clearer. Assays of immuneglobulins are just one part of the diagnosis. How about the complement function, leukocyte functional assay, receptor level abnormalities and others? Our fellows vehemently chased the diagnosis, but we are financially stressed. We did not want to burden the parents over massive expenditure on investigations. Has anyone come across cases like this anytime? How did you go about the diagnosis? Also of interest is the methodology to be followed in India if a suspected case of primary immune deficiency comes when the immune globulins are of normal levels. Please let us know your viewpoints on it.
UNGUARDED EBSTEINS
What is the DD for Ebsteins anomaly!? The question sounds a bit tough, as there can hardly be any. The picture of Ebsteins is so clear that even partially trained fetal echocardiographers vouch by the diagnosis. We had a baby with such an eventuality. It was reported as Ebsteins from outside. What we found surprised us. It was a case of unguarded tricuspid valve! The leaflets were in the right place with no displacement. But, none of them coapted with each other, leaving an unguarded opening to allow a free to-and-fro movement of the blood. The RA was enlarged and the moderator band looked thick and mobile, giving an impression of displaced STL. Is this condition common? It is possible to have missed this condition for Ebstiens. Please let me know if you have seen such entity earlier.
AGELESS REGURGITATION!
How would the pulmonary regurgitation behave with age in setting of absent pulmonic valve? We had a 24-year-old with TOF and absent pulmonic valve! His PR was minimal, but the PAs were huge. The latter findings suggest that the PR must have been there and significant. How to explain the minimal PR that we find now? No one could recall any patient of this age with such findings. Does the free/severe PR improve with age in absent pulmonic valve syndrome? If anyone has come across such a scenario, please let us know.
PEDIATRIC CARDIOLOGY PEARLS:
26. There is a sub-variant of Partial AV canal defect called Transitional type. In the transitional form of partial AVSD, there is aneurysmal replacement of a portion of the inlet ventricular septum, leaving a minimal VSD with a tricuspid pouch which usually obstructs any major shunting at the ventricular level. (Seward JB, Tajik AJ, Edwards WD, et al. Congenital heart disease. In: Two-Dimensional Echocardiographic Atlas. Vol. 1. New York: Springer-Verlag, 1987)
27. In 1973, when echocardiographic evaluation was not a part of diagnosis, it was suggested that the diameter of the ventricular septal defect compared to the diameter of the ascending aorta could be used in determining the prognosis. When the ratio was ≥ 0.8, this defect was considered large, was unlikely to spontaneously close, and the infant would have a large pulmonary blood flow and pulmonary artery hypertension. Although the determinants are changed with the advents of Echocardiography, few still consider this point as a significant one. (Rowe RD. In: Barratt- Boyes BG, Neutze JM, Harris EA, eds. Heart Disease in Infancy. Diagnosis and Surgical Treatment. Proceedings of the Second International Symposium. Edinburgh: Churchill Livingstone, 1973 page 121)
28. In Atrial Septal defect, Eisenmenger reaction was found to be 7% in the first decade, 8% in the second decade, 10% in the third decade, and 11% in the fourth decade and beyond. (Cherian G, Uthaman CB, Durairaj M et al. Pulmonary hypertension in isolated secundum atrial septal defect: high frequency in young patients. American Heart Journal 1983 page 954)
29. The commonest congenital heart disease with right aortic arch is common arterial trunk (popularly called Truncus arteriosus) (Anderson RH, Thiene G. European Journal of Cardiothorac Surgery 1989 page 481)
30. In d-TGA newborns, increased numbers and size of pancreatic islet cells, and increased weight of the adrenal cortex are found. These findings in the pancreas and adrenal cortex are similar to those seen in infants of diabetic mothers and support the contention that the higher-than-usual glucose concentration in the descending aorta during fetal development may play a role (Naeye RL. Archives of Pathology 1966 page 412)
This brings us to the end of one more post. I had sent the emails to all the known followers last time. If anyone is following the blog and has not become a follower for any reason, please send your email id to me on drkiranvs@gmail.com I shall include your mail id in the list to be informed. Also, send your feedbacks by email or via the comments section.
Regards
KIran
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