Tuesday, April 13, 2010

Welcome to NH Blog. This is Dr Kiran anchoring you to this journey. We shall continue with anecdotes that convey more meanings.

I recalled this story when my erstwhile boss was narrating her experience in one of the hospital as attendant of a patient.

Divya was a cherubic, bubbly girl of 4 years. She started going to a nearby school. She was supposed to come back from the school with another baby from the neighbourhood along with an attendant. One day, the attendant of the neighbour boy told Divya’s mother that Divya refused to come with him and she is staying back in the school.

Her mom was surprised. Although Divya was naughty girl, she never did anything similar before in the past 4 months of school. A bit tensed, her mom walked towards the school.

At a small bench near the play area, Divya was sitting alone. Her face was not its usual bright.

“What happened to you?” demanded her mom.

“Nothing, mom”, replied Divya, still with some gloom on her face.

“Did anyone say anything to you?”


“Then why are you not home yet? Why did you refuse to come with that uncle?” her mother sounded angry now.

“Actually, mom” Divya started. “My friend, you know, dropped her doll and it broke”


“I was with her.”

“Did you stay back to repair her broken doll?” ridiculed her mother in a taunting way.

“Oh! mom. I don’t know how to repair her doll. I just stayed back when she was crying”

“Which friend? What is her name? Where is she now?

“I don’t know her name. She is my friend. She left just now with her dad. I saw you coming and stayed back.”

“What did you say when she was crying?” asked her mom, getting more curious now.

“I did not say anything. I just cried with her”

Her mom was speechless with overwhelming emotions.

It is quite satisfying to have a person standing by you silently in times of agony. It is probably one place where the hospital management has to look at. We usually have indifferent staff, busy nurses, super-busy doctors and all the other people in the hospital. Management is usually engaged in the balance sheets. Hardly anyone thinks of the situation from the point of patient’s family. Should we really face the situation head-on as a patient before realising the feelings they go through? That is too expensive way of learning things. Can we be more sympathetic for situations which demand common emotions from the entire humankind? The little girl in the above anecdote is probably teaching us a superior method of living as humans.

Let us get back to the section of interesting learning scenarios once again:


We recently had a couple of children with abnormal pulmonary venous connections associated with tetralogy of Fallot. First baby which was 1-year-old had two pulmonary veins entering the RA and the other 2 entering LA. This had gone to OT table, unnoticed in the echo. Second one was a much higher shocker! This 4-year-old had very poor echo windows and cath study was suggested to evaluate for additional VSDs. In the cath, the RA catheter entered RUPV. Hand injection of contrast showed the dye entering RA. The surgeon was informed about the association of PAPVC. However, on the table, the surprise was revealed. The baby had TAPVC! Was the hand injection of dye in cath not enough to opacify common confluence? We went back to the echo recordings, but the windows were so poor that we could not get any information on pulmonary venous return, especially in this baby with very small Qp. I am seriously considering a prospective study on the differences found on the OT table against the final diagnosis provided by the cardiology team. How are the experiences of other centres? Please let us know your experiences.


We came across a 3-year-old operated for Tetralogy 2 years back. The boy was followed up in his native and came to us for the first time after the surgery. He was otherwise doing well, with no symptoms. On echo, we could not find LPA either in 2D or colour in any of the conventional views. The flow across RPA appeared normal. However, on clinical examination, his left lung had normal breath sounds, no added sounds. We wondered why the LPA was not visible. Small clue on chest radiograph was that the Left dome of diaphragm was high up with normal vascular pattern on both lung fields. It was probably paralysed during the surgical procedure and must be partially recovering now. It was likely that the orientation of lung has changed in such a way that the LPA must be traversing in a very odd angle and limited the visibility of LPA. This was only a hypothesis and we could not find any better explanation. We did not get any further investigations, as the clinical picture was very satisfactory and virtually no clues of abnormality in physical examination. Any experiences with such a pattern? If anyone has any better explanations, I would like to hear. How do you think such kids should be investigated? Please let me know your opinions on it.


Many times, we come across number of children with ventricles looking similar to non-compaction. What are the actual criteria for this diagnosis? Is a simple visual impression enough to say this? Are there any clear cut guidelines to say so? The text books describe it as spongy appearance of ventricular surface with thin epicardial layer and a thickened endocardial layer with prominent trabeculations and deep recesses. How to objectively evaluate this entity, which has only visual description? How many times do we really see ventricular dysfunction associated with this picture? How are the experiences with other centres? Please let me know your take on it.


It was a child which disturbed our team a lot. This 3-month-old boy had truncus arteriosus. However, the truncal valve was quadricuspid and dysplastic. There was no other reason why this baby should not have had further procedures. However, is it worthwhile to convert this leaking dysplastic valve (which is not even repairable) into the future aortic valve? Is there any other option than rejecting the scenario as “untreatable”? Has anyone come across a similar phenomenon earlier? Please let me know your views on this.


On an interesting note, we had three children with AP Window on a single day in our OPD. It was more than a coincidence. One among them was a 9-month-old with type 1 APW. This child also had mitral and tricuspid valve prolapses with severe regurgitations along with moderate aortic regurgitation. The net result was dilatation of all the cardiac chambers with reversal of flow in the aortic arch. The pulmonary venous return on the echo could not be assessed satisfactorily. Now the question was: How would one assess the operability on the echo for such children? The child saturated 93% in room air. Is that enough to claim operability? Is the cath study mandatory? Let me know how you would handle this issue.

Some of my friends who are pediatricians with lots of academic interest had an objection about the blog. They claim that it is too much of pediatric cardiology alone. They wanted something that would interest the general pediatric person with interest in Pediatric cardiology. Also, the post-graduate students in pediatrics wanted something that would interest them. With these in mind, I have decided to start a new section from now on. This section would be called “Pediatric cardiology pearls”. I would give 5 interesting and practical points in pediatric cardiology from a known work, along with the source. It should be good for the practitioner and students for management and quoting in the scientific meetings as well. Here goes the first instalment:

1. In the ECG of ASD, one can often see a notch near the apex of R wave in leads 2, 3 and avF which resembles the croche needle. This is called the crochetage sign. This has high specificity for the diagnosis of ASD if found along with the rsR’ pattern in the ECG. Contrary to the popular belief, the crochetage sign does not have a steady correlation with the shunt severity and is often found with PFO also. (Heller et al in JACC 1996, page 877)

2. An Eisenmenger VSD (also called Eisenmenger malalignment) is a perimembranous VSD with an anteriror deviation of infundibular septum. This has nothing to do with Eisenmenger syndrome or Eisenmenger complex (shunt reversal due to high pulmonary vascular resistance). (Fukuda et al in Cardiology in the Young 2000, page 343)

3. PDA is classified into 5 types: wide aortic end, wide pulmonary end, tubular, multiple constrictions and bizarre. (Krichenko et al AJC, 1989, page 879)

4. In the AV canal defect, distance from the cardiac crux to the left ventricular apex is foreshortened, and the distance from the apex to the aortic valve is increased. As a result, the LVOT is longer and narrower than normal and produces the “gooseneck” deformity. (Moss and Adams Pediatric cardiology text book, 7th Ed, page 646)

5. A combination of persistent left superior vena cava terminating in left atrium, atrial septal defect, and absence of roof of coronary sinus is called Raghib complex. It is associated with cyanosis – one of the few causes for cyanosis in ASD without Eisenmengarization (Raghib et al Circulation 1965, page 912)

With this, we come to the conclusion of another post. Please mail your suggestions and feedback to drkiranvs@gmail.com or use the comments section. Thanks for all the new followers. Please let me know how the new segment can be improved with the defined objectives that I have mentioned.



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