Pediatricians should recognize that recurrent or persistent pneumonia (defined as ≥2 episodes/year or ≥3 episodes lifetime with clear lungs between infections, or symptoms lasting >1 month despite appropriate antibiotics) requires investigation for underlying causes rather than simple antibiotic treatment. Key red flags include wet cough with sputum production, recurrent otitis media, failure to thrive, clubbing, and electrolyte abnormalities. Common underlying conditions include cystic fibrosis (characterized by thick secretions, pseudomonas infection, and pancreatic insufficiency), primary ciliary dyskinesia (with situs inversus in 50% of cases), and primary immunodeficiency (meeting Jeffrey model criteria). The diagnostic approach involves thorough history-taking, chest imaging (preferably contrast CT over HRCT), and targeted investigations including sweat chloride testing, lymphocyte subset analysis, and whole exome sequencing when indicated.
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28.5.26 Young Voices Experts WisdomAñadido:
Yeah.
>> Good evening, sir.
>> Good evening.
All right. Dr. Shila you can start.
>> Yeah. So Dr. >> Yeah. Yeah.
>> Uh madam should I start? I want to say there was some anthem.
>> Yes, you can start actually. Yeah. Yeah.
Right sir.
>> Thanks. So I I I will on behalf of Mahip I welcome everybody the participants.
Uh plus today we have got a very special guest who is going to give us expert wisdom in form of Dr. Jagish Chinapa. I welcome Dr. Jagish Chinapa to this Mahip forum to give his expert wisdom. Today we have got a very experienced moderator and Dr. Shilpa Hazare who also happens to be a GM set. So both the expert moderator and me myself are all GM sets GMC Mumbai. So that is a very nice thing to note today. And we have three young ones today who are going to present their perspectives on pediatric pulmonology. Dr. Kaus Moy Dr. Kausum Moit Dr. Siddhant Dalwani and Dr. Balopal group Dr. Balopal is a ET surgeon and Dr. Sidant and Dr. Kausubar pediatric pulmonologist. So it is going to be a very interesting mix to know what is going to uh what is going to be the current management in the terms of pulmonology and what is going to the to be the future and how we should adapt to it and to guide us through today's program will be Dr. She'll pass but before that I would like to invite Dr. Sanju Zoshi sir followed by Dr. Reu Burakar madam to give their perspectives on this program and then I will personally hand over the proceedings to Dr. Shilpazar. Dr. Sanju Zooshi sir.
>> A very good evening to all. I think I am muted. Okay. No, I'm okay. Uh a very good evening to all uh esteemed colleagues from the Maharashtra IP, OBS and EVs, central IPs.
Then uh dignitaries from the central IP and of course today's guest and all speakers, moderator, our team of the young boys.
Uh it's a great privilege and honor to welcome a towering personality like Dr. Jagdish Shinupa an astute academician teacher par excellence. One important thing about him I always appreciate that he is always outspoken about if at all things are going against science in the academic. So I have really high regards for you uh sir it's a really a blessing to have you here. Uh of course uh we all have our three young guns uh Dr. Kowu, Dr. Siddhant and of and Dr. Bal Gopal. I came to know that he is a pediatric ENT specialist. I also appreciate the auspicious presence of our past national secretary Dr. Vin Sakena. Sir, welcome sir.
uh we all know that uh the purpose of today's uh the webinar or the uh our academic sessions are transforming the cutting edge protocols into the frontline physic care and we all know respiratory medicine is a bread and butter for the practicing pediatrician and through our uh this clean uh this webinar we always uh provide a standard uh treatment protocol all to our most peripheral pediatrician trying to bridge the gap between the busting metros and the most peripheral part of the state.
And of course as uh Preven has already stated this is going to be a very lively session and uh so friends who has joined on the virtual platform from across the state let us plunge into the ocean of science. Over to you Provin.
>> Yeah, I will.
>> Thank you all.
>> Thanks President sir. I will request our my secretary Dr. Reu Bakar madam to put in a word.
>> Yeah. Good evening one and all and welcome Dr. uh respected Jagish China as our expert today's pulmonology uh young voices experts wisdom program and also I would like to welcome Dr. Vini Sakasar our past CIP uh secretary uh who has come for this today's program and the young voices as we know today are Dr. Sidan Dr. Kosuk and Dr. Kurup uh they are all going to give us the insights in the pediatric pulmonologist aspects with expert guidance from Dr. Jagdish and our moderator for today Dr. Dr. Shilpa uh is there. So uh actually I would like to thank our team of young voices expert wisdom Dr. Pravin Gokles and uh Dr. Mahesh Sakshane Dr. Klay and all who has taken the efforts uh for arranging this program and for uh your information today we have one MMC point.
So to all those who have joined who are kindly put your name IP number MMC number mobile and those who are nonappens you can put your name MMC number mobile and please so this is from my side over to you Dr. Goki sir thank you so much >> thanks uh present sir and secretary madam without much ado I would like to hand over the proceedings to eminent pulmonologist Dr. Shilpa Hazare who will conduct a further proceedings. Uh as decided she will proceed with the introduction of all speakers and then I think the young guns will take over with expert wisdom followed. I would request the audience to stay put till the very end because the lively chat session will be at after all the presentations are completed. You are welcome to put in your questions in the chat box. Plus you at the end of the program you can easily type it out in the chat box. whatever you want to require require to be answered. You will also get some opportunity to ask the question directly to the speakers and experts at the end of the program. So please be patient uh to allow this program to proceed. Over to you Dr. Shilpa, you can take over now the program.
>> So good evening uh all of you. Uh so this is the fourth episode of uh young voices and expert uh wisdom and uh the theme is pulmonology. Uh and we have a uh expert uh uh person in pulmonology uh a pioneer in pediatric pulmonology actually as an expert uh who will give his uh pearls of wisdom at the end of each talk and he is none other than Dr. Jagish Chinapasar. He's cluster head pediatrics Manipal Manipal Hospital Bangaluru and uh he's past president of IIP National Respiratory Chapter uh from 2019 to 20121 and he's CEO of uh Bangalore uh Met Train uh LLP. So welcome you sir uh to this uh program.
Uh we have three young speakers uh who are doing very good work in pediatric pulmonology.
um they will be delivering uh their talks and the first uh speaker is Dr. Siddhant Lalwani. He's pediatric pulmonologist at Lalwani mother and child care hospital. An honorary consultant uh in pediatric pulmonology at Bharti hospital and Dinanat Mangeshkar Hospital and KM hospital also at Pune. Uh the second speaker is Dr. Kowub Mohit. uh he's consultant pediatric pulmonologist interventional broncoscopist and sleep medicine consultant at Sai child care hospital and uh he's attached to multiple hospitals like Jupiter uh Apollo MMR SRCC Hinduja KDA 40s and Surya hospital at Mumbai.
Our third speaker is Dr. Balopal Kuruk.
uh he is a consultant ENT uh pediatrics uh ENT surgeon uh who has a interest in um uh airway uh procedures uh uh he is at department of pediatric autoarangology at Baiji via via hospital for children at Mumbai. So welcome uh all three of you and uh let's begin with the first uh talk uh of this uh session uh that will be given by Dr. Siddhant Lalwani uh on what lies beyond pneumonia as a diagnosis. So >> yes, thank you madam. Uh firstly I would like to thank Mahayip and Goku for giving me this opportunity for presenting today. I'm just going to share my screen quickly and you all can tell me if it's visible. Okay. Is my screen visible and am I audible as well?
>> Yes sir.
>> Okay. Yeah. So perfect. So I know the title is a bit confusing him and I found it a bit confusing when I got it. But what lies behind beyond pneumonia as a diagnosis is basically we all pediatricians do diagnose pneumonia. But at what point do we say well this is not a simple pneumonia. We need to think further or diagnose further is what I'm going to talk about. essentially a case of recurrent pneumonia or persistent pneumonia. So we all know pneumonia is an acute respiratory infection of the lungs uh which presents with cough difficulty in breathing alongside with rapid respiratory rate or tacipnia with chest and drawing as it is stated by WH1. Because of these criterias, we rampantly label children as pneumonia itself. Even if it's a child who's having an acute wheezing episode, he qualifies as a pneumonia. But I would like to say that we should add one more point to that is along with the above uh definition. We should also add infiltrates on the chest X-ray. We should rather see infiltrates on the chest X-ray and also have some oscultator signs suggestive of pneumonia. And we should always question ourel is this really pneumonia? The reason I'm saying this is we get a lot of referrals at our unit when the parents say you know the child has been admitted for almost four five six episodes of pneumonia. Uh we have to you know think upon are those episodes actually pneumonia firstly and are they recurrent or are they persistent pneumonas. So I'm just going to take you through a few cases first. We'll just ponder upon the gist case and then we'll discuss individual cases in detail and then we'll go to some theory part as well. So my first case was this young male you know first issue of a non-contangonist marriage uh referred by a pediatrician from Dur and he was brought by his parents with complaints of multiple admissions for respiratory infections right since one and a half years of age. Uh the the parents say that the child always has a fever and a wet cough on and off that has been ongoing for almost last 7 months. So though the infections were there since uh the admissions were there since 1 and a half years of age but it has gotten much more worse in the last 7 months and this fever associated with wet cough as well. The parents also noticed that now since last 3 months there is some difficulty in breathing post activity as well. Now mom says that the cough is wet. It is associated with some sputum production which is yellowish in color and the mother categorically says it gets better on oral antibiotics or whenever he has been admitted IV antibiotics. So these episodes have recurred persistently over last few years. Uh each episode parents say stays for about at least 5 to 7 days and gets better on as I said antibiotics oral versus IV. Fever is present during most episodes and uh there is documented relief on antibiotics. On further probing, mother does say that the child has had a few episodes of acute separator otitis media, sometimes unilateral, sometimes bilateral and about two to three times a year which again probably at times need antibiotics. The child has never had a severe infection warranting PICU admission. So a few questions we as pediatricians must think of is is this a simple pneumonia?
I mean we just should just treat the current pneumonia and that's about it or should we try you know think deeper down or dig deeper down what is causing this pneumonia and should we refer this child to a specialist now that the child has had so many infections so these are some questions we should think upon keep this thought in your mind I'll just go to go to the next case uh the next case is again a three and a half yearear-old girl fifth issue of a third degree consangus marriage recurrent complaints of uh chest infections chronic cough cough and a recurrent runny nose ongoing since infancy. Again the cough was wet as I said here was persistent and uh mother always said that the child has a runny nose as well. This child was born at term but had a stormy neonal ICU course and was ventilated for almost 3 weeks. Uh mother has had a bad obstetic history and again this child has had about four episodes of pneumonia in an outside hospital requiring antibiotics IV versus oral. Again this mother recalls having some uh of the child having some acute separator otitis media episodes as a kid. Now again is it a simple pneumonia? Are these acute separative utitis media episodes normal?
I mean are these ENT symptoms linked to pneumonia as well? So these are some questions we should think as pediatricians.
The third and the last case I'm going to discuss upon before >> sorry before discussing deep into these cases. The third case is a 15-month-old girl born of a non-consuous marriage and bought with complaints again of a cough daily for the last 5 months. Parents saying that the child is not thriving well and not growing as compared to her peers. The child has had three episodes of pneumonia again requiring antibiotics. Cough again is wet. The child is faltering on her growth charts.
Uh mom here says that the child has some bulky stools. This is only on probing and questioning not up front. And mother says this child has been admitted once for dehydration as well 4 months ago.
Now again again is this a simple pneumonia? Is dehydration here affected or rather related with these pneumonas as well? And do these bulky stools or oily stools do have some correlation with the pneumonas? So we need to introspect all what is common amongst all these three cases is all these three cases are cases of recurrent pneumonas.
Okay. And uh we should definitely treat them but we should also dig down probe and try to find the exact diagnosis why this child is having recurrent pneumonia. So we must know what is a recurrent pneumonia visav what is a persistent pneumonia. A recurrent pneumonia are basically two or more episodes of pneumonia within a single year or three or more episodes during any time during the life. A critical requirement is that the lungs must be clear and radologically clear lungs should be there between these two individual infections as well. Now persistent pneumonia when pneumonia have persistent clinical symptoms like cough and fever with radological abnormalities on an X-ray which lasts more than a month despite receiving a full course of appropriate antibiotic therapy that would deem as a persistent pneumonia. So first we should think is it a pneumonia.
Second is it a recurrent or a persistent pneumonia and also sorry I mean I mean these are three sorry important factors we need to think on every case who present again and again to you in your oper IBD practice. Now just slightly enumerating in detail the first case as we discussed was 11year-old with a non-contagonist marriage resident of DUI had a wet cough fever and multiple respiratory infections ongoing for the past few years some difficulty in breathing. Now what are the red flags that we picked up here in the history that every pediatrician must pick up?
One, the cough is wet. So when you say it's a wet cough that is recurrent or persistent with sutum production, you should think about an underlying chronic separative lung disease. Amma or other wheezing episodes or airway problems will cause more of and will cause a dry cough rather than a wet cough. Again these episodes were persistently recurring over the last few years and most of them got better on oral versus IV antibiotics. So they were severe enough. Fever is also present saying that it is definitely infection and the child is also having acute separative otitis medias which is again a problem here that does that does say that there is some problem at the immunity level that the child is suffering probably to have these recurrent episodes.
So the child also has some difficulty in breathing. Probably the symptoms are worsening over the last 3 months. So for these complaints the child had had multiple doctor visits. I still remember this pro child has had almost about seven or eight admissions. Uh multiple pediatricians. Some labeled him as am as gave him some inhalers. Some said it was TB and gave him empirical AKT for almost 6 months but there was absolutely no response. So this child eventually was referred to us. on examination. What was again alarming was that the child had grade two clubbing uh on general examination was thin built. Tonsils were not very well visualized in this child and the child was failing to thrive. On systemic examinations the child had coarse creps on the uh on the right side but there were some preparations on the left as well. Other systemic examination were normal. So now this this was a x-ray there were I mean there have been a series of x-rays for this child but this is one of the x-rays that was that was that I've put here. So, so the pneumonia were not massive pneumonia but they were definitely pneumonia. So, you can see there is some haziness bilaterally right more than left on the right mostly in the right paricardiac region uh there is some haziness saying that definitely it is a pneumonia. So there was a CT done outside as well but the CT plates were horrible and the quality wasn't the best. So we repeated a contract chest in our institute uh in which you can very well see that there is certain degree of bronchiactis that the child has developed bilaterally right more than the left side. In this case we landed up doing a broncoscopy with bal and we grew pseudomonas. Now whenever you isolate pseudomonas it is a signature bug for two or three conditions which we'll talk about. It is an alarming bug because it is very difficult to eradicate this bug because they eventually fall form bofilms in the airways and it's quite notorious. They usually become as uh uh you know they become commensal in the airway and cause recurrent problems and infections. So this child was started on some antibiotics receive some airway clearance measures with hypertonic saline and we send an whole genome a whole genome sequencing actually we have a study ongoing. So instead of sending an exom, we have sent a genome sequencing for this child and the genomic sequencing reports are awaited.
But now should we stop here? We want to find the underlying cause of this condition. So we dig deep further. So we said that with recurrent wet cough with a child having repeated acute separator otitis media episodes. We also landed up doing a sweat chloride for this child which was negative and we also send a primary imino deficiency panel in which we do lymphosy subset analysis. uh we do DHR or dihydroamine dihydroamine testing and we also send imoglobin levels. So this is a report that we normally send to NIH at Bombay and you can see here very well that the absolute TH lymphocytes in the lymphosy subsets are low and uh the absolute NK cells are also low. If you come down on the left hand side you can see that the memory B cells are low and the class switching memory B cells are zero. That means your B swells that usually form the imunoglobulins are zero. So there is no class switching. So invariably the imunoglobins or imoglobins here are low IGG, IGA and IGM. So this was a case of primary immuno deficiency that is CVID.
In the second case uh we the the girl was a three and a half year old girl fifth issue of a third degree kzangonous marriage recurrent chest infections chronic cough stormy NICU course being a term baby uh and mother had a bad obstetric history with three abortions was again referred for recurrent chest infections now again wet cough persistent cough runny nose which was a persistent hormma the mother kept saying the mother was a daily wage worker the child also her grade three clubbing was failing to thrive as well and again she required antibiotics to clear an infection and again this child had acute separative utitis media on examination again tacipnia was there there were crepetition sas for borderline clubbing was there a child was failing to thrive now this x-ray initially I think one of my juniors said x-ray but this x-ray is absolutely right so in this x-ray we can see that there are two three pointings one or two three features rather one there is dextrocardia there is situs inverses as well and there is a pneumonia on the left side in the retrocardiac region and the paricardiac region on the left so whenever you say dextrocardia with situs inverses and the mother also then eventually revealed that during the nu stay she was told that the child's organs are flipped and will need further workup but the mother never bothered we ended up sending an whole exom sequencing for this child uh and which actually showed primary celery diskynesia homozygous autotosomal recessive. We also did a nasal eno for this child which was significantly low. So that was a second case. Now this is a third case. In this case 15-month old girl, non-consanguinous marriage again daily wet cough for 5 months not gaining weight as compared to peers. Three episodes of pneumonia. And one additional pointer, the child was admitted specifically for dehydration 4 months ago. On on whisking through the files, they said it's a hyponetromic dehydration. Again, same features. Cough was wet, growth was faltering, but there were some GI complaints as well. Here there were some occasional bulky stools.
On examination there were tacipnia, there were crebs bilaterally, saturations were borderline, clubbing was there. Child was again failing to thrive. This was an X-ray. There was some hyperinflation bilaterally and significant paricardiac infiltrates on the right side. We landed up doing a CCT chest for this child and you can see uh again I don't have an arrow to point it but uh you can see inspecated mucus secretions bilaterally and you can see bronchitic changes that were starting to develop as well. So serum electrolytes in this case uh I've already popped in the diagnosis sorry the serum electrolytes in this case uh it was not only hyponetriia it was hyponetriia hypoglymia and hypocalemia so it was all three were low so it was a pseudobarter like presentation broncoscopy with bal for this child was done which again grew pseudomonus again a signature bug with MRSA infection as well we suspected cystic fibrosis in this child and sent a fecal elastice that was significantly low suggesting there was pancreatitic insufficiency and a sweep chloride which is positive. In order to get or confirm the mutation now that we have CF modulators, we sent an exom sequencing which show which showed a homozygous autoomal recessive CFTR mutation suggestive of cystic fibrosis.
So what do we learn from all these cases? One pneumonia definitely has to identified to be identified and documented. You have to identify if it's recurrent or persistent pneumonia and you have to try to find out the underlying cause. Even if we keep treating each and every episode, we have to dig down deep that why is the child having recurrent or persistent pneumonas. Now certain red flags that we can pick up on history for cystic fibrosis as you can see respiratory wise. So in CF the child has a chronic thick mucus uh has a thick mucus, chronic wet cough, recurrent lung infections, pseudomomas is a one of the signature bugs in this condition. The child may have wheezing because of secretions. The child will have a salty taste tasting skin. If you do newborn screening, you'll pick up pick it up on that. You'll have clubbing of fingers, poor appetite, bulky, oily, greasy stools and because of pancreatic insufficiency, there is severe failure to thrive, poor growth and they can also be nasal polyp and chronic sinusitis.
These children don't only present with licorant LRTI. Actually, in the first few months of life, they can present as hyponitriic, hypocalemic, hypocchloric dehydration. The respiratory symptoms usually develop after infancy. It is predominantly GI symptoms that these children might present initially. So any child with this kind of electrolyte picture with dehydration and respiratory issues please think about CF with primary celia diskynesia as we said again a chronic wet cough recurrent chest infections again sudomonus will be one of the signature bugs with the child will have chronic sinusitis chronic nasal congestion and a runny nose that is going on throughout. Again one of there is a picadar scoring for PCD or primary celia diskynesia which says that a term child having respiratory distress or congenital pneumonia it ticks one of the boxes for primary celery dischasia.
The child may also have recurrent acute ottoitis medias or cirrusitis medias and can also have hearing problems. Situs inverses with dextocardia may be present in 50% of the cases but if it's absent you should still think of primary cy disynesia and infertility is common in adulthood. Uh now from diagnosis again a chronic wet cough with respiratory symptoms persistently and situs inverses should point towards PCD. Now coming to primary immuno deficiency this is a Jeffrey model criteria for diagnosing primary immuno deficiency and these are 10 steps that you should just follow. If a child has four or more new ear infections in one year, think of P. Two or more serious sin infections within one year, think of P. Two or more months on antibiotics with little effect. Two or more pneumonas within a year. Failure to gain weight normally. Recurrent skin absesses or deepseated absesses or organ absesses. Persistent oral thrush with fungal infection on skin. Need for IV antravenous antibiotics to clear infections persistently and again deepseated infections or septicia and obviously a family history of primary immuno deficiency. Now these were three possible you know conditions that cause a persistent pneumonia. You should always ask in such cases about foreign body aspiration uh because that always remains a ask for history of choking or coughing during feeds and after feeds.
Failing to failure to thrive asking is an important finding in these conditions. Always ask for noisy breathing as well as a symptom. Assess the child's neurological status because if the child's neurological status is slightly backward, it can cause aspirations resulting into recurrent pneumonia. So there's an excellent article by Dr. Kabraasar at all. It's an old article from 2000 uh but uh I mean it's it's uh it's it it very well enumerates about the different causes of recurrent and persistent pneumonia and it stands true even in 2026. So one congenital mal forations children with purean sequence cleft pallet airway issues tracal fistulas and trachomalias are also possibly they can cause recurrent pneumonas or persistent pneumonas. Lung malf formations like pulmonary sequestration or hypoplasia may may look like a patch. So whenever you have repeated infections in one particular area of the lung think about a congenital mal for it's a multif focal infection then other possibilities are true. If it's a fixed uh malf for one of the part of the lung, think of hypoplasia sequestration, CPAM or a broncogenic cyst if it's in the midline.
Now cardiovascular malf forations definitely congenital heart disease may present again and again with respiratory issues. So that has to be ruled out and even for vascular rings hence for noisy breathing which will give I mean like strider wheezing which will give a clue to a possible vascular ring causing these repeated episodes as well.
Aspirations very important. So recurrent aspirations not only aspirations from above that means swallow abnormalities but aspirations from below that is gastroesophedial reflux disease can also cause recurrent pneumonia foreign body as we have discussed anomalies of the upper airway we've already discussed now defects in clearance of secretions that we saw at cystic fibrosis primary cerees secondary infections to congenital defects any airway compression within the lumen outside the lumen or in the wall can cause problems uh disorders of local and systemic immunity like primary or secondary immuno deficiencies malnutrition and imunosuppressive therapy so I'm not saying we should do blanket tests to find out the underlying condition one is take a very good history think clinically and on history based on where your diagnosis inclining towards get a chest x-ray in such conditions to say whether it's actually a pneumonia or not also whatever past history is there take that properly Because five episodes of pneumonia may not be all five may not be pneumonia.
Some might be just wheezing episodes. If you're getting a if you're getting a chest CT done, majority of the CTS that we get from outside that the child has already done is RHRCTS. HRCTS won't give a lot of information. Always get a contra CT of the chest. It will help us diagnose vascular mal forations and will give us some idea upon the lymph node status if it's necrotic, non- necrotic, how big they are. So it gives us a better clue uh versus a HRCT of the lung. Look at a basic CBC. Look for lymphopenia. Look at the tonsils when you're examining the child. A general a good thorough general examination is also equally important. Look for electrolytes if the child pres you know comes with a lower respect infection with dehydration uh symptoms. In CF specifically uh sweat chloride is usually done. Whole exom sequencing and fecal elastasis are done. In primary celery diskynesia you can get nasal eno celerary brushings and whole exom sequencing in aspiration. Most of the big hospitals now barerium swallow studies are definitely done that is to give us an idea about reflux. Uh but we should also get a voflloroscopic swallow study done to now find out problems in swallowing issues resulting into aspiration. And if you do a broncoscope you can send lipid laden microfasages on the bronchial lavage to get an idea about whether the child is aspirating or not. in a child with primary immuno deficiency get a lymph lymphocy subset analysis get an imoglobin level and get a DHR uh if you're ruling out chronic granulomatus diseases so uh just conclusion I try to keep it short so always take a good history a good history is cardinal for you know pointing towards a possible underlying condition of a recurrent pneumonia uh identify if it's a recurrent or persistent pneumonia never ignore a persistent wet cough you should you should ponder upon the thought that what could possibly go wrong for the child having a persistent wet cough. You might think this child, this man is talking about CF, PCD, P they are so rare. Trust me, they are not rare. We are just touching the tip of the iceberg. We have more than 25 CF patients under our belt in last 2 years that we have diagnosed PCD and P cases all also increasing.
Always ask for feeding issues and feeding problems. They might give underlying clue to your possible recurrent pneumonia episodes. Document proper anthrop anthropometry. I know all of us are busy pediatricians. So a good history and proper anthropometry and proper saturations is essential and key.
Do not forget to examine the ears, the nose and the oral cavity in each case where you are suspecting a recurrent infection of the chest. Uh and also please other system examination also should be done just because we are pulmonologist. So look at one system other should not be neglected and always think of a specialist referral if there is a diagnostic dilemma. Thank you so much.
Uh thank you Dr. uh Siddhant for elaborating uh the topic so nicely and uh you are spot on on how do uh we know that it is not a simple pneumonia that is the most important thing and history is the most important. Many things you will come to know just on the history.
By and large we are diagnosing these cases very late once they develop clubbing but they should be diagnosed much earlier if we want to decrease the morbidity in these children. So thank you very much uh excellently uh delivered this talk u thank you ma'am >> we have Dr. Rajendra Kulkarni sir as a MMC observer I welcome you sir on behalf of MahaP and I request Dr. Dr. Jagd Shinapasa sir for your expert comments.
>> Uh thank you very much Dr. Shalpa and excellent presentation Sedant. Uh I will just make four comments. The first comment is uh much of what we practice is pattern recognition.
That means please remember that you cannot overdiagnose or underdiagnose a condition. Now for example an X-ray is probably not required in the garden >> routine garden variety of pneumonia you do not need an X-ray and usually cough need not be there in a patient who's got pneumonia because ultimately it's not an airway disease. So what must be kept in mind is that if this child continues to have cough as a predominant symptom then you are on to an airway disease you are not onto a parenal disease so that's the first thing that you should recognize straight away the second point which I want to bring out is that go back to park is our preventive and social medicine textbook always look at host agent and environment because many times you may Yet the environment causing a lot of recurrent infections in children, pneumonia and infection especially if there is overcrowding and cigarette smoking and uh exposure to uh various uh indoor pollutants. So that's another important history that should be taken.
The third thing which I would look at is what is called as Daniel Kman. He is one of my most favorite authors. He has come up with a basic thing that human beings think in two ways. Either you think fast or you think slow.
In vast majority of OPD practice, you need to think fast because you cannot spend too much time on this. But at the same time, you must know which patient you need to think slow. So therefore in the patient who comes to you recurrently or who does not improve with whatever you have done needs slow thinking needs to look you need to go back to your board and see what the history is what the examination is what are the clues and finally Dr. Andrew Bush has given a beautiful article on how to look at um you know immuno deficiency in clinical practice. Look for a severe it goes by spur if it is a severe infection a persistent infection an unusual infection or a recurrent infection. And here you have got in all the cases that you have mentioned here you have either recurrence or you have persistence or you have an unusual organism or something of the sort. So the moment you see that you're on to an immuno deficiency. So I think the uh cases were well brought out a lot of good points and I think your last slide I think is the most important for a general general pediatrician. Always get back to your history always go back to your physical examination and yeah investigations are going to be there done in a few but again think through is this patient coming to you with recurrent wheezing.
If there is vising then definitely there is it is an airway problem causing causing some parental changes. In fact the commonest cause of recurrent pneumonia is a child who's got asthma because every time the child has got some wheezing and some parental this thing is on some antibiotic. So I think the important thing is there to say is yes this is not a pneumonia this is a vising disorder that needs treatment and if you look at the vast amount of literature even in the west the most common diagnosis of recurrent pneumonia is a vising disorder. So uh excellent presentation and a lot of very good points that came out.
>> Thank you sir. Thank you.
>> Uh thank you sir for that very practical pulse of wisdom. Uh Shil, our MMC observer is also uh in the meeting Dr. Rajendra sir.
>> Yeah I yes I have already welcomed uh Dr. Rajendra Kulkarnney sir.
Yeah. So our next talk is on TB diagnostics and we all know that the new end tape guidelines uh they insist on microbiological diagnosis in TB and if you see since last so many years we are struggling to diagnose TB microbiologically.
uh but now we have uh significant technological advancements and it has become easier to diagnose microbiological uh leo1 TB and so the next talk is on IBUS as a diagnostic multiplier in TB management and that will be given by uh Dr. Kub moit from Navi Mumbai. Over to you Kub.
Yeah. So I'm audible and is my slide visible?
>> Yes sir. Yes sir.
>> Yeah. Perfect. So that was a great session by Sedant and uh he had many cases to share. However, I'm not that lucky to have cases to share, but I will try to make it as interesting as possible focusing on the diagnostic modality. So, as things have been already mentioned, what we used to do and what we will be doing in the near future, let's just compare these two things. So, let's do some time travel.
You have a child with persistent fever, cuff for more than 14 days and weight loss. What would you think? Very obvious. It is a first clinical differential diagnosis would be tuberculosis. But things are growing much slower much faster and you have many more diagnosis to look for and also to differentiate it for to make sure what you're dealing with. You have certain baseline first line investigations as already mentioned could be an X-ray could be a simple mantto test which is actually obsolete now and could also be something like sputum test you'll be lucky if you get positive microbiologically in these at least in pediatric age group then we have something which is more advanced maybe a CT scan and based on CT scan we as pulmonologists have our very personal favorite procedure called as broncoscopy and b now even in broncoscopy there have been issues because there have been many instances in which the child typically fits into tuberculosis but still we don't get any bug then what what next the CT is showing something we need not be radiologist to say what is very obvious in this CT but you can see multiple media and lymph nodes lingering around along with parentheses what next what do we do for these kids with this short introduction I would like to introduce myself I'm Dr. I'm a pediatric interventional pulmonologist in multiple hospitals across Mumbai and Mumbai and we'll be talking about images of Ebus biopsy as this micro invasive technique not only in TB we'll talk about TV but also in various other medastinal lymphopathies.
So first of all what is Ebus? Let's just cut down this word. Ebus is endobil ultrasound. So after using this modality of endob bronchial ultrasound, two very important things that we can find out is either you can do a trans bronchial needle aspiration to give you a slide or you could take a direct core biopsy to give you a section a frozen section. Now with this let's just ponder upon these four main points how it works what are the benefits over the obvious modalities some few practical cases and then we'll talk about my personal experience. So what is zebus? So there are like mainly two types of the one which we use very commonly is something called as curvy linear rebus. The other which adults use more commonly is called as radial levers for more deeper loads. So what this curvy linear rebus is as you can see the tip it is a broncoscope with a ultra sonography probe curved uh placed on a on a on a linear form which angles to around 80 to 120° away from the scope.
So this is a 5 to 12 MHz per curve ultrasound transducer at its distal tip with a field of view. You can see that there is a camera angle just above the tip from where the needle is coming out.
That is the camera and under vision both you can see the needle as well as the ultrasonic view of what you're taking a biopsy from. The needle can vary from as big as 21 g to as fine as 21 25 g depending upon the size of the child, the age of the child and the weight of the child. So using this we go and scan across all the media lymph nodes and at an angle of this this transducer scans at 90° from the bronoscopic longitudinal axis and provides a realtime visualization. As you can see we can also give you a Doppler effect to make sure that you're not hampering or puncturing the nearby vascular structures. And once you're at place what you actually see is something like this. As you can see that it's a very well-capsulated uh lymph node and under direct vision you can punch in your needle and take samples both for trans bronchial needle aspiration as well as core biopsy. Now having known this we should know which lymph node to be biopsied. We are not that fortunate to have classification for pediatrics but what we use is as for as per adult guidelines as per the international association for study of lung cancer guidelines in which uh lymph node station starting from 1 till 14 are according to the location and situation of the lymph node along the anatomical structures. So having known these there are certain ebus guidelines. So once you're inside the airway now this and this EUS broncoscope ranges somewhere between 6.5 to 7.9 mm mark that a pediatric airway the trachea of a 6-year-old child a 7-year-old child is somewhere between 7 to 8 mm. So an endob bronchial ultrasound guided biopsy if you want to take it through the airway can be done only in above maybe 6 years of age. There are ways to do in the same procedure in younger kids but these are certain landmarks which we should know because once you're in the airway you practically cannot see anything as you can see in a broncoscope. So based on what you see on ultra sonography you have to go and guide yourself to make sure that you are hitting the right target benefits over your usual modalities as we've already mentioned it's a very minimal invasive procedure and can be done under a daycare procedure. The child doesn't require any admission. The procedure is directly done under vision and there's no age barrier which we'll be focusing upon uh in the coming few slides. It is relatively safe and the biggest advantage is that we get both hystopathological as well as microbiological diagnosis as opposed to only microbiological once it comes to bronkel at large. With this let's go through some interesting cases. So first we'll talk about some non TB cases and then we'll focus upon TB cases. So first this is a 13year-old girl persistent fever for for last 4 weeks on and off dry cough complaints of eye pain in the past 2 weeks weight loss and the outside chest X-ray was this very obviously one very major finding that you can see is there is significant medastinal whiting and you can see nicely uh demarcated shadows of what probably could be medastinal lymph nodes. Now having known this a CT was done and we were right.
There were there was a huge subcarina medastinode which was averting the angle of corina. Before going for a biopsy this child underwent a broncoscopy as you can see there are multiple nodul nodulations all across the airway which is not very common. Now being said that this is kind of a subaccute to chronic infection the the reason for these nodes should be found out. It could be seen in tuberculosis but tuberculosis is not the only condition in which such uh nodilations are seen. So along with a uh uh endob bronchial biopsy which also adds to one of the other microbological diagnosis we went went ahead and got an ebus biopsy done. So here as you can see under end bronchial guidance and doppler guidance this is a station 7 so subcurren lymph node the biopsy was done and the sample was taken out. So here as you can see you can make slides which can be used for cytologology. So under microscopy you can do something called as rose rapid onsite evaluation to find this child luckily had granulum but these were non-necrotic granomomas which was very typical for something called as saridosis. Now if you go back the eye pain probably because of lugiitis and on and off cough probably because of lymph node compression and now coming with fever was all pointing towards a non-tuber classifying of saridosis.
Another child is a 20-month old child, a young child. Acute onset dis a well-groomed child. Respiratory system examination showed bilateral VS but decreased air entry on the right lower lung field. Now again acute onset right lower air entry gone. What is the first thing that you would think of? A foreign body. Nothing you would not think too much about any some long long-standing chronic or subaccute infection. So clinical diagnosis yes was foreign body.
But again something was not fitting in the while while referring itself a CT was done which showed multiple medastinal lymph nodes. Now in this child there was absolutely no sign of any foreign body at least on CT. But one thing that we should know that many foreign bodies could be missed on a CT.
But here having known that there was medinal lymph nodes. This child underwent again a neighbor's biopsy to find that there wereypical lymphoid cells and which on imunoparoxiding was CD45 as well as CD20 positive which went towards diffuse B cell lymphoma. So again before going towards TB let's search for something which could also be other than TB. So first was an inflammatory second was a malingan disease which could be diagnosed using this novel modality. So next for ebus for analytical mal forations. So this is 11year-old adulphin girl had three episodes of massive hemoptis over the past 6 years in between episodes. Vitals were all stable examination showed occasional crepitations in the right mid zone and lower zones. chest showed groundlasting opacity involving both right middle loop as well as lower loop.
Now to find the possible cause of the source of bleed first we got a broncoscopy and found this nice pedulated mass cell non-pulset lesion noted in the right lower low bronus. Now this mass looks very tempting to take a biopsy from but note that this child has had massive hemopasis even touching this uh this mass there have been instances in which kids have kids mainly in adults they have they have bled to death on table. So before confirming what you're biopsying you have to we have to make sure we should know what is the content of this uh mass. So this was scanned using an eoscope and as you can see that it was completely filled with dense vascular structure. So good that we didn't touch the structure and this was the heoscope was just placed over this mask to make sure that what are we dealing with a bronchial angog was done which showed that there were multiple uh draining structures multiple abnormal dilated torturous vessels overlying the lesion with bronco pulmonary shunting and finally this was coiled obviously to make sure that the bleeding uh was reduced to that blood site. So having known that this was cicile mass with which was which had dense vascularity and had uh multiple bronchial lorision this was something like called as bronchial deloy syndrome. Again a very rare but again seen in uh respirator is more commonly seen in uh GI system but again the point to be noted is that we should not be taking biopsies once we see something which which is which is just hanging out in your airway. So this is something which is non TV. Now let's move towards TV. So this is a two-month old child complaints of cough for the last 1 month. So imagine a two-month old child with 1 month. So in a very early age intermittent fever, decent onset respiratory distress. Initially this child was well, good weight gain. Mother had viral program. So was discharged with suggestion of something called as bronchilitis. Again after 2 weeks this child came with increasing tachypnia, labored breathing, persistent cough, not feeding adequately.
significant tacipia intercostal as well as subcostal retractions were were found out bilateral vis more on the left side and threats were hurt investigations were absolutely non-suggestive PCR again knowing the fact that it was lower respiratory upper had had no meaning it was negative this was the x-ray now the x-ray showed that there was significant hyperinflation on the left side with almost shift of the mediainum towards the right so there was if you could make that there was at least something which is compressing the bron bronchial I mean the left mainstream bronchial lumen which is partially compressing causing ball wall mechanism causing hyperinflation of the left lung which is causing pressure effect on the medastinum to move towards the right side. A CT was done which was we were not surprised that there was significant medastinal lymph nodes and as you can see the right the left bronus was almost compressed by the medasty the subcranal lymph node and in this case our procedure was very helpful but now as I had mentioned earlier a eboscope like a 2-year-old child will have 5 to 6 mm of tracheal diameter now this is a 2 month old child so imagine what would be the diameter of the trachea not more than 3 to 4 mm and the eboscope that we have is 6.9 mm. So in order to take the biopsy the same mediainal lymph nodes could be mapped from the esophagial end which is called by a procedure called as esophagial ultrasound guided media lymph nodes. So EU so esophagial ultrasound broncoscopic guided fine needle aspiration. So the same lymph node few lymph node actually you cannot mark all the lymph nodes from the esophagus but most of these the important lymph nodes could be mapped from the esophagus as well. So first the child was intubated to make sure that the airway is secured and then I'm passing my eboscope through the esophagus as you can see goes down and opens up into the stomach. These are the rugi of your stomach. Then pulling it up gradually and moving toward the right left side. You get to see again the media channel lymph nodes. This was a subcrinal lymph node which under vision and Doppler guidance biopsy was taken and not surprised that we directly got pus which was aspirated through this lymph nodes and this puss was directly positive for uh had necroizing granuloma and also was positive for gene expert.
So there was no other way this actually child also underwent uh bal. So point to be not noted that many a times even bal could be negative but the source what we used to read in our textbooks the source all these these these uh the infantile TV being possibilityary most of the bacterial node is concentrated in the media lymph node. So here the lymph node came positive AFB was positive even on the lymph node and pathology showed necroizing granuloma with epicoid cells which was predominantly on lymph node which was negative for bal. So again plus point is that we also get hystopathology along with microbiology once it comes to an ebus biopsy. So like we mentioned about certain landmarks for ebus there are also some ultrasound for I mean esophagial ultrasound landmarks this becomes a relatively a difficult thing but again once we get used to it it is not that difficult I would say but uh anatomy or first year MBA subjects needs to be sorted out very thoroughly.
Now in the last 3 years my personal experience in the last 3 years I've been doing these procedures in three centers across Mumbai done a total of 102 cases age ranges the case that I showed you was the youngest case 2.5 month to as old as 12 years symptoms predominantly were fever cough weight loss radiologically again the medastinal lymph the most common lymph node was subcrinal lymph node and again Bombay being one of the epicenter for TB was no shocker that most of these cases were tuberculosis now this data is under is is undergoing publication. So it will be the biggest e pediatric ebooks to be documented from our unit. So we've did found four lymphomas, two sarcidosis and eight were reactive. So moral of the story is yes these this newer modalities are picking up uh tublossis much better in cases where you are not finding it positive or not getting positive through other investigative procedures. Of course we need an excellent team. The anesthetists play the major role as well as technicians because uh without them you are absolutely helpless and just last month we finished 100 cases. So this is all thanks to our team. So finally so today we at least know that there is a diagnostic modality that we could use for prompt diagnosis.
Interventional pediatric pulmonary is all about jugard. There is nothing which was no official ent transophial biopsy but this is something that we have derived in the past few years.
absolutely say no no antibiotics or no empirical equity without finding an uh the microbological diagnosis or linenosis and finally we know that tissue never lies if it's not I think uh Dr. Kausub uh >> sorry I got disconnected.
>> Yeah. Yes.
>> So I want to thank Dr. Kaus Mohit for uh excellent talk on Abus. uh though it is not available at many centers especially in the periphery but it is available and uh one can use this facility whenever uh we have a difficulty in diagnosing uh especially uh uh not only in TB but even the other cases uh I request Dr. Chinapas to have his uh expert comments.
>> Uh thank you Dr. Costume for that mind-blowing presentation and I think you know when I was when I first had the uh ebus for my patient close to maybe 10 years back with Dr. Dr. Shikant in Bangalore. I was thrilled with the uh with the result and I can see that it has progressed quite rapidly under your expert you know intervention and I always am in awe of Kosu because he has really put his heart and soul into this kind of interventional bron broncoscopy and ebus for diagnostic purposes and also this thing. So I think it was a fantastic presentation and keep it up and I think you must be having the largest series I don't know in the world by now in pediatric ebus. So so it is a it is a it is a really great achievement. So congratulations and again the only thing that I can relate back is that you know Dr. Dr. P. Mudani used to take classes on tuberculosis when I was a student and he always used to say that the subcaranal node is the node that you need to look for in a chest X-ray in a patient and and you are only you know coming circle around and coming back to the same kind of conclusion that the subcaranal node is the probably the most common site from where you could get a a good thing. The other point which I also um was very impressed is that you did not touch that uh vascular malfformation but I think there you would have landed up with a mess and I think it was really a a wonderful decision not to do. So I think a lot of very good learning points.
Thank you Kosub. I learned a lot. Thank you very much.
>> Thank you sir.
>> Yes. So it's already 10:00 and uh we have to uh have one more talk by Dr. Dr. Bal Gopal Kurup who is a uh pediatric ENT surgeon. He's going to talk on congenital airway anomalies and endoscopic solution. I request him to be uh very crisp uh as otherwise we'll be very late.
>> I'll try to be as crisp as possible.
Yes.
>> Good evening everyone. I'm Dr. Balu Balur. Uh I'll share my screen.
Is it visible?
>> Yes sir. Kindly make it full screen.
>> Yeah. Just a second.
>> Yes. Thank you. Uh so yeah topic that I have been given by goer and thanks to Mahayap I'll be talking about minimally invasive uh uh endoscopic treatment that can be given for uh congenital airway anomalies in uh infants. I work as a pediatric ENT at children's hospital. Uh so I'm uh actually blessed to have lot of cases referred to me. Uh second yeah uh so as an ENT uh how am I involved here? Uh so most of these children who are referred to me come with either increased work of breathing noisy breathing uh with cyanotic spells or acute life-threatening events. Most commonly failure to thrive with recurren pneumonia or aspiration or v cry or hostess. they're already through the pulmonology department and they end up with us for some surgical intervention.
So we again uh purely uh look into what our pulmonology colleagues would have missed. We look at the onset of symptoms if the respiratory distress or uh events have occurred at birth after a few days after a few months or after a few weeks.
Are there any aggravating or relieving factors? Is it more on trying feeding any positional variations or if there's any syndroic association? We grade the uh respiratory issues based on uh if the child is uh comfortable uh is playful accepting feeds. If the child has a strider, if the child is not comfortable, anxious, restless and is refusing to feed, not interested in playing or if the child is about to give up. Uh if the child is exhausted, uh is the respiration is slowing down. Uh the child is already sweat a lot, is dehydrated. Uh based on that we grade, we uh decide what needs to be done next.
So what we do is we do an airway assessment. We first do a flexible laryingoscopy. Then under anesthesia we do an asleep flexible scopy. Then we go on to a total intravenous anesthesia residcopy. Then we suspend the larynx.
Look for any cliffs. We do an east veoscopy. And then at times we might have to do a fee in the beginning of this. So not all airway pathologies are aminable to endoscopic repair. Uh there are few I have listed here. We'll go through it one by one. So pling Malaysia as you guys know better than me uh present in the first few weeks of life with inspiratory strider develops uh uh might go on to uh have uh uh failure to thrive. It might worsen on uh positional changes uh on supine position gets better with prone position. There might be issues with feeding crying it might increase uh there might be recurrent pneumonia. Most of them are self-limiting and only about 10% of them require treatment. So uh how do we uh diagnose them? We do a transnasal flexible langoscopy and based on paper from 99 we grade them into three different types. These types are not absolute absolute types. Type one which has prolapsing prolapsing aretinoid mucosa. Type two when the arpiglotic folds a short and have the classic uh omega- shaped epiglotus. Type three is when the epiglotus is very floppy and gets sucked in with each inspiratory attempts. You can have a combination as well of all of them together. So uh these help us uh these types help us decide in what surgical uh intervention we are going to perform. We do a supra gllotolasty in children who come to us uh with uh recurrent symptoms and failure to thrive. In a type two langoia we just cut the short area pigotic folds uh which can be done with cold steel instruments or with laser. Uh then we for the type one langomalias we remove the uh redundant mucosa of the aretinoids and type three lingoas which is when the epiglotus is collapsing. We uh suture the epiglotus to the bon which again can be done uh with cold steel instruments. You don't need any complicated instruments for that. This is the epiglottoexi being performed.
Uh the same thing can be done with laser. the cost goes up. Uh it can't be done in all institutes. So uh it's easier to do a cold seal surgery. But if at the right institute uh we can do with laser it causes less handling less edema postoperatively. Uh this is a child who presented with a valicular cyst with type three languia.
Most of the times any cyst of the upper airway can have some associated langomalia with it. And you can see the result one and five we improved the laryngel inlet and the airway improved.
This just a child who came to us with failure to thrive one and a half months old had type 1 and type two lingo malaysia on posttop day three of supratolasty. The child is comfortable.
Uh looks like the child had nothing to begin with and the child and the mother after one year for followup happy faces.
So it's a simple intervention and uh the uh child who actually requires it benefits from it a lot. The second most common cause of strider that we get uh is bilateral vocal fold immobility presence with bifphasic strider at birth. The children often require uh airway support. It can be easily diagnosed with a transnasal flexible laryingoscope. uh we do an MRI for all children because there can always be an associated GRE malfformation in such children. Uh many of them present to us with uh an NIV uh attached. At times they can come with severe audible strider. Uh at times they can come almost at the uh just about to get intubated. So what we believe is it's always better to do an endoscopy to find what is wrong prior to an airway intervention. So before we intubate, we take the child in the OT and we do an assessment. At times the child can present you with an extation failure as well as this child, this child was one and a half months old had multiple extation failures. Every time he would get reintubated. So these are the things we look out in children. So what do we see uh when we do a flexible langoscopy?
We look for paramedian vocal folds. Any sort of anesthesia might miss this. So we do without any anesthetic agents being given. And if there is history of intubation, we always palpate the criccoiteninoid joints because any uh emergency intubation can cause dislocation or fixation of these joints.
So we always look for that. The only way to confirm it whether it's a neurological entity is by doing a langel EMG which is uh not done in children. So once we diagnose then what do we do for these children? So world over the most commonest uh procedure done is a lateral fixation of the vocal folds in neonates especially. So uh once the child is diagnosed we uh counsel the parents and we go ahead uh with a suture lateralization of the aritenoids. Here I'm checking for uh aritenoid fixation again in a child with abductor pulsy. We pass a 22 gauge needle with a proline suture in the infra glotus and this is the external picture and just around 5 mm above we pass another needle perccutaneously and we suture lateralize the aritenoids to buy a few millmters of millm of airway so that the child can breathe. So we get about 16 to 20 children with bilateral vocal fold pulsy a year. In about 10 to 12 of them I'm able to get away with not doing a tracheosttomy. Trichosmy being the traditional treatment for such children.
This is just an example. Uh the child presented with a abductor paly. This was a child at 3 months of age.
uh there's always some amount of aphonia associated with suture lateralization but luckily this child we were able to give a good result uh avoiding a tracheosmmy gives a lot of pleasure to a surgeon because I really do not like to put these children on a tracheio tube it's easy for us to do a trachiommy but it becomes very difficult for the parents to manage at home especially if they're from a very rural setup uh some children get referred with a trricchosmmy with a endotrical tube in there and these children cannot be extated. So I offer them an option called an endoscopic cricoid split where as you can see this child has already been on the ventilator for a couple of weeks. The larynx is edimatus. So we cut the cricoid cartilage posteriorly and anteriorly. We split the cricoid cartilage and we balloon dilate the cricoid cartilage to separate the posterior glauus to buy some space. uh and we keep the child intubated for a couple of weeks uh from around 7 days to 10 days and after that we extate them.
We balloon dilate them again once more and this is the result we get. This is a child who presented uh with extation failure. This was at 3 months. This child had other neurological anomalies as well. There's some amount of dysphonia but the child at around one year of follow-up had done really well.
So yeah so I avoided a tracheostomy in this cell as well. So it gives a lot of pleasure in not doing a tracheostomy. Uh next uh pathology which we can give a good result with endoscopic surgery is cysts of the airway especially valicular cyst and subglottic cyst. Uh there are other cysts which are not aminable. So I've not included them here. Uh valicular cysts are quite common. They present with strider feeding difficulties failure to thrive. There can be epic episodes. They can be easily diagnosed with a transasal flexible langoscopy. Subglotic cysts can present with recurrent crew like symptoms. They can have a history of intubation. They need to be diagnosed with the rigid langoscopy to see the number of cysts uh which are there in the subglotus. Uh many of you might encounter a situation like this. We get calls once in a while for difficult intubation. This is a child with valicular cyst. The larynx is not visualized. There's a panic call that uh the child cannot be intubated. A simple thing take an 18 gauge needle, a 5 cc or a 10 cc syringe. Just poke the cyst. At that site, there can be no vascular entities appearing. You poke the uh cyst. It's just clear cirrus fluid that comes out. Uh you get to see the airway. You can do an airway intervention there itself. uh at the cyst fills up and can always be removed at a later stage. Removal of the cyst can be done with a laser or with cold steel methods or uh you can use micro debriders, coblation, anything. Uh they give good results and it's a near 100% success rate. Subglottic cyst uh generally there's a history of intubation in these uh children. So you have to look for those cysts. uh there can be multiple at times this is due to uh implantation of certain uh salivary glands in the subglottus or mucus glands in the subglottus. So you handle them one by one you marelize them. We avoid trachos in these children too. Another entity that can be handled endoscopically is lenel cliffs. There are different uh types of lenel cliffs.
They present with recurrent aspiration choking with feeds. Can have cyanotic spells during feeding. The higher grade cliffs can present with strider recurrent pneumonia. Uh a rigid laryingotric broncoscopy with a suspension langoscopy and palpation is the gold standard to uh recognize a cleft video studies of swallowing and a fees aid in the functionality of the uh swallowing and you can assess pre-operatively and postoperatively as to what amount of aspiration is happening. Benjamin English has classified cliffs into multiple types. I won't get into it deep uh into the deeper part of it. Type one clefts are very controversial uh whether to be treated or not. Many of these children can have some uh developmental issues as well. So we once we diagnose type 1 clefts if we are suspecting aspiration on a fees or a VFSS we go ahead and we do an injection laryangoplasty in such children with hyaluronic acid. So that sort of bulges up the posterior glauus.
If the child does well for the first couple of months after the injection then it's sort of diagnostic to know that this cleft has been contributing to the aspiration. Then we go ahead and do a formal repair. Type two type two cliffs uh which involve partially the cricoid also are pretty straightforward.
This was a one-year-old child who presented to us with cough after each uh spoon feeding of liquid fluids. So we went ahead and did a scopy. We found a ridge between the arenoids. As I mentioned uh cliffs are not a visual finding. You need to palpate them. So we use a vocal fold separator and we put a probe to see that the ridge is going beyond the vocal folds. Uh in such cases we do a endoscopic repair. We can either use a laser or a cold steel method and we repair the cleft. There's the same child. After the repair around 6 weeks post repair, she's able to drink water.
Now all all this while the parents used to thicken her feeds and give her water.
Now she's able to drink liquids as well.
Type three cliffs are a little more difficult to handle endoscopically. But uh type 3A ones where the cleft involves the entire cricoid cartilage. As you can see here, there's a a mucosa over the arettoid which is collapsing in. They can present with strider as well. So not all striders are lingo malaysia. So we need to scope and palpate to find out.
Here you can see on palpation uh my probe is going beyond the vocal folds into the subglotus. There is no posterior cartilage of the cricoid. So it was a difficult case. Uh we went ahead suture. The child is doing well now. Uh type 3 B cliffs are not aminable to endoscopic uh suturing. I have a video of a child required open surgery had child had multiple issues. This is uh the cleft going up till the tracheosttomy. The child required a tracheosttomy as well. Uh so it's very difficult to manage. Uh next although not purely endoscopic peer robbing sequences we scope them to look if look for if glossopexy if uh pulling up the tongue can help this cell. So during the flexible endoscopy we take a tongue stitch to see if the larynx opens up. Uh in such children who show uh that the langel inlet opens up. We go ahead and do a uh glossopexy but it's not a 100% thing. Many children do end up with a tracheosttomy as well but it's worth a shot.
Uh htype fistlas again can be detected quite late in life. We have had children coming to us at age of 12 to 14 with an ht type fistla with a bronchitic lung.
So uh broncoscopy is superior to any imaging. In this case this was a neon who presented with recurrent pneumonia.
This is a fistless site in the mid trachea. We do canulate these uh fistlas to see where they go. And in the same setting we put a ureric catheter to canulate it. See it sort of confirms that this is going in the esopus and we loop it out and in the same setting with our pediatric surgeons we uh do a small surgery or through a lower neck incision. The looping helps us identify the fistula clearly between the trachea and esagers. Uh this avoids a lot of dissection in and around the trachea and esas causing lot of damage to structures. uh as a last pathology I would like to concentrate on congenital nasal pyroform aperture stenosis we get around two to three cases a year where the child has cyclical sinosis they're referred to as failure to us for failure to thrive and repeated nasal obstruction most of them can be managed with just uh deconistent nose drops but many of them are not diagnosed that they have a CNPS uh so what do you look For when you see from the outside you might see their nasal aperture might be small and on a CT you might see the uh distance between the frontal process of maxillon bilateral uh sides might be less than 8 mm on coronal as well as auxiliary cuts.
So traditionally I used to do an open approach subli but lately I have started doing balloon dilotations for these children. It's almost non-invasive. No sutures. Uh this is a child prior to surgery that the endoscope wouldn't go in and we put in the balloons and post dilotation we have our endoscope going in completely. We stand them uh but we also look for other associated anomalies in these children. Almost 60% of them have a central mega incizers. They do not have two incizes. they have one incizer. Most of this can be detected on the CT as well. So they also have midline defects. They can have uh hypothalamic pituitary axis hypounction and hollow proincense other things as well. So uh we involve our endocrinologist in this uh so something to look out for. Thank you.
Hope I was >> Thank you Dr. Bal Gopal Kurup. Uh it was an excellent talk and uh excellently delivered. Uh so many of anomalies actually nowadays can be corrected endoscopically and so well with so minimal um um uh surgical interventions actually open surgical interventions. So it was a excellent talk by you. Uh I request you to also uh mention that langotracho Malaysia. Yeah.
Laringo Malaysia cases like which cases needs surgery like which of them >> mentioned madam most of them are self-limiting. Uh we first see them first approach we don't go with surgery.
If the child keeps coming back to us or if the child is not leaving the hospital then we need to do something so that the child goes home. So uh if the child has failure to thrive uh keeps getting admitted for multiple issues, respiratory issues then we automatically get a call then we intervene but we do scope all children with rider so that we know what the child has first so that if the child requires an intervention we can uh tailor the requirement accordingly.
>> Yes absolutely fully agree that all striders are not lingo Malaysia. I have had children who have uh subglottic who had sublottic hemangiomas where um they were told that it's just laryngia and it will go with age. So it is very important that if the child is having failure to thrive if the strider is progressive if there are retractions failure to thrive one needs to scope them and have a clearcut diagnosis uh uh of the strider. So thank you Dr. Bal Gopal Kurup. I request China to have his expert comments.
>> Yeah, I think it's uh nearing the end and I don't think I will be very exhaustive in my comments. Uh it was an excellent presentation Dr. Bal Gopal and I think the need of the hour is our are bright young ENT surgeons like you across the country. Unfortunately there are very very few of them. Uh at least in my hospital we have Dr. Ramen doing a lot of airway work for many many years and we have seen many of these conditions. I have just one question for you.
>> What is your incidence of recurrent you know papillomosis of the airway? Uh >> we get about four to five cases a year.
>> Now with HPV vaccination the cases have gone down. uh we used to get at least 7 to eight cases before but now with uh uh vaccination our uh cases have gone down I mean which is a good thing I'm not saying I wouldn't like to operate more uh good that there are >> now the male so now with the male vaccination it'll go down even further I think so >> I hope so too so anyway uh excellent presentation thank you very much a lot of and the slides are really outstanding congratulations >> thank you sir Uh Jooshi sir any closing comment >> actually I have one uh uh I just want to have point of view of our expert Dr. Jagish sir we see lot of parallel shift in the presentation of the common respiratory pathogens post pandemic.
phenomena of what you call his immune death. what are your expert comment on him on it like >> yeah I think you're absolutely right and I think it's seen globally that there has been a rise primarily in uh two or three things one is viral infections different viral infections especially if you go to see adino virus which was not a very big pathogen has come back as a very major pathogen there other viruses like for example the respiratory sensitial virus again is another major problem which was there before but we just come in. The third thing is that in the viral infections is co- infections.
If you look at much of the uh lower respiratory infections that we see in admitted to our hospitals, we see multiple viruses causing uh disease. So there is a definite increase. The other also issue is the um you know the because of the immune deficit many of them come with lower respiratory rather than the upper respiratory issues. So the immunity definitely has changed and we also are seeing a large you know primarily viral thing but also to some extent myopplasma was an issue which came in a in a kind of an epidemic then subsequently we had also pneumocal necroizing pneumonia and invasive pneumonia. uh so we are having a uh burden but uh there had something has happened after COVID in terms of the immune system of uh the human beings but again the other thing also is that we also faced with the environmental crisis of global warming and uh you know spread of the viruses across many uh countries.
So these are some of the issues and of course the latest now two cases of Ebola being dis discovered in in in India. So that again is going to be a major issue.
Then we had the hunter virus scare a couple of weeks back. So I think with global travel, global warming uh relative uh you know suppression of immune function after covid we are going to have a lot of issues.
>> Thank you. Thank you sir. Excellent pearls of wisdom and for your auspicious presence.
>> I have one question uh for Dr. Kuru.
Yeah, >> I wanted to ask far as uh uh like the comparison between a cold cotry and a laser uh like uh uh from your talk you preferred laser over that uh so just want the comparison of that and is there any risk of ARDS post uh laser use in airways? So >> uh I use very less laser ma'am because the cost goes up uh at VIA where I work cost is a big issue. So I rarely use it but uh the results are superior because I don't touch the tissue much. It's a beam laser so it cuts precisely. I don't need to keep holding things. Uh post laser uh we switch off the oxygen while we use the laser. So there is no laser burns. We take all laser precautions. If there is no uh injury or if there is no charing then it doesn't cause ARDS. We have an evacuation system as well. So the smoke doesn't get uh uh transmitted to the lower airways. So we I have not encountered any post laser ARDS.
So thank you. Thank you. First of all I would like to thank uh our expert Dr. Jagish Shinapa sir. Uh then I want to uh thank all our young guns Dr. Siddhant Lalwani Dr. Kausub Muhit and Dr. Bal Gopal group for the excellent uh sessions which they have delivered.
I want to thank Dr. Sanjiv Zoshi sir and Dr. Renu Buralar madam for uh have for having this brainchild of young uh voices and expert wisdom. Uh so fourth going on with lot of attendance and interest uh by all the general pediatricians. So really want to thank both of them for the opportunity also. I want to thank uh Dr. Pravin Goklay, Dr. Mahesh Sulakshnay and Dr. Sep Carlay uh for uh like planning of this uh session.
Um I want to thank uh our MMC observer Dr. Rajendra Kulkarni sir uh uh for being a MMC observer and uh all the uh EBS and OBS and the most important I want to thank the audience uh for this uh session. So if anyone has any questions they can type it. I don't see any questions up till now. Uh it's already late so I'll just wait for a minute or so.
There was a question in the chat box uh that I saw that whether the biopsies can cause any fulus tracks to remain by one participant Dr. Sapray I think had asked that question. Uh our our young voices and experts can give comment on that.
>> I think Sedat has already answered >> already that's what I saw. So there we we don't we don't get fistulas post procedures madam.
>> So thank you very much and uh good night.
>> Thank you. Good night.
>> Thank you everyone. Thank you.
>> Thank you.
>> Right. And thank you and uh wonderful session. Uh thank you Mahap for this uh invite and uh I must really uh I have learned a lot today. So thank you very much.
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