This video presents a clinical case of a 15-year-old male with uncontrolled bronchial asthma who developed complications including allergic bronchopulmonary aspergillosis (ABPA), demonstrating the importance of comprehensive history-taking, systematic differential diagnosis, and adherence to GINA guidelines for asthma management, including addressing non-compliance, inhaler technique, environmental triggers, and co-morbidities.
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Post Graduate Clinics in PediatricsAdded:
Shall I start?
>> Yeah. Yeah. So, good evening everyone.
Uh I'm Dr. Anis Dave and uh from Gangaram Hospital and uh today our DNB first year Dr. Ana who joined few months back is going to present an interesting case of uh asthma. Uh so she's going to tell us about the case and little bit about the uh uh little bit about the asthma because asthma itself is a very very big topic not able to cover up in a in our time. So Na you may start now.
>> Yes sir.
So uh here is a patient of 15year-old male who resides in Delhi presented to SG on 28th of April 2026 with the chief complaints of cough since 15 days, fever since 4 days and shortness of breath since 1 day. History of presenting illness. The child presented with cough since 15 days on and off type. Initially mild and intermittent, non-productive in nature, non-spasmodic, no postessive vomiting, cough more pronounced at night, associate with noisy breathing, sneezing and nasal block. There is history of seasonal variation and he also complains of fever developed 4 days prior to the admission. Low to moderate grade. Maximum temperature documented 10.1 degree Fahrenheit which two to three spikes per day. Not associated with chills or rigers. No dal variation relieved with oral antipariatic medication. He also complains of history of shortness of breath since one day progressive in nature. Increased work of breathing.
complained of while uh increased work of breathing while climbing stairs.
Negative history. There is no history of ear pain or ear discharge. No history of skin rashes or eczema. No history of mouth breathing or excessive snoring. No history of chest tightness. No history of exposure to known allergen. No contact history of tuberculosis. No weight loss or night. No history of weight loss or night sweats. No history of hemoptasis and no history of chest pain.
Past history.
>> Okay, hold on. Hold on. An hold on.
>> So depending on these few slides, the initial presentation you have said told us.
>> So what do you think this child is suffering with? Now I'm not asking for a specific clinical diagnosis but I'm just asking you about in general when you were taking history what was coming to your mind that this child has primarily >> cough and fever sir >> no >> disease of is possibly suffering with a disease of >> respiratory system >> likely lower respiratory likely a parenyal disease.
>> Yes sir.
>> Right. So >> yes sir >> and the second question to you is why you are taking all these negative histories? You can tell us the importance of all these negative histories.
>> Yes sir. uh history of ear pain or ear discharge is to rule out any or history of URTA or uh rule outitis media and history of skin rashes or eczema to rule out any attopic autotopic triad like uh in bronchilma there is attopic triad bronchilasma allergic rhinitis and attopic dermatitis and to uh to uh no history of mouth breathing and excessive snoring to rule out adoid history and uh history of chest tightness is to rule out uh complicated uh complication of ama and uh to exposure >> coordinate matter for any parenyal disease tightness is a different feeling which only a patient of asthma can feel.
>> Yes sir.
>> Right. And this ear discharge is important because if there is a history uh no he is a 15 year old but in a small child if there's a history of ear discharge or recurrent ear discharge then immuno deficiency is a very you know we have to think of im primary immuno deficiencies.
>> Okay sir. Similarly for a patient to skin rashes or ear discharge combination with chest uh issues then then you always think of uh LCH >> of course >> okay then history of tuberculosis is obviously >> yes sir >> then weight loss why weight loss and night sweats >> is to rule out tuberculosis or >> any chronic infection or any chronic infection yes sir M >> and to uh no history of hemoptasis uh to rule out any bronchectasis or bronchectasis history and uh no history of chest pain.
>> Okay, go ahead.
past history. Uh at the year of 2016 when he was 6 years old, he had uh multiple episodes of recurrent cough where he showed to the nearby clinic and had taken symptomatic treatment which was undocumented and uh and he had a uh he was asymptomatic for one one two years and then in the year of 2019 he had similar episodes of recurrent cough. So he went to the uh private clinic nearby where they had done the pulmonary functions test and they started on uh inhaler inhaler corticosteroid but he was non-complent he taken only for one year which was on and off and lost to followup due to covid in the year of 2021 similar complaints he had persistent cough he went to the different private clinic and there also they started started the inhaler meter dose inhaler corticost uh corticosteroid for one year and uh which he did not continue. he stopped on on his own and in between 2021 and 25 he had uh no severe symptoms of cough. Uh uh and then in 2025 he was admitted in SGS with complaints of abdominal pain and constipation and complaints of cough. uh uh gastro reference was sought and was managed conservatively in in view of cough on chest findings and inhaler for aoc 200 microgram microgram BD one puff BD was prescribed but they did not continue it and uh there is a history of taking aya medication uh for the mentioned complaints of abdominal pain which he mentioned he got relieved after taking Right.
>> Okay. Ana, one precaution to all the DNPs including you that during presentation and during exam don't mention forot. You do not mention the marketing name of brand names.
>> You mention you say the child was put on inhaled corticosteroids with long acting betagonist for lava.
>> Yes sir.
>> Okay. That's a precaution every DNB should take.
>> Yes sir.
Birth history full uh full term uh LSS m because of muconium stain but he cried spontaneously after birth. There was no history of nu stay family history.
>> Okay go back go back go back go back.
>> Now you tell us the importance of each of these factors.
You know this child has asthma.
>> Yes sir.
>> So what are the what are the risk factors at birth or in the neonatal period in the or in the perinatal period which are associated with the asthma in childhood.
uh muconium stain if mucconium aspiration happens >> that can cause into uh repeated infection and there can be bronco pulmonary displacia.
>> No that is a different disease that is a dis different spectrum.
>> Yes sir. Mhm.
>> So at birth the risk factors which are associated with as childhood asthma are prematurity.
>> Okay. That is early early visas they're under five visas what we used to call them.
>> So now they prematurity low birth weight monium strain lier all these are important histories one has to take.
>> Yes sir. And of course the patient is symptomatic uh without all these risk factors but still symptomatic and has nose block or cough from the early neuronal period and presents to you uh with wheezing then we should keep in mind the one of the differential diagnosis of primary celery disynesia PCD patients do quite often they present early neuronal period. Yes sir.
Okay.
>> Yes sir.
>> Uh family history there were no his family history of bronchila no contact history of tuberculosis. There was a history of allergic rhinitis in father uh where he used to take uh symptomatic treatment legoin and it used to get relieved on its own.
uh developmental history no developmental delay. He had a good school uh scholastic performance and he was good in academics.
Nutrition history there was no deficient in the nutrition.
Immunization history he was humanized till date as per national immunization schedule.
Socioeconomic history head of the family is grandfather. The number of family members who stayed together are 11.
Housing 3 BHK uh paka house filtered uh drinking water they use. There were no history of any indoor plantation. No history of any contact to pet animals or any smoke or any construction work nearby. Uh uh sanitization and hygiene was good. No smoker at the home. overcrowding was present and belongs uh he belongs to lower middle class according to kusquami classification.
So what is the importance of all these features that you have asked?
>> Uh so the number of family members uh s shows the there is a overcrowding in the home which can cause repeated infection uh I mean uh allerg respiratory infections.
Yes sir.
>> Okay.
>> And indoor uh history of indoor plantation moisture uh that also can cause infection like fungal infection.
History of pet animal is that uh like non allergic trigger like poland dust smoke >> pet animals and uh smoking like uh cooking whether it's uh normal gas or uh wood would be like cooking use by using wood and uh by sanitization and hygiene if it's good or Yes, it's very important to take the history of any type of smoke in the house. Whenever you tell the parents what are the sources of smoke in the house, they always think that we are talking about cigarettes.
>> They they will never accept that the bbati can also produce the smoke because that is that is part of their household.
So we have to go into the detail and dig out dig on these questions and you know get an reply on these particular aspects. Second uh uh another thing which you should add in the socioeconomic history is exposure to pigeons because there are there are many people are living in flats you know the multi-story buildings or uh you know uh first floor, second floor, fifth floor and there is always a shaft in the house and these shafts are are housing for pigeons. Yes. So they have exposure to they have exposure to pigeons.
>> Okay sir. Okay.
>> Right.
>> So we have to go into these details and exposure to cockroaches.
>> Yes sir.
>> These are important histories.
>> Yes sir.
>> Hello.
>> Yes sir.
>> Hi. So summary 15year-old male born of fullterm ls delivery belonging to lower middlecl class copus scale all developmental milestone achieved normally and fully immunized with no dietary deficiency of calories and proteins known case of bronchilma non-complent to medications was admitted in our hospital with a chief complaints of non-productive cough associated with rhinitis and history of seasonal variation along with acute onset of low to moderate grade fever without cells and riers and comp and increased work of DIY.
Differential diagnosis based on the history is first my first differential diagnosis is uncontrolled ama or difficult to treat amma ama with LRTA which can be due to bacterial or viral infection or complicated ama with uh suggestive of ABPA or pulmonary TV.
Generally >> Ana ana go back go back go back one slide more okay this is the history no go further go further next slide please yeah this is a differential diagnosis you have to justify you know give points for and against >> yes sir uh uncontrolled ama difficult to treat ama is mainly he was not complained multiple times he has been prescribed incorticosteroid But he was not compliant throughout his course. And Aama with LRTI bacterial or viral because cough was associated with fever which can be a cause of bacterial or viral and um complicated ama with ABP or pulmonary TB had a chronic cough for 2 weeks. So that can be uh comes to pulmonary TB.
>> Hello.
Uh is there any point against the diagnosis of asthma? Forget about difficult asthma or uncontrolled asthma.
Yes sir.
Uh I I don't know sir.
>> No. So what is the definition of asthma?
>> Ama is chronic obstructive disorder where there is revers it's caused because of uh reversible bron bron bronchial changes.
>> No that is not the definition of asthma.
You are you are giving a pathological or pathophysiological definition of asthma.
What is asthma? How do you define asthma?
>> Uh sir, um aa ama is like a obstructive disorder which is characterized by the uh reversible airway obstruction >> and with recurrent episode of cough, chest tightness, breathlessness.
So it is a disease where the cough is dry. It is a non-productive cough with with with airway hyper >> variable variable expiratory obstruction.
It's a disease of obstiratory obstruction.
>> Yes sir.
>> Okay. So it's a disease of chronic cough with chest tightness, non-productive cough with variable expiratory obstruction and and with reversibility >> or response uh reversibility is now changed to responsiveness. Now the reversibility is no more used. Now the term that they use is responsiveness to betaist.
Okay sir.
>> So there is no doubt about the asthma but uncontrolled asthma. Okay. We'll talk about it later.
>> LRTI you're saying because he has a history of fever ur and all.
>> Yes sir.
>> Yeah.
And complicated asthma is because you're saying because it's a long history >> since two weeks. Yes sir. Yes sir.
>> Yeah. So that is a query query thing.
Right. Go ahead.
uh general examination uh on time of admission the temperature of the patient was 99.4° 4° F. Pulse rate was 112 which is regular normal volume and character.
Respirator rate was 28 cycles per minutes and SPO2 was 93 percentage on room. Blood pressure was 112 uh 68 mm hg. There was no paral, no icus, no sinosis, no clubbing, no lympidopathy, no pedal edma.
Head to examination, skin, no uh articular or eczema. There was no rash.
Eyes no redness, no watery discharge.
nose. Uh there was bilateral nasal cavity, purolent discharge, severe DNS towards the right. Oral examination, gray to tonsil, there was good dental hygiene.
Neck, there was no palpable lympadinopathy.
Chest elliptical in shape, bilateral symmetrical, abdomen not distended, umbilical central and no dilated veins.
Anthropometry his weight is 45 kg, height is 160 cm, BMI is 18 which is between 15 to 25th percentile systemic examination.
>> So, so you said that he had good nutrition. He there was no deficit in nutrition but his height and weight both are uh below 50th percentile.
>> Yes sir.
Below 50 is entire. What is the explanation for that?
Do you have any explanation for that?
>> No sir.
>> No can be constitution.
>> Yeah. Usually asthma patients are are not deficit uh they don't have growth deficit but if they have associated chronic infections particularly ABBA or when they develop bronchitis uh because of the chronic infection or because of uh because of uh ABA or because of tuberculosis particularly in Indian scenario then there can be possibility. So if there may be a discrepancy uh discrepancy in the nutrition uh what you have been told and uh you know that may always explain. So this this is quite a significant growth retardation.
No.
>> Go ahead.
Systemic examination RS examination uh inspection chest shape was elliptical and symmetrical chest movement is reduced bilateral typia was present prolonged respiratory phase use of accessory muscle present no chest wall deformity scars or sinuses.
Palpation trachea felt to be in the midline.
Movement with respiration chest expansion is symmetrical on both side.
No intercostal tenderness. Vocal fame is normal. Chest circumference on inspiration 84 cm and on expiration 78.5 cm.
RS examination on percussion was resonant in supraclavicular, intraclavicular, mammary, axillary, infrailary, suprascapular, intertcapular and intrascapular region.
>> Can you go back to the previous slide, please?
>> Yes sir.
>> Chest circumference.
What do you expect in patients of asthma?
>> Yes sir.
>> What what what do you expect in patients of asthma? What type of chest deformity types of deformity do they get?
>> H >> uh they will have because of they can barrelshaped chest >> barrel shaped section that is because of >> that is because of >> increased >> chronic chronic expiratory obception.
They they they are they have air trapping.
>> So that is why their entroposed diameter increases.
>> Yes sir.
>> That is why there is a barrel-shaped chest.
>> Yes sir.
>> And and the and the difference between this is 84 and 78. It is almost 5 and a half cm.
I think this is more.
So there may be some air trapping happening at this stage because of the chronicity possibly. Yes.
Okay. Go ahead.
>> Percussion felt resonance in all.
>> Yeah. Yeah.
Go ahead.
>> Assultation normal vascular breath sound heard in all the areas. There was bilateral air entry was present.
Expiratory V present on bilateral diffused lung fields. There was no creps.
Other systemic examination cardiovascular system S1 S2 her no murmur abdomen soft not distended labor and spleen not palpable CNS conscious oriented no focal neurological deficit there is no managial signs >> okay particularly in obstructive airway disease or any chronic respiratory disease during examination don't just forget to say P2 P2 not loud or P2 normal because whenever you have P2 loud it indicates there is a chronicity of pulmonary system. So there can be a possibility in a particularly in adolescent child it is very important.
So particularly mentioned that there are there P2 is normal.
>> Yes sir. So loud P2 is is indicative of a of >> pulmonary hypertension >> pulmonary hypertension or culmin for that matter. I'm not saying particular in asthma but in any respiratory case you should always uh you know speak that the P2 is normal.
>> Yes sir.
M >> summary 15year-old male child born with full-term LCS delivery belonging to lower middle class copus scale all developmental milestone age normally fully immunized with no dietary deficiency in calories and protein and known case of bronchial amastema was admitted to a hospital with chief complaints of cough fever and increased work of breathing associated with noisy breathing on examination the child was taknic with intercostal retraction and bilateral expiratory vis was present.
>> What is your diagnosis now? Okay.
>> Uncontrolled bronchial asthma presenting with acute exasperation is my >> what are the causes of what are the causes of uncontrolled asthma?
>> One is non-compliance.
non-compliant to >> uh to the medication >> and uh um and the uh usage of not usage of MDI spacer and uh not proper technique.
So uncontrolled bronchilasma.
>> Yes sir.
>> What are the causes? What we these are this is very important. If you do not recognize those features which are responsible for uh uncontrolled asthma then how will you how will you treat this child?
Yes like not uh complaints is one thing and one more thing is no proper technique usage >> uh >> and uh uh other like environmental triggers around by >> uh dust poland >> and um recurrent viral infection that can trick cause even more complication.
>> So that is overcrowding.
>> Yes sir.
>> This child has overcrowding.
>> Uh yes sir.
>> So there are many factors which are responsible for uncontrolled asthma in this child. First is non-compliance. So many times he started and he stopped treatment. Then second is inhalation technique.
Whenever a patient like this comes to the clinic or in the hospital in the OPD we have to we have to uh ensure that the inhalation technique is correct. We can we just don't assume that we have told the patient on the last visit. That is how it is. He's going to you know must be taking his medications properly. We should not assume every time they come we always ask them to bring their uh inhalation devices and then we go ahead and always get a demonstration done or ensure that the technique is correct.
>> Okay. Many times they they just especially for the MDI they just keep on using it uh the you know empty canister they do not now the most of the MDIs are with counter dose counter but previously when the counters were not available those counters were not available then they they discontinued because some bit of gas you know the carrier gas or vehicle gas used to be there so ensuring the adherance ensuring the technique.
Then you said overcrowding. So these are the environmental factors. Then what else? Exposure to allergens. Indoor or outdoor allergens.
>> Sure.
>> Then always look for co-orbidities.
So what are the co-orbidities which are associated with asthma?
Uh comora like viral infections.
>> That is not that is that comes with the overcrowding.
>> Yes sir.
>> Uh he had he had allergic rhinitis and uh >> yes allergic rhinitis as you said nasal septum as you said.
>> Yes sir. Okay. Then second another attopic dermatitis.
>> Dermatitis.
>> Allergic allergic conjunctivitis.
Adinoidal hypertrophy.
>> Yes sir.
>> Okay. So whenever you are treating these patients you have to treat all these features all these associated problems.
Then only your child patient will respond to treatment of asthma.
always do uh you know you have to see for the overweight or the obesity >> obstructive sleep >> that's a that's a very very important uh co-orbidity >> yes sir >> so all these co-orbidities you have to take into account rhinocitis atic dermatitis allergic conjunctivitis then uh uh uh obesity even smoking in the house any type of smoke exposure in Indian families especially Hindus the the hams are very common they do hmon at home so that's very common so all these things need to be considered before you label this child okay there everything is clear so I have to modify my treatment I have to step up my treatment so every time a child comes to you you don't go into the history and details of these issues and you Just increase the dose of inal corticosteroids that is not going to help you.
>> Yes sir.
>> Okay.
>> Yes sir.
>> So why did you write acute exuberation?
Was this child in actual acute exuberation?
>> No sir but he had one day history of increased work of breathing.
>> That can be because of asthma only. No.
>> Yes sir. Or there may what is the classification of acuteation?
>> Mild, moderate, severe, >> mild.
Read about it.
>> Yes.
>> Okay. Go ahead.
>> Investigations.
This hemoglobin was 15, TLC was 12,000.
DLC neutrfilic picture 82 and lymphosy were 11. Absolute eosinophilic count was 126. Absolute neutrfilic count was 10,348.
Apa panel was sent. Total IG was 1.
Hello.
Hello.
Hello.
Your voice isn't cut. We can't hear you.
Yes, sir.
>> I'm joining you.
Good network is going Sorry sir. Uh >> yeah go back to the blood investigation start from there.
>> Yes sir.
>> Investigation.
>> Uh his ABPA pan uh his hemoglobin was 15 total lucaside count was 12.62.
Differential luccoside count neutrfilic picture was 82. Lymphosy was 11.
Absolute eosinophilic count was 126.2.
Absolute neutrfilic count was 10,348.
ABPA panel total IG was 1,985.
Aspel specific IG was 5.05. Aspel fumigator specific IGG was 28.10.
Attopic screening test fattop was 9.27 respiratory bophile came positive for human rhino virus.
>> So what is your interpretation of these investigation?
uh the main uh ama which aggregated first main because of viral infection >> and his as his total IG was raised and ABPA panel showed asperella specific IGG is also raised so can be because of asperilosis p in asperilosis uh infection fumigatorus infection And what about far? What about fartop?
>> Fiotope is a little contradictory thing like in attopic screening test fiotop usually asperellis is not included in this >> but this is raised.
>> Um >> so why it is contradictory?
Why it is contradictory? M >> actually a topic this far top screening includes house dust mite and and few fungi but not espilus >> and family cockroach is not there. So mainly the HDM HDM means house might.
>> So this child may be originally sensitized to house might that is why fartop is significantly positive and he has now acquired he sensitized to now espilas also >> it is very much possible.
M we have to go in for you know uh further testing especially uh in such a case we should go for the skin pre testing so this >> yeah go ahead >> uh it it is a PA view and it's showing uh increased broncovascular marking hard borders are visible able and uh hyperinflation of the lungs are seen >> central.
Any other feature? Any other feature of uh hyperinflation? What are the features of hyperinflation in this?
Increased lung fields. Um three.
>> What are the features of uh hyperinflation?
>> The uh lung looks more h uh radio >> more >> lucent uh radolucent.
They're more dark. Okay.
>> Yes. Yes. In simple words, they are looking more dark.
>> Then second, >> second >> and third, >> second uh diaphragm. Look at the diaphragm.
Hello. And uh hello >> diaphragm diaphragm.
>> See the diaphrag flattened sir.
>> Yeah diaphragms are flat. The dome is gone.
>> Yes sir.
>> And >> how many intercostals number of uh anterior and posterior ribs.
>> What is that? 1 2 3 4 5 6 7 >> eight. almost eight on the right side.
>> So how do we define hyperinflation?
>> And there is more than eight ribs.
>> Eight or more than eight, right?
Sometimes some people say nine also.
There's one more feature.
>> Tubular heart you see.
>> Yes. Very important. Heart looks small.
>> Yes sir.
>> So these are the four features here.
Yes sir.
Okay. Bronco marking is a very very non-specific thing. It is not at all suggestive of obstructive airway disease at all.
>> Yes sir.
>> Okay.
What what next you will do?
>> Uh HRCT.
>> Why?
>> It is to look for any parental changes.
In view of In view of >> hyperinflated lung field.
>> No.
>> In view of >> AB. Uh >> yes. In view of >> APA.
>> Sensitization.
>> Sensitization. Yes.
>> Sensitization.
>> Yes sir.
>> Espilla sensitization.
>> Yes sir.
>> Okay. ABPA is a disease. Espilla sensitization. You still not sure whether it is disease or it is just a sensitization.
>> Yes sir.
So here uh it reveals bilateral lung mo.
>> What type of what type of window is this?
>> This is what um >> in CT scan you see one some frames are more dark some frames are like that like this. So what is this?
>> This is what is this? Yeah.
You have one more frame. Go to the next frame. Next slide.
Oh, you have removed that. Okay.
So, there are two windows. What window is this?
>> What window is this?
This is lung window.
>> When you want to look at the para then you look for window lung window. When you are concentrating on the heart or the media other media spinal structures then we look at the then we look at the >> lung window medinal window. This is lung window where you can see the lung parind.
I think you're gone again.
No.
Got up.
Got up.
Go up.
Hello.
It's not Hello.
>> Yeah. Go ahead.
>> Yes sir.
So um in this HRCT we see mosaic pattern with air trapping and uh with bronchial wall thickening and um mucus plug secretions.
>> Can you can you can you pinpoint to that?
>> Yes sir. Uh mucus plug secretion.
>> Yeah. and air trapping. We can see the difference. Here it is dark and here it is comparatively lighter >> and >> and mosaic pattern can be seen. So >> this is whatever you're explaining is is making the mosaic pattern. No.
>> Yes sir.
M and >> and bronchial wall thickening with the mucus blood.
>> Okay. Is there bronchial places >> in this?
It's not seen. So uh what is this where you are pointing out?
What is this? There's a long streak going towards the periphery. Yeah, this one >> bronchasis changes.
>> No, this is not bronchasis.
This is not bronchasis. This is possibly segmental latasis or it's a fibrootic band.
>> Yes, sir.
>> No, this is not bronchitis. The bronchial wall thickening evidently seen uh as as you pointed out and on the left side as you can see the signaturing type of thing. Yes sir.
>> Yeah these one.
So these one also the bronchial. This is a cross-sectional view and the other one is the the along the length of the bronus and there is retention of the secretions.
>> Yes sir.
>> Okay. The bronchitis is not yet evolved but likely to evolve looking at all these changes.
Right. Go ahead.
Next slide and name >> HRCT report.
>> Okay, you have so said that. Okay, go ahead.
>> So we had done the impulse oscillator in this patient to look for the broncoilator response.
um in this uh this lighter color shows the pre- bronco dilator and the darker color shows the post broncoilator effect. So at the five hertz region there is a increased amplitude which shows that small airway uh airways are responding to the broncoilators which is suggestive of small airway obstructive disease where there is reversibility post broncoilators.
So let me tell to tell all the DNB students here that oscillometry is not the standard investigation for judging the obstructive airway pulmonary function that is spyometry is the standardized thing. It's a validated and standardized tool. So in exam don't say oscillometry as a first but if the examiner ask you which what how will you assess the reversibility or responsive responsiveness to bronco dilator so please say spyometry don't say oscillometry oscillry is yet not a standard of standard investigation or for the asthma patients right but as she has rightly said at five hertz that is sound waves there is a reversibility so it's It's a pure small airway disease. So this is another talk you know it's a impulse osometry or oscillometry is different talk. So we'll not go into these details. Okay. Go ahead.
>> Go ahead. Yeah, >> we had planned uh we had done the broncoscopy on fourth >> which showed cell count 85 per uh and RBC cells was 1,000 corrected TLC was 83 pH was alkaline cell type neutrfilic picture was 64%age lymphocytic picture 36%age absolute eosinophilic count was zero and the gram stain was negative TB gene expert MTB was not detected Koh fungus was negative. Galactoman and asperilus is yet to come.
>> Why the broncoscopy was done?
Asthma patient don't need bronoscopy.
>> Yes sir.
>> Then why it was done? to look >> uh to >> look for the uh aspirus.
>> So you already said that this in in CT scan there was evidence of uh retained secretions. Okay. Bronchial secretions.
>> Yes sir. So it is very important to uh you know do the lavage and see for any any tuberculosis or any CT doesn't differentiate will not tell you everything about tuberculosis or AVPA we already know that the child is sensitized to esperilus but the CT scan is showing retention of secretion of the bronchial secretions fluid fil broni so important to rule out secondary infections and then to rule out tuberculosis And if there if this the Q comes positive then it becomes a case of invasive espigilosis.
So when you grow aspigilus from the bell in a case like this. So then it becomes a case of invasive bronco the treatment becomes little more uh you know it's a different type of treatment.
So that is why it is important to do broncoscopy and lavage in these patients.
Yes sir. Okay, go ahead.
>> Ama is a chronic inflammatory airway disase which is characterized by reversible airway flow obstruction and airway hyper responsiveness treatment of ama in this child gina guidelines 2025 as he's 15 year old. So based on adjust review assess method uh there are two tracks track one and track two. Track one is usually the preferred one where uh in step one and track one is more we preferred one as we use inhaled corticosteroid formol is used both as a controller and reliever. In step one and two we use low dose of inhaled corticosteroid with formol. In step three low dose as smart maintenance therapy therapy and step four we use uh medium dose maintenance inial corticoststerol and in step five we add llama and biologics like antiig and antiil 5 antiil4.
So this is at every step you have to go back. You can see a uh circle on the top review, assess, adjust, adjust.
>> So this circle has to be followed on each visit.
>> Excellent.
>> On each visit you always have to go look look at these the treatment non-farmacological studies asma medication including ICS education and training of the patient confirmation of diagnosis. Whenever the patient is not responding always go into the modifiable restractors, lycomorbidities, inhaler techniques, adherence that's what we have already talked about and the patient and the parent given preferences and the goal. If they are not happy with with the MDI, you give them an alternative.
So it's always and as far as the review is concerned, you always go into the details. Why are the exhibitionations?
Why are there any side effects? Are there any co-mobilities? Are the what are the lung functions at this moment and consider the uh biomarkers if you want to do bio what are the biomarkers >> IG IG >> IG >> IG pheno fractional excretion of nitric oxide that is a biomarker for this all these guidelines have revised every year Gina Dina 26 released this this week only recently in May.
So Dina 26 is available on the net now.
So this is a different now but okay then anything else you want to tell us now.
>> Uh so based on the methods if the patient is responding well and patient is if suppose uh the patient is in step three treatment and is responsing well we step down to step one and two >> after how much time?
Uh >> right >> that is important. You see if the patient comes to you and you give step three after two weeks he comes where he says I am all right I have no symptoms will you will you bring down to step one two no change for 3 months.
>> Yes sir.
>> So he has to continue step three treatment at least for 3 months.
>> Okay sir.
>> Go to next slide now.
Uh what is uncontrolled ama? Difficult to treat ama and severe ama.
Uncontrolled ama is uh the patient who has poor symptom control who has frequent symptom activity limited by ama because of ama symptoms and night walking due to ama. And if there is frequent exasperation of more than two episodes per year that requires him or her to have oral corticosteroid or severe exasperation more than one episode per year which requires hospitalization.
difficult to treat ama that is uncontrolled despite prescribing medium or high highdose inhaled corticosteroid with second uh controller or with maintenance oral corticosteroids.
Severe ama is a subset of difficult to treat ama where ama is uncontrolled desp despite good aderance to the optimized high dose of inhaled corticosteroid lava treatment and it is also called as severe refractory ama.
>> So severe asthma is a subset of uncontrolled asthma.
>> Yes sir. not difficult to control as right.
>> Yes sir.
>> Okay go ahead.
>> So am aa and abpa correlation if any ama which is poorly control uh controlled and if there is recurrent exasperation with elevated IG with elevated eosinophilic count we have to suspect ABPA.
Diagnostic feature of ABPA uncontrolled ama with total IG of more than 1,000 international unit per ml asperella specific IG increased with peripheral eosenophilia with central bronctasis changes on HRCT the stage stage wise management of patients with ABPA any patient who are newly diagnosed with ABPA we should start with oral gluccocortic corticids or itchonazoo for 4 months and we have to follow up with spyometry and serum total IG and chest X-rays radioraphs and we have to look for the response. If the patient is stable for 6 months the patient will be in remission.
If not then we have to start oral gluccocorticoids or itchonosol for 4 months with frequent oral gluccocorticoids and itchonosols for 4 months and then treatment dependent ABPA is with oral azoles anti-ype to biologic biological agents or nebilized amphoterisin or low dose of gluccocorticids.
Management of ABP is mainly with oral corticosteroids atroconosal antifungal therapy and to optimize the ama control.
So uh so this patient comes under abpaab criteria.
So based on the HRCT finding if there is uh no bronchasis only cerological test will be pres positive then it is categorized as APA S and if the patient is having bronchasis changes it is categorized as ABPA B and if the patient is having mucus plugs in the SRC finding uh uh it is categorized as APA MP And uh if the patient is having uh central uh and here in our our patient the childhood the patient had child history of ama with sensitization of aspergilus fumigatus IG with total IG was 1,985 with increased eosinophila and aspergilus IGG and here suggestive of APA the bronchitasis changes.
This is not exactly bronchiticis but yes the the where the we could see the thickening of the bronchial wall it is all central and likely to how do you say that the bronchasis is there >> based on the HRC finding >> HRCT finding but there are criteria that the the size of the bronchi and the pulmonary vessel pulmonary artery the pulmonary artery is bigger than the bronai Okay. So when the bronchi becomes equal or rather more than the more than the diameter of the pulmonary artery then it is bronchitis.
Okay. That has yet not happened in our patient but yes we have to treat him for asthma and ABPA. Okay. Next.
Thank you. So uh any questions in the chat box?
Nobody has written any questions.
>> You can unshare na.
>> Yes sir.
>> Thank you sir.
>> So this was a case of childhood asthma who has now gone into the complication of APA. So we have to treat both. But very important is as they were missing the treatment for so many times. So we have to ensure that they don't miss the treatment and child if we can save the child from going into uh bronchitic tasis complication that would be good.
Okay if there are no questions in the chat box no queries then good night to everyone.
>> Good night.
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