UDLCO CRH: Residency curricular evolution from apprenticeship formative assessments entry to written summative assessments entry

Summary 

The conversation provides a detailed historical narrative of the evolution of residency curricula in India, focusing on the transition from the *1+2 system* (one-year house job followed by a two-year MD) to the *three-year direct PG system*. The participants recount their personal experiences during residency, including the challenges of intense workloads, competitive exams, and significant strikes that shaped postgraduate medical education. Strikes by Resident Doctors' Associations (RDAs) in the 1980s and 1990s were pivotal in standardizing the three-year postgraduate (PG) curriculum across India. The discussion also highlights formative assessments during the older system, the introduction of thesis requirements in the modern curriculum, and the camaraderie, hardships, and institutional politics that defined the residency experience.

Key Words

- *Residency Curriculum*

- *1+2 System*

- *Three-Year PG Program*

- *Resident Doctor Strikes*

- *Formative Assessments*

- *Summative Assessments*

- *Medical Council of India (MCI)*

- *NICU/PICU Duties*

- *RDA (Resident Doctors’ Association)*

- *PGI (Postgraduate Institute)*

- *AIIMS*

- *Singularity of Events*

- *Camaraderie*

- *Workload and Pressure*

UDLCO Keyword glossary:

http://userdrivenhealthcare.blogspot.com/2023/11/glossary-of-user-driven-healthcare.html?m=1

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Conversational Transcripts:

[31/08, 22:50] hu1: Yes… it was really tough back then, with no DM seats and only 10–15 selected for MD each year. Unlike now, where almost every department has 40 MDs and 4 DMs, per year our journey was very different.

I was mostly posted in NICU and PICU, and I hardly remember much of OPD postings. Even when I did get OPD, I would often be shifted back to ICU as replacement. Nights in PICU were intense—I would wake up to the sound of alarms in the middle of the night even after completion of night duties . After long duties, we would eat at nearby dhabas or relish the frozen food kept aside at the South Mess by Kalyan (the ever-smiling guy).at 12 MN 😊

Because we were in a separate building, a little away from other departments, we all shared great bond with batchmates, juniors, and seniors /staff . My ICU duties were made tolerable thanks to the great company of @⁨& @⁨ @⁨ and many other contemporaries. My teachers were truly caring and supportive—many of whom I’m still in touch with even today. 

During those years, we built our own little world inside that building. I maintained the “coffee club” for almost two years, and we celebrated birthdays, small get-togethers, and countless moments of joy amidst the workload. Though it was three years of hard work, plus one more as SR, they are memories I deeply cherish.

I truly miss my residency days… unforgettable times that I could easily write a memoir about. 🥰

[01/09, 06:27] hu2: How are the work demands today in ...?

Are there more residents per bed or is it still as demanding?

Who does the sampling and basic case sheet maintanence?

[01/09, 07:26]hu3: Demanding ..🤔hmm

Recall 1 house surgeon ..me.on alt days ,..2 jrs 1 year ahead of me sharing alt with me.

With the damocles sword of 1 plus 2..I.e.no guarantee of a pg seat, needed another all india exam to clear..

36 hours official duty for 8 hours sleep

We had to organise a strike to get a 3 year direct pg for the rest of you ..

Deserve a plaque in our honour..mine and preceding batches..

[01/09, 08:39]hu4: Yes, those days 1+2 were very tough...the tension of no guaranteed PG seat after a full year of Donkeys Job.. Fortune has to smile twice at you before one walks out of PGI - Pressure Generating Instrument. I know a few people had to quit the Institute due to the Pressure of Work and Study!

[01/09, 08:46]hu5: 1+2 Means ??

No guaranteed seat ?? Elaborate sir

When selected through entrance why not guaranteed seat ?

[01/09, 08:53] hu6 : I don't think entrance exam existed in their time..

[01/09, 08:54]hu5: Ok 

Then selection basis ?

[01/09, 08:54] hu6 : @⁨  Enlighten the curious minds sir.. I dunno..😅

[01/09, 08:55]hu4: Practical Exams  interview

[01/09, 09:01]hu4: Before 1983, ... entrance exams were of a 2-point entry. The first entry exam is only a Theory paper with Negative marks, each MCQs have 5 options to mark YES or NO, similar to MCRP exams. The toppers select Medicine, Paediatrics, Surgery & OBGYN. This is for a one-year term to work as a House Physician in the selected departments. At the end of the Year, again sit for a PG entrance exam comprising a Theory Paper and a Practical, including a Viva Voce, for a 2 Year MD/MS exam with no Thesis.

[01/09, 09:11] hu4 : _The Clinical Skill test in Medicine comprises 4 sections, each with 10 marks. All are Objective in each System: Neurology, Cardiology, Respiratory & GE. One may be asked only to inspect, palpate, percuss, or auscultate. Only 3 Questions - Diagnosis, 3 relevant Labs to confirm the diagnosis, and the treatment. Viva is a rapid-fire test. Ten questions are asked to all the examinees, and the one who answers the most, of course, gets selected. The theory portion in the chosen subject has 50 marks._

[01/09, 09:45]hu3: Good summary..

This lead to a piquant situation..

Where after 1 year of " Hamali" where one couldn't study..you faced another all india exam with diploma holders from all over india..often top students with experience. 

The viva in this exam provided you made the theory grade ( i know some who did not )  now became a test indeed..because your practical experience in phlebotomy, general sucking up, and running around doing unskilled work,  was pitted against real practical experience..

In general medicine, peds etc,  say 4 Seats..there were 4 internals, and 8 externals..and at least one dch brain from bengal and one MLAs connect..

So 2 persons would be left hanging around hoping for an act of God.. or reasearch post

The home state bridges would have been burnt so no going back..

[01/09, 09:45]hu3: Nobody had the guts to protest.

[01/09, 09:46]hu3: The association office bearers were basically trying to ensure they got Best outgoing awards

[01/09, 09:47]hu3: So how did it change..?

[01/09, 09:49]hu3: If anybody is interested indicate this old man will share.🙂

[01/09, 10:32]hu7: This is amazing and I wonder if all this has been formally documented somewhere and if not it should asap!

I guess they were trying to forge an apprentice model that may only be assessed formatively and the upcoming summative assessment evolution was just short of bursting forth into the firmament that created this unholy atmosphere that you have so well outlined here

[01/09, 10:33]hu7: Do we have the contacts of those who had to return after a year? What happened to their careers eventually?

[01/09, 12:17]hu4: That's true. 4 long cases in Medicine - in each System of Neuro, Cardio, Respiratory and GE. 

Each case may have multi system involvement and to face 8 examiners.. luckily, most of the candidates pass out due to objective assessment.

Cases are first given to the external examiners to take History including Physical examination and note down their findings. 

When they examine the candidate they are supposed to match with their own findings, if the candidate scores equal, then only one passes. 

During my exam, my Cardiac case was Mitral Stenosis.  The Cardiologist who examined me wanted to fail me as he missed PSS - Progressive Systemic Sclerosis in the same patient. 

The system did not allow him to fail me as he himself missed a major disease in the patient. My HOD won the argument and I was promoted. 

He further advised me not to allow any one in my practice to fail me.

[01/09, 13:01]hu8: It means that you had to do one exam to be selected for house job/ man as it was called then . After one year house job you took another exam for getting a PG seat for the 2 year MD course- no guarantee. 

For example I did 6 months house job in Bangalore and the next 6 months at ... after taking the entrance. In the first 6 months you didn't get any of the coveted postings( cardiology, neurology,chest etc) which would help you in the entrance for the MD. My first posting was the private wards. 

As a back up during the MD selection,I had appeared for pathology also

The MD entrance was a written and practical exam

[01/09, 13:06]hu4: Yes, I know several people who couldn't make it at the First entry or the Second, many had their fortunes overseas. Incidentally, while working in Gulf, few Members and Fellows from Royal College recognised me and admitted that they did not make it PGI and soon left India did PLAB and after their training from UK they came back in the same Hospital where I was working with 3 times the Salary of mine. Sadly, Postgraduates from India are recruited as Specialist and Members, Fellows from Royal College as Consultants 😔

[01/09, 13:22] hu7: This is an amazing history around ... that i learned for the first time today

[01/09, 13:32] hu4: Those who attempted to get into PGI and could not make it also has carved a niche in our Profession. As matter of fact getting a Call letter  - Interview is in itself is a honour as there is a pre Test Screening. Only 500 people during my time are called to take the entrance. Only 50 get selected . I do not know now, may be the same system except it is One point entry with 3 Yr PG with added Thesis.

[01/09, 13:37]hu4: Answering the Query of hu3, the system of 1+2 changed to One point entry to PG after RDA went on strike during 1982 which was never heard of in ... and after a Roar and Cry  administration recommended 3 Yr PG course to MCI and was soon implemented in 1983.

[01/09, 14:14] hu4: Adopted Standardization Across India

- The Medical Council of India (now replaced by the National Medical Commission) standardized postgraduate medical education to ensure uniformity.

- Most MD/MS programs across India are 3 years long, so PGI aligned with national norms

[01/09, 14:16] hu4: Could any one tell me still PGI & AIIMS conduct their own entrance for PG or is it INI - CET ?

[01/09, 14:17]hu3: Aha..as one who was a jt secretary of the RDA who organised the strike..lots of trivia to share

[01/09, 14:19]hu4: Which batch was yours hu3 ??

[01/09, 14:22]hu3: It started innocuous.. a patient complaint against an SR who couldn't attend as he was doing a procedure.

... Administration set up an inquiry and found the concerned doc guilty..😳

He  finds this when he reads his name in  the Sunday paper

Everybody is furious..no amount of Bete..tussi naraz  na hona..pacifies

The RDA head has Akali connections so the association is emboldened

The strike in right earnest complete with parallel opds ..near the car park

Mess is closed..🫩

 The minister comes and is presented with a 16 point charter of demands..

Reinstatement of doc..etc.. but 4th point..3 year direct ms/MD.. 

The minister asks the ias ..he asks director..long explanation..to which he asks again what is system in AIIMS..3 years..so why this 1 plus 2 ..

Voila a 10 year demand is accepted..the same obstructers are now agreeing vehemently..

All kinds of changes in the aftermath.

People are scared that simple logic will be applied elsewhere

[01/09, 15:32]hu2: We had a ARD strike during our times when they retrospectively applied electricity charges on all residents to the extent of Rs 33,000 ( worth many lakhs of contemporary money’s worth). Our residency ended on January 1st instead of Dec 31st, after our successful strike.

[01/09, 15:51]hu3: Which year?

[01/09, 16:38] hu3 : recall an army col who did his Neurosurgery Mch..saying on his last working..I have worked in this hospital now can work in Andamans..😳

[01/09, 17:07]hu2: 1997 sir, we were exam going in 6 months time when this happened. Again same apathy and threats to residents to withdraw strike. Some idiots had siphoned power from resident hostels and the residents were easy bakras to pass the buck.

[01/09, 18:26]hu3: Some trivia of strike

Me and a friend..mess closes..go to sector 17 every evening..for dinner..salary 550 a month..that also stopped..dad retired..

So found this restaurant..2 parotas, chicken do pyaza.. with 2 pieces of chicken in gravy..

Shared

After one week..the restauranter got suspicious..

We had to fight as there was only one piece of chicken..from then on

We argued  Chicken do pyaaza.. so two ..he came back..with do pyaaz milega..

Luckily strike lifted soon after.

Thematic Analysis

1. Evolution of Residency Curriculum

- *1+2 System*: The older system involved a one-year house job followed by a competitive exam for a two-year MD/MS program. This system placed extreme pressure on residents, as PG seats were not guaranteed after the house job.

- *Three-Year PG System*: Standardized across India in the 1980s after a major RDA strike, this system eliminated the need for a second entrance exam and introduced a thesis requirement. The change aligned PGI and other institutions with AIIMS and international norms.

2. Strikes and Advocacy

- *Catalyst for Change*: The RDA strike in 1982 was pivotal in transitioning from the 1+2 system to the three-year PG program. Residents protested over workload, unfair assessments, and systemic inequities, forcing administrators to adopt reforms.

- *Camaraderie and Struggles*: Strikes brought residents together in solidarity despite financial hardships, threats, and apathy from authorities. Stories of shared meals, makeshift arrangements, and resilience highlight the human aspect of the struggle.

3. Assessments and Workload

- *Formative Assessments*: The older system relied heavily on formative, practical assessments with viva voce, clinical skill tests, and subjective evaluations by examiners. These methods often lacked transparency and fairness.

- *Summative Assessments*: The evolution toward written exams and objective assessments marked a shift toward more standardized and equitable evaluation systems.

- *Workload*: Residency involved long hours, with residents juggling clinical duties, exams, and personal challenges. The NICU/PICU postings were particularly intense, with night alarms and extended shifts.

4. Institutional Politics and Inequities

- *Selection Bias*: The older system often favored candidates with political or regional connections, leaving many deserving candidates without opportunities. This created a culture of frustration and resignation among residents.

- *Systemic Inequities*: The conversation highlights how some residents had to leave India for better opportunities abroad, where their qualifications were recognized more generously.

5. Personal Narratives and Camaraderie

- *Memories of Residency*: Despite the hardships, residents fondly recall the camaraderie they shared with peers, mentors, and staff. They created informal support systems, such as "coffee clubs" and birthday celebrations, to cope with the intense workload.

- *Cultural and Social Context*: The stories of shared meals, financial struggles, and relationships within the residency environment underscore the human dimension of medical training.

6. Standardization and Modernization

- *Role of MCI (Now NMC)*: The Medical Council of India played a key role in standardizing postgraduate medical education, ensuring uniformity across institutions.

- *Current Landscape*: The conversation touches on modern entrance exams like INI-CET, which have replaced earlier systems, and asks whether the same challenges persist today.

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Comparative Reflection

The discussion highlights a significant transformation in medical education, moving from an *apprenticeship-based formative system* to a *standardized summative assessment model*. While the older system emphasized practical, hands-on skills, it was fraught with inequities and subjective evaluations. The modern system, with its structured curriculum and objective assessments, aims for fairness and uniformity but may lack the personalized mentorship of the past. The personal anecdotes humanize the narrative, emphasizing the resilience and camaraderie of residents during a time of systemic change.

Feedback from other human users hu1,2,3,n:

[02/09, 10:48]hu1: Brilliant piece in fact a lot more can be added to it

[02/09, 13:19]hu2: Please do and even if you share the text here I can add

[02/09, 21:29]hu2: Here's some additional feedback by another reader:

[02/09, 19:07]dhu1: At AIIMS, New Delhi ours was the first batch of MBBS graduates to face this sudden transition from 2 + 1 to 3 year MD/MS with a thesis requirement. For me the challenge was even greater as I was using my spare time to read Indian History and Political Science for the IAS entrance exam while the rest of my batchmates were preparing for the ECFMG (precursor to the VQE). 

Towards middle of October 1977 (during my internship) I had to decide whether to continue preparing for the remaining two papers for the IAS which I had to take on October 31, 1977 or get back to medical books for the entrance examination of MD/MS in the third week of December for AIIMS, New Delhi. At that time, we were treated as equivalent to outsiders appearing for the entrance exam for an all Indian competition. 

Anyway, I decided to write the remaining two written exam papers for the IAS. 

On November 1, 1977 switched back to medical books. Topped the entrance exam for MD pediatrics which had three open seats. Joined MD (Paediatrics) on  1.1.78 but left it on 12.7. 78 to join the IAS.

My formal practice as a doctor was limited to pro bono practice in Arunachal Pradesh where I was Deputy Commissioner of a district. 

I left IAS in Nov 93 to join the World Intellectual Property Organisation, Geneva, Switzerland, from where I retired on 31.08.2017. 

The only time I practiced medicine full time (again on a pro bono basis) was during the height of Covid-19 when I was working remotely for patients in dire need for almost 16 to 18 hours per day for a few weeks. 

At present, my medical practice is limited to pro bono practice with friends and family. Mostly for second opinions.

Lecture module: Current role of AI in diagnostics and decision support and tech singularity driven merger of system 1 and 2 cognition

Learning objectives:

1) Clarifying terminologies: Diagnostics (process) vs Diagnosis (product)

2) Decision doesn't end at diagnosis: resolving therapeutic uncertainty (the final product)

3) Introduction to a real world, 24x7, AI LLM user driven diagnostic and clinical decision support workflow with it's past and current background

4) The AI and human driven user vs developer perspective in clinical decision making 

Introduction:

Diagnostics (what is the process):

Conversational Transcripts from an interaction between a developer and user (to also understand the differences in their perspective)

[30/08, 22:06]hu1: Our wearable device captures a comprehensive set of physiological parameters, including:

Cardiac

• 4 Lead ECG

• Pulse Rate

• HR / HRV

• Stroke Volume

• Cardiac Output

• Cardiac Index

• Pulse Pressure

• Arterial Mean Pressure (MAP)

• SVR

• NiBP (under validation)

Respiratory

• Pleth-SpO₂

• Respiratory Rate

• Thoracic Impedance

Other

• Body Temperature

• Accelerometer (patient position)

All data is collected with *medical-grade accuracy*, seamlessly streamed to a bedside monitor (tablet) and securely transmitted to the cloud for *AI & algorithmic computation*. This enables near real-time alerts with *Early Warning Score (EWS)*, *Sepsis prediction*, and *Heart Failure (HF)* detection.

We are actively advancing toward *CDSCO* regulatory clearance

[31/08, 12:36]hu2: Medical grade accuracy is good but one needs to keep the broader process of diagnostics in mind along with the initial product (diagnosis) and final product (therapeutic outcome).

These data points are currently given a lot of weightage in diagnostics so much so that the meaning of the term "diagnostics" has changed to mean something limited to lab or imaging based parameters and this is something that needs to be debated.

Diagnostics is a collage of multimodal data points tied into an ontology:

It begins with patient history as in life events data points that can be discreet or continuous.

Trying to understand patient requirements from life events generated data can be analogous to prompting an AI LLM!

https://userdrivenhealthcare.blogspot.com/2024/08/template-for-pajr-user-driven-history.html?m=1

The other milestones in a diagnostic workflow process:

Clinical examination

Physician or Machine driven Objective vs patient driven Subjective data points 

Labs

X ray

MRI

How much weightage can one give to each in the decision making workflow?

Diagnostics (what it isn't)!

Throwing a few lab reports (currently masquerading as objective data but actually suboptimal data) to a human posing as a physician agent and expecting him her to create magic with suboptimal data!

Your diagnostics and decision support will be as good as the data you share! Beware of GIGO!

The role of laboratory vs clinical encounter 

Methods: 

Clinical problem solving workflows 

Medical cognition and procedural workflows toward diagnostic and therapeutic outcomes 

Layers of diagnosis:

Anatomical

Etiologic 

Past published discussion on critical realist heutagogy CRH and AI driven workflows: 

Narketpally syn as a case based blended learning ecosystem CBBLE and it's PaJR pajr.in platform with detailed description of CRH and our medical cognition workflow 

https://pubmed.ncbi.nlm.nih.gov/40674544/

CRH first signposted here: https://medicinedepartment.blogspot.com/2024/10/critical-realist-pedagogy-and-theatre.html?m=1

CBBLE as an early progenitor of the current Narketpally syn: 

https://pmc.ncbi.nlm.nih.gov/articles/PMC6163835/

Current regular methodological uploads archived:

2024:

https://medicinedepartment.blogspot.com/2024/11/technology-end-user-driven-ecosystem.html?m=1

2025:

https://userdrivenhealthcare.blogspot.com/2025/07/analysis-of-participatory-medical.html?m=1

2020:

https://medicinedepartment.blogspot.com/2020/06/daily-workflow-of-our-case-based.html?m=1

Results:

Recent real patient outcomes:

An individual patient problem necessitating diagnostic and clinical decision support (human as well as AI driven): https://pajrcasereporter.blogspot.com/2025/08/56m-traumatic-pain-in-left-great-toe-1.html?m=1

More individual AI driven real patient diagnostics and decision making process regularly updated here: https://pajrcasereporter.blogspot.com/?m=1and past 5000 records here: https://medicinedepartment.blogspot.com/2022/02/?m=1

Discussion: 

Decision support toward diagnosis and therapy:

The pandemic of Over-testing and Overtreatment resulting from misinformation of diagnostics:

The process of Medical cognition (meta cognition, thinking about thinking to integrate medical education with practice):

System 1 cognition: default fast thinking mode and it's evolution in the dyadic doctor patient relationship 

Past lecture: https://sites.pitt.edu/~super1/lecture/lec54941/003.htm

to

System 2, the slow thinking mode with the added advantage of collective sharing (blessing of dimensionality reduction) and the disadvantage of missing data (curse of dimensionality reduction)

https://userdrivenhealthcare.blogspot.com/2025/08/udlco-crh-reducing-multidimensional.html?m=1

AI and system 2 beginning with primordial asynchronous intelligence to current day automation unleashing an era of pre-tech singularity Orwellian data capture and sharing that will eventually merge with system 1 cognition with further 

https://userdrivenhealthcare.blogspot.com/2025/07/user-driven-orwellian-eyes-at-pivot-of.html?m=1

Feedback conversational learning loops:

[01/09, 06:17]hu1: Nice!

Have you presented an innovation or analysed issues with deployment and usage of any digital health tool?

[01/09, 08:08]hu2: Both perhaps.

I began by clarifying current misperceptions around the labels diagnostics vs diagnosis and then proceeded to describe our team based learning workflow (not sure if it can be called an innovation but it's a variation from traditional dyadic workflows as described by us a decade earlier here: https://pmc.ncbi.nlm.nih.gov/articles/PMC4587042/ and recently here: https://pubmed.ncbi.nlm.nih.gov/40674544/ where we use critical realist heutagogy driven by AI LLM users as well as non AI users in our CBBLE (case based blended learning ecosystem).

We discussed the current issues with it's usage both from the AI as well as non AI users perspective

[01/09, 09:20] hu1: Thank you

Do they all need facebook accounts and internet access?

[01/09, 09:30] hu2 : Not Facebook currently but WhatsApp.

Previously I was a laptop user as far as mobile computing would go and our ecosystem was in Facebook, which had it's advantages of having individual threaded conversations in groups but had it's own privacy issues and when I found that majority of my patients were WhatsApp users I ditched the laptop (those days WhatsApp wasn't easily accessible from the laptop) , to become a full time mobile phone user and expand our patient user base.

[01/09, 09:39] hu3: Fantastic 👍

[01/09, 10:43] hu4: Thank you for sharing it. Very encouraging approach.

[01/09, 10:51] hu4: *My critique developed with Gemini Pro:*

The current lecture module on AI in diagnostics requires a complete pedagogical overhaul to become an effective educational tool. To fix this, the module must be redesigned into a highly granular, interactive learning experience grounded in specific, actionable frameworks.

*Phase 1: Foundational Redesign and Reorientation*

The first step is to transform the module's core content into a coherent, easily digestible narrative. This involves moving beyond the raw conversational transcripts and reorganizing the material into a clear, progressive structure.

*A. Clearer Core Concepts through Analogies:*

The module needs to start with crystal-clear definitions. Complex ideas should be introduced with simple, relatable analogies.

* *Diagnostics vs. Diagnosis:* Explain this with a cooking analogy. *Diagnostics* is the entire *process of baking a cake*—gathering ingredients, mixing, setting the oven temperature, and monitoring the bake. *Diagnosis* is the *final product*—the finished cake. The ultimate goal, or *therapeutic uncertainty*, is whether the cake will be delicious and meet the needs of the person eating it. This analogy makes the distinction concrete and memorable.

* *Multimodal Data:* Break down the concept of multimodal data into distinct, understandable categories with real-world examples.

    * *Level 1: The Raw Data:* This is the most basic layer, comprising objective metrics like lab results, ECG readings, and imaging scans.

    * *Level 2: The User-Driven Data:* This is the patient's narrative, their subjective symptoms, and their personal history, which the module rightly calls "life events data." This layer is crucial for a complete picture.

    * *Level 3: The Clinician-Driven Data:* This includes the physical examination findings, the physician's observations, and their professional judgment.

    The module must explicitly show how all three layers are essential for a complete diagnosis.

*B. Redefining Learning Outcomes with Dual Taxonomies:*

The current objectives are too broad. They need to be rephrased as actionable, measurable goals using two complementary frameworks: *Revised Digital Bloom’s Taxonomy* and *Fink’s Taxonomy of Significant Learning.*

* *Revised Bloom's:* This provides the *cognitive scaffolding* for the learning journey.

    * *Remembering/Understanding:* "Students will be able to *define* the difference between diagnostics and diagnosis using the provided analogy."

    * *Applying/Analyzing:* "Given a provided patient case, students will *analyze* and *classify* the data points into objective, subjective, and life events categories."

    * *Evaluating/Creating:* "Students will *evaluate* a hypothetical AI diagnostic report and *critique* its potential for bias, proposing a more holistic diagnostic workflow."

* *Fink's Taxonomy:* This adds the *affective and human dimensions* crucial for medical education.

    * *Application & Integration:* "Students will *integrate* their understanding of AI and cognitive bias to *develop* a strategy for a collaborative human-AI diagnostic process."

    * *Human Dimension & Caring:* "Through a role-playing exercise, students will *demonstrate empathy* and a *commitment to ethical care* when discussing a sensitive diagnosis with a virtual patient."

*Phase 2: Building Interactive, Heutagogical Components*

This phase focuses on making the module's core philosophy—*critical realist heutagogy (CRH)*—a tangible reality. The goal is to move beyond simply referencing a methodology to actively implementing it.

*A. Turning Abstract Concepts into Concrete Experiences:*

Abstract ideas like cognitive bias and systemic distortion must be illustrated with concrete, engaging examples.

* *The Mercator Projection Analogy:* Don't just mention it; use it as a central teaching tool.

    * *Explain the Distortion:* Acknowledge that the Mercator map is useful for a specific purpose (navigation) but grossly *distorts reality* by making landmasses near the poles appear much larger than they are. Use the "flattened orange peel" analogy to explain this visual distortion. 

    * *Draw the Clinical Parallel:* Explain that a diagnostic model based on a limited data set—for example, only lab values—is like a Mercator map. It provides a useful, but *distorted view of the patient's reality.* This limited view can lead to a diagnosis that over-emphasizes one metric while missing the patient's full story.

    * *The Solution:* The comprehensive, multimodal approach to diagnostics is the *3D globe*—a complete, accurate representation of the patient's health.

* *Cognitive Bias Simulation:* Create a granular, interactive exercise. Present a virtual patient with a clear "red herring" symptom that would trigger a common cognitive bias, like *anchoring bias* (over-relying on the first piece of information). An AI chatbot can act as a Socratic challenger, prompting the student with questions like, "What other possibilities could explain this symptom? Have you considered the patient's social history?"

*B. Implementing the PaJR/CBBLE Workflow:*

The module must explicitly guide students through the *PaJR (Problem-Analysis Journal & Reporter)* workflow, which is the practical application of CRH.

* *Step 1: The Initial Case Prompt.* Students are presented with a de-identified case in a *PaJR format*. They must act as the "user," deciding which data to input into an AI system.

* *Step 2: Collaborative Analysis.* Students use a platform (simulated or real) to share their initial diagnostic hypotheses with peers. This peer-to-peer feedback is a cornerstone of heutagogy, where learning is self-determined and collaborative.

* *Step 3: AI as a Metacognitive Partner.* The AI system does not give a direct diagnosis. Instead, it provides a "metacognition report" on the student's decision-making process. The report could highlight:

    * *Missed data points:* "You did not consider the patient's socioeconomic status, which is a key social determinant of their health."

    * *Potential biases:* "Your rapid diagnosis suggests premature closure. What steps could you take to avoid this bias?"

    This feedback loop teaches students *how to learn* by helping them think about their own thinking.

*Phase 3: Final Touches for Implementation and Assessment*

The last phase ensures the module is fully functional and ready for deployment.

* *Portfolio-Based Assessment:* Move away from a single final exam. A *digital portfolio* allows students to demonstrate their learning journey, aligning with the heutagogical philosophy. 

The portfolio could include:

    * A completed PaJR case study.

    * A reflection on their experience with the virtual patient and the AI chatbot's feedback.

    * A critique of a recent article on AI bias in healthcare, using the module's new frameworks.

* *Sufficient Context for Educators:* The module should include a detailed "Teacher's Guide" that explains the pedagogical basis, the CRH/PaJR workflow, and how to facilitate the collaborative learning process. This ensures that the module isn't just a document for students but a comprehensive tool for educators.

Clinical problem: A middle aged man with traumatic pain in the left knee and base of the left great toe

56 years old man walking his two dogs in the morning, was suddenly taken off guard when the dogs got excited after spotting a herd of pigs and pulled free from the leash toppling the man in the process. As soon as he fell he suffered from excruciating pain in left knee and base of left great toe and barely managed to walk home limping with pain.

On examining of the knee and toe in the evening:

Radiology of the foot:

Day 2 morning:

Day 2 evening:

Objective examination and interpretation: Swelling persists due to traumatic inflammation. 

Confirmed on palpation with no palpable fracture dislocation

Subjectively as related by the patient and interpreted by physician:

The pain exacerbates on prolonged sitting and produces marked stiffness in surrounding muscles which reduces slowly on prolonged walking suggestive of ligamental inflammation or enthesitis

Day 4 update:

Left Metatarsophalangeal joint looks even more spell and pain appears more than day 1!

The swelling and pain of left knee is persistent. Patient hasn't taken any analgesics till now 

Day 7 evening update:

Subjective: The swelling and pain of left knee is persistent only in a different flavour as the morning pain immediately after waking up and after initial mobilization is slightly less but every time the patient sits for sometime and then attempts to get up and walk the pain and stiffness keeps recurring. Patient hasn't taken any analgesics till now 

The left MTP swelling is not reducing and pains often during walking with shoes when it gets compressed antero posteriorly by the shoes. The patient recalls having much milder version of similar pain and swelling of the left MTP induced by footwear since last few years. The incidental findings in the foot x-ray appears to point toward a prior gout.

UDLCO CRH: Participatory medical cognition in online user driven Clinical Biochemistry learning sessions

Summary: A chance post on a global CBBLE creates intrigue in a critical realist heutagogue (aka CRH where H is more often used to mean heutagogy) and leads the CRH human user to search and share more on this topic.

UDLCO Keyword glossary:

http://userdrivenhealthcare.blogspot.com/2023/11/glossary-of-user-driven-healthcare.html?m=1

Conversational participatory medical cognition aka Web 2.0:

[19/08, 19:01]gm:

 https://cmeindia.in/if-serum-uric-acid-level-is-%E2%89%A42-0-mg-dl-should-you-proceed-to-investigate-hypouricemia/

[19/08, 19:25]cm:

Thanks for sharing.

Was also stimulated to find out more.

As far as the patient data here is concerned, it appears to be a real patient experience although it's mentioned as case scenario so can't be sure. The case narrative indicates certain highlights around his exercise induced AKI that was later suspected to be due to RHUC. 

Found another real case from Hyderabad, Telangana here: https://pmc.ncbi.nlm.nih.gov/articles/PMC8330661/

And another from Kolkata here: https://journals.sagepub.com/doi/10.1258/acb.2012.012017?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

Till 2020 the Hyderabad case report was the second to report this condition from India along with the genomic analysis.

AI driven medical cognition offering further structured summary and analysis

Online Clinical Biochemistry Learning Session: Renal Hypouricemia (RHUC)

Core Concept: Renal Hypouricemia (RHUC) is a rare genetic disorder characterized by a defect in the renal tubular reabsorption of uric acid, leading to abnormally low serum uric acid levels (< 2.0 mg/dL) and increased urinary uric acid excretion. It is a significant, though often overlooked, cause of exercise-induced acute kidney injury (AKI).

---

1. Pathophysiology: How the Kidney Handles Uric Acid

To understand RHUC, one must first understand normal urate handling (as depicted in Figure 1 of the Hyderabad case report).

· Filtration: Uric acid is freely filtered at the glomerulus.
· Reabsorption: ~90% of the filtered load is reabsorbed in the proximal tubule. This is the key process disrupted in RHUC.
  · URAT1 (SLC22A12): The primary apical (luminal) transporter responsible for urate reabsorption from the urine into the tubular cell.
  · GLUT9 (SLC2A9): The major basolateral transporter that moves urate from the tubular cell into the blood.
· Secretion: A smaller portion is secreted back into the tubule via other transporters (e.g., OAT1, OAT3).

Genetic Defects:

· RHUC Type 1: Caused by loss-of-function mutations in the SLC22A12 gene encoding URAT1. This is the most common type, especially in Japanese and Korean populations.
· RHUC Type 2: Caused by mutations in the SLC2A9 gene encoding GLUT9. This is rarer and often leads to more severe hypouricemia, as it blocks the final exit step from the cell into the blood.

---

2. Clinical Presentation: The Case Studies as Examples

The shared cases illustrate the classic and a variant presentation.

A. The Classic Case (Hyderabad Report):

· Patient: 15-year-old boy.
· Precipitant: Strenuous anaerobic exercise (sprint run).
· Symptoms: Severe bilateral loin pain, extreme fatigue, oliguria/anuria.
· Key Biochemical Findings:
  · During AKI: Serum Creatinine 7.4 mg/dL, Uric Acid low (noted as "extremely low").
  · After Recovery: Confirmed hypouricemia. Fractional Excretion of Uric Acid (FEUA) = 52% (Normal <10%). This is diagnostic.
· Notable Absence: No significant rise in Creatine Kinase (CK=280 IU/L), ruling out rhabdomyolysis as the primary cause.
· Genetics: Compound heterozygous mutation in SLC2A9 (GLUT9), confirming RHUC Type 2.
· Family History: Mother also had hypouricemia (1.8 mg/dL), suggesting a hereditary pattern.

B. The Variant Case (Kolkata Report):

· Patient: 19-year-old man.
· Precipitant: Rigorous gym exercise.
· Symptoms: Muscular pain, weakness, dark urine.
· Key Biochemical Findings:
  · During AKI: Markedly elevated Creatinine (736 μmol/L) and, crucially, CK was very high (10,127 U/L) indicating rhabdomyolysis. His uric acid was normal (243 μmol/L) at this time.
  · After Recovery: Profound hypouricemia (17 μmol/L) with high FEUA (151%) was discovered.
· Family History: Brother also had hypouricemia and exercise intolerance.
· Key Learning Point: This case demonstrates that RHUC and rhabdomyolysis are not mutually exclusive. A patient with RHUC can also develop rhabdomyolysis from extreme exercise. The initial normal uric acid during AKI is a red herring and highlights why follow-up testing is essential.

---

3. Why Does Exercise Cause AKI in RHUC? (The Proposed Mechanism)

The exact mechanism is not fully proven but is thought to be a multi-hit model involving loss of antioxidant protection:

1. Exercise-Induced Renal Vasoconstriction: Strenuous exercise shunts blood away from the kidneys, causing transient ischemia.

2. Oxidative Stress: Upon reperfusion, a burst of oxygen-free radicals is generated.

3. Lack of Antioxidant Defense: Uric acid is a potent intracellular antioxidant. Tubular cells in RHUC patients have a depleted uric acid pool due to their reabsorption defect, making them uniquely vulnerable to this oxidative stress.

4. Result: Severe acute tubular necrosis (ATN) and AKI, often with the characteristic symptom of severe loin pain.

---

4. Diagnostic Approach (Answering the Original Question)

Yes, if serum uric acid is ≤2.0 mg/dL, you should absolutely investigate hypouricemia. The investigation is simple and non-invasive.

Step-by-Step Workup:

1. Confirm Hypouricemia: Repeat the test on a fresh sample when the patient is well and hydrated.

2. Check 24-hour Urinary Uric Acid Excretion or Fractional Excretion (FEUA):

   · Expected in RHUC: Normal or high total urinary uric acid excretion, with a FEUA > 10% (often >50%, as seen in the cases). A high FEUA confirms a renal cause (over-excretion) as opposed to reduced production (e.g., Wilson's disease, SIADH).

3. Exclude Other Causes: Rule out generalized proximal tubular dysfunction (Fanconi syndrome) by checking for glycosuria, phosphaturia, and aminoaciduria.

4. Genetic Testing: The gold standard for confirming and typing RHUC (SLC22A12 or SLC2A9 gene sequencing). This was elegantly done in the Hyderabad case.

5. Family Screening: As shown in both cases, screening first-degree relatives can reveal an inherited pattern and identify other asymptomatic affected individuals.

---

5. Management & Counselling

· There is no cure. Management is preventive.
· Patient Education: This is the cornerstone. Patients must be counseled to avoid strenuous anaerobic exercise (e.g., sprinting, repetitive weightlifting, competitive swimming).
· Hydration: Maintain excellent hydration, especially before any physical activity.
· Avoid Nephrotoxins: Be cautious with NSAIDs and other potentially nephrotoxic drugs.
· Antioxidants?: Some case reports suggest a potential benefit from vitamin C and E supplementation due to their antioxidant properties, but this is not proven.
· Allopurinol?: Paradoxically, there are reports of allopurinol (a xanthine oxidase inhibitor) being used to raise serum urate levels and potentially prevent AKI, but evidence is anecdotal.

Take-Home Messages

1. Think Beyond Rhabdo: Not all exercise-induced AKI is due to rhabdomyolysis. RHUC is an important differential diagnosis.

2. Check the Uric Acid: Always include uric acid in the initial workup of AKI. A low or normal uric acid in the context of AKI is unusual and should prompt further investigation.

3. Follow Up: The diagnostic hallmark (hypouricemia) may only be visible after the AKI has resolved.

4. FEUA is Key: The fractional excretion of uric acid is a simple, crucial calculation to confirm renal wasting.

5. Genetic & Family Impact: RHUC is a genetic disorder. Identifying a case has implications for genetic counselling and screening of family members.

These cases from India highlight that while RHUC is most reported in East Asian populations, it is a global condition and likely underdiagnosed. A high index of suspicion is required.

ProJR viral fever heart failure in metabolic syndromes presenting with consolidation and clinical complexity

Project Title:

*Loculated Pulmonary Edema: Revisiting Phantom Tumors and Diagnostic Challenges in Viral Fever-Precipitated Heart Failure*

Summary:

This study investigates the phenomenon of loculated pulmonary edema, often misdiagnosed as pneumonia, in patients with viral fever-induced heart failure. Drawing from clinical observations, imaging findings, and literature, the study explores how atypical radiological patterns—such as consolidation resembling pneumonia—are manifestations of pulmonary edema.

 

The research aims to elucidate the pathophysiological mechanisms behind loculated fluid accumulation, its prevalence, and diagnostic implications while highlighting the need for refined imaging interpretation and clinical correlation. The thematic analysis underscores the gap between textbook descriptions and real-world clinical presentations, emphasizing the importance of interdisciplinary approaches to improve diagnostic accuracy.

---

Keywords:

- Loculated Pulmonary Edema

- Phantom Tumor

- Viral Fever-Precipitated Heart Failure

- Pneumonia vs. Pulmonary Edema

- Diagnostic Imaging

- Pathophysiology

- Consolidation Patterns

- Clinical Complexity

Pilot case data links:

1) https://userdrivenhealthcare.blogspot.com/2024/04/cbble-case-report-60-year-old-woman.html?m=1

2) https://pajrcasereporter.blogspot.com/2025/05/68m-metabolic-syn-hfpef-pulmonary-edema.html?m=1

3) https://pajrcasereporter.blogspot.com/2025/03/74m-with-neck-pain-hypoglycemic-coma.html?m=1

IMRaD Format Plan:

Introduction:

- *Background*: Discuss heart failure precipitated by viral fever and the diagnostic challenges posed by atypical imaging findings. Introduce "phantom tumors" and loculated pulmonary edema as phenomena requiring deeper investigation.

- *Objective*: To analyze the prevalence, imaging characteristics, and pathophysiological basis of loculated pulmonary edema in heart failure patients, distinguishing it from pneumonia.

Methods:

- *Clinical Case Review*: Analyze serial chest X-rays and HRCTs of patients presenting with fever, alveolar opacities, and heart failure. Include cases like the "Narketpally syndrome" and others with loculated pleural effusion patterns.

- *Imaging Studies*: Compare radiological findings (X-rays, CT scans) between heart failure pulmonary edema and pneumonia using published literature and case-specific data.

- *Literature Review*: Include thematic analysis of relevant papers, such as Stark and Leung’s study on pleural effusion distribution and recent studies differentiating cardiogenic and infectious edema.

Results:

- *Imaging Findings*: Present patterns such as sharp fissural margins, unilateral or loculated consolidation, and rapid resolution with diuresis. Highlight discrepancies between textbook descriptions and observed cases.

- *Pathophysiological Insights*: Discuss mechanisms like negative intrapleural pressure (suction effect) and systemic factors influencing localized fluid patterns.

- *Comparative Analysis*: Detail similarities and differences between heart failure pulmonary edema and pneumonia radiologically and clinically.

Discussion:

- *Diagnostic Challenges*: Explore why loculated pulmonary edema mimics pneumonia and its implications for misdiagnosis.

- *Clinical Significance*: Highlight the importance of serial imaging and clinical correlation in distinguishing between pulmonary edema and infectious processes.

- *Future Directions*: Suggest the need for pathophysiological models to explain loculated patterns and a narrative review to synthesize findings across cases and studies.

Conclusion:

- Summarize key learning points: the prevalence of loculated pulmonary edema, diagnostic criteria, and the importance of interdisciplinary approaches.

- Emphasize the need for awareness and updated clinical frameworks to address atypical presentations of heart failure pulmonary edema.

---

Thematic Analysis:

Themes Identified:

1. *Diagnostic Complexity*:

    - Loculated pulmonary edema often presents as consolidation indistinguishable from pneumonia on imaging.

    - Rapid resolution of opacities with diuresis is key to recognizing pulmonary edema rather than infection.

2. *Pathophysiological Mechanisms*:

    - Negative intrapleural pressure and localized factors like atelectasis may contribute to fluid loculations.

    - Systemic factors like heart failure drive pulmonary edema, but local variations in fluid distribution require further elucidation.

3. *Clinical Implications*:

    - Misdiagnosis can delay appropriate treatment for heart failure pulmonary edema.

    - Serial imaging and clinical correlation are essential for accurate diagnosis.

4. *Textbook vs. Practice Gap*:

    - Textbooks fail to comprehensively describe loculated pulmonary edema patterns, leading to diagnostic challenges.

    - Real-world clinical observations suggest this phenomenon is far more common than traditionally believed.

5. *Interdisciplinary Learning*:

    - Collaboration between clinicians, radiologists, and researchers is critical to understanding and addressing these atypical presentations.

    - Integrating imaging findings with clinical history and pathophysiology can improve diagnostic accuracy.

---

This project plan provides a structured approach to investigate loculated pulmonary edema, bridging gaps in understanding and refining diagnostic practices.

[14/08, 17:07] Meta AI: References for the Project:

1. *Severe Localized Re-Expansion Pulmonary Edema*

Gowrinath K, Reddy SP, Jyothi P. _Severe localized re-expansion pulmonary oedema: An unusual instance._

Natl Med J India. 2023;36:310–11. DOI: [10.25259/NMJI_838_20]((link unavailable))

This case report sheds light on the phenomenon of localized pulmonary edema, specifically after pleural drainage procedures, and discusses predisposing factors like atelectasis and pleural fluid dynamics.¹

2. *Differentiating Heart Failure and Pneumonia via Imaging*

MedRxiv preprint: _There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected, and septal thickening between heart failure and pneumonia. However, features like peribronchovascular thickening and fissural thickening were more common in heart failure._

DOI: [10.1101/2020.03.04.20031047v1]((link unavailable))

This study highlights the radiological overlap and subtle differences between cardiogenic pulmonary edema and infectious pneumonia.

3. *Pulmonary Pseudotumors*

(link unavailable) _A pulmonary pseudotumor is often caused by loculated pleural effusions trapped in pulmonary fissures, mimicking a solid mass._

[Pulmonary pseudotumor | Radiology Reference Article]((link unavailable))

This resource provides insights into how pleural effusions can mimic tumors, emphasizing loculated effusions as a diagnostic challenge.²

4. *Pleural Effusion Management*

Folch E et al. _Principles and Practice of Pleural Diseases._

This comprehensive guide discusses loculated effusions, their imaging characteristics, and management strategies, including diuresis and thoracentesis.³

5. *Effects of Lobar Atelectasis on Pleural Effusion Distribution*

Stark P, Leung A. _Effects of Lobar Atelectasis on the Distribution of Pleural Effusion and Pneumothorax._

Chest. 1989;95:1170. DOI: [10.1016/j.chest.1989.1170]((link unavailable))

This older yet foundational paper provides a theoretical basis for localized fluid accumulation due to atelectatic forces, offering potential explanations for the phenomenon of loculated pulmonary edema.

6. *British Thoracic Society Guideline for Pleural Disease*

Roberts ME, Rahman NM, et al. _British Thoracic Society Guideline for pleural disease._

Thorax. 2023;78(Suppl 3):s1-s42. DOI: [10.1136/thorax-2022-219784]((link unavailable))

This guideline discusses pleural effusions, including loculated presentations, diagnostic challenges, and treatment options.⁴

These references provide a strong foundation for the study, addressing both clinical observations and literature-based insights into loculated pulmonary edema and its diagnostic complexities. Let me know if you'd like more detailed explanations or additional references!

Conversational Transcripts:

[18/05, 07:19]cm: Our current heart failure clinical complexity projects are picking up a lot of viral fever precipitated heart failures manifesting with fever and alveolar opacities in the chest X-ray, initially interpreted as pneumonia because of fever and consolidation signs in the chest X-ray (very similar to what we saw during the covid period) and finally after a few days when it all resolves dramatically we realise that the consolidation opacities were all due to heart failure pulmonary edema precipitated by a viral fever in people with a metabolic syn phenotype and not due to pneumonia as one initially misinterpreted them as!

The recent most example we published is the Narketpally syndrome sample patient!

[03/06, 14:48] Dhu1 Pulmonary Edema: Good afternoon sir,

I had been busy with exams recently sir so I am going through some of these messages a little late.

I wanted to ask whether these opacities you mentioned were significantly indistinguishable as pneumonia vs edema on the imaging itself?

[03/06, 17:00] Rakesh Biswas: No in imaging they would simply be labelled as consolidation

[03/06, 17:13] Rakesh Biswas: Take a look at this patient's serial chest x-rays and one HRCT showing his loculated pleural effusion and consolidation that eventually vanished one day after few days of admission and recovery from heart failure which is when we became sure that it wasn't pneumonia but pulmonary edema👇

https://pajrcasereporter.blogspot.com/2025/03/74m-with-neck-pain-hypoglycemic-coma.html?m=1

[03/06, 18:04] Dhu1 Pulmonary Edema: Quite interesting sir, this xray from the case most certainly does not seem like it could be pulmonary edema.

[03/06, 18:06] Dhu1 Pulmonary Edema: But why would pulmonary edema due to heart failure be restricted to the right upper lobe as it appears to be, instead of being more uniformly bilateral?

[03/06, 19:43] Rakesh Biswas: Exactly! These kind of loculations due to pulmonary edema are far more common than text books know!

Text books may teach about phantom tumor as a short note, which is what this phenomenon is and we used to think it's relatively rare when we started gradually seeing it in practice till it's become so very common as to make us believe that it's much more common than pneumonia!

So learning points here are:

1) (Known previously) Phantom tumor is a pulmonary edema with loculated pleural effusion that is known to disappear rapidly in chest X-ray with diuresis 

2) It's actually much more common than pneumonia if one has a high index of suspicion for all patients with rapidly resolving pneumonias 

3) Why pulmonary edema gets sometimes (and for us often) in this peculiar loculated manner is what needs more elucidation with pathophysiological models

[03/06, 19:51] Rakesh Biswas: Yes but a pneumonia can't vanish overnight!

The sharp margin of the displaced pleural fissure that you may notice in this and the other serial chest x-rays is the one indicative of the loculated pleural effusion.

Again in the past Phantom tumors were probably termed for loculated pleural effusions due to heart failure although it's logical that they would also have had alveolar edema? @⁨Meta AI⁩

[03/06, 19:51] Meta AI: You're right, pneumonia typically doesn't resolve that quickly. The sharp margin of the displaced pleural fissure is indeed indicative of a loculated pleural effusion. And yeah, "phantom tumors" was a term used to describe loculated pleural effusions in heart failure patients, which likely had accompanying alveolar edema. It's interesting how terminology and understanding of these conditions have evolved over time. Are you looking into the specifics of how heart failure can manifest in chest x-rays?

[03/06, 19:51]cm: @⁨Meta AI⁩ alright share the specifics

[03/06, 19:51] Meta AI: Heart failure can manifest in chest x-rays in several ways, including:

1. Cardiomegaly (enlarged cardiac silhouette)

2. Pulmonary venous hypertension (distension of upper lobe veins)

3. Kerley B lines (short, horizontal lines at lung periphery)

4. Perihilar batwing opacities (alveolar edema)

5. Pleural effusions (often bilateral and loculated)

Loculated pleural effusions, like the one you mentioned, can mimic masses or "phantom tumors" on x-ray. Serial chest x-rays can help track changes and response to treatment.

Would you like more details on these findings or their implications?

[03/06, 19:52]cm: @⁨Meta AI⁩ strange that text books never make this mention about their being manifest as consolidation!

[03/06, 19:52] Meta AI: Textbooks often focus on classic presentations, but heart failure can indeed manifest in various ways, including consolidation-like patterns on chest x-rays. This can be due to pulmonary edema or hemorrhage. Some cases might show atypical patterns, making diagnosis more challenging.

In clinical practice, radiologists and clinicians consider the entire clinical picture, including patient history, symptoms, and lab results, to interpret x-ray findings accurately.

Are you finding that your clinical experience is diverging from textbook descriptions, or are you preparing for exams and wanting to bridge that gap?

[03/06, 20:25]cm: @⁨Meta AI⁩ here's something interesting around this, although not representative of a single chest X-ray for single patient findings but rather findings from a study utilising many chest X-rays for a single patient from different directions inside a tubular body shaped electro mechanical contraption aka CT scan and I quote from that paper 👇

"There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected and septal thickening between heart failure and pneumonia. However, less rounded morphology (8.3% vs. 67%, p=0.003), more peribronchovascular thickening (75% vs. 33%, p=0.041) and fissural thickening (33% vs. 0%, p=0.028), less peripheral distribution (33% vs. 92%, p=0.003) were found in heart failure group than that in pneumonia."

https://www.medrxiv.org/content/10.1101/2020.03.04.20031047v1.full

[03/06, 20:25] Meta AI: That's fascinating! The study you mentioned highlights the complexities of differentiating between heart failure and pneumonia using CT scans. The findings suggest that certain radiological features, such as peribronchovascular thickening and fissural thickening, are more common in heart failure, while rounded morphology and peripheral distribution are more characteristic of pneumonia.

The overlap in features like ground glass opacity, consolidation, and crazy paving pattern between the two conditions underscores the importance of clinical correlation and careful interpretation of imaging findings.

Did you find any other interesting studies or insights that might help in distinguishing between cardiogenic and infectious pulmonary edema?

[03/06, 21:19] Dhu1 Pulmonary Edema: Precisely sir, the sharp demarcation at the right horizontal fissure is very suggestive of localized consolidation.

[03/06, 21:23] Dhu1 Pulmonary Edema: As for point 3 I do indeed think it's very curious how something like this might come to occur. 

How common would this be? Perhaps something that could warrant a narrative/literature review sir? I will read up and think about what could be causing this.

[03/06, 21:45]cm: More sharper due to a loculated pleural effusion

[03/06, 21:47]cm: To answer the commonality question I had shared the quote from the link earlier which I am pasting here again 👇

@⁨Meta AI⁩ here's something interesting around this, although not representative of a single chest X-ray for single patient findings but rather findings from a study utilising many chest X-rays for a single patient from different directions inside a tubular body shaped electro mechanical contraption aka CT scan and I quote from that paper 👇

"There was no difference of ground glass opacity (GGO), consolidation, crazy paving pattern, lobes affected and septal thickening between heart failure and pneumonia. However, less rounded morphology (8.3% vs. 67%, p=0.003), more peribronchovascular thickening (75% vs. 33%, p=0.041) and fissural thickening (33% vs. 0%, p=0.028), less peripheral distribution (33% vs. 92%, p=0.003) were found in heart failure group than that in pneumonia."

https://www.medrxiv.org/content/10.1101/2020.03.04.20031047v1.full

[05/06, 00:30] Dhu1 Pulmonary Edema: I went through this paper which led me to go through some of the literature I could get my hands on for this topic after my duty hours. I found this which you might find interesting:

[05/06, 00:31] Dhu1 Pulmonary Edema: An atelectatic lobe can develop a recoil equivalent of 50 mm Hg; normal lung has aretractile pull of only 5 mm Hg (4). When a lobe develops a greater retractile tendency than the rest of the lung, local variations in pleural pressure ensue. This variation results in greater negative intrapleural pressure surrounding the atelectatic lobe and produces a suction cup effect. Thus, when a buffer medium such as liquid or gas is present in the

pleural space, it will preferentially be attracted by the atelectatic lobe (Figs. 1-5).

Therefore, any atypical configuration of pleural effusion or pneumothorax should direct attention to the underlying lung parenchyma (5). An atypical arrangement of pleural effusion caused by focal alteration of intrapleural pressure can be readily differentiated from loculation due to adhesions by positional maneuvers that test the mobility of the effusion. Obstructive atelectasis develops the largest retractile forces and attracts a disproportionate amount of pleural effusion. An increased atelectatic

tendency in the lower lobes may explain large subpulmonic effusions (6).

~ Effects of Lobar Atelectasis on the Distribution of Pleural

Effusion and Pneumothorax (Paul Stark, M.D., and Ann Leung, M.D.)

[05/06, 00:34] Dhu1 Pulmonary Edema: It is a rather old paper but I believe it provides a theory for this phenomenon that is something along the lines of what I was thinking, since I have a strong feeling there is localized factor at play to explain the specific pattern of fluid accumulation, either by itself or in addition to a systemic factor like heart failure.

[06/06, 12:39] Rakesh Biswas: Excellent! 👏👏

Please share the URL to it

[07/06, 17:47] Dhu1 Pulmonary Edema: https://pubmed.ncbi.nlm.nih.gov/8820023/

This is the paper sir, I had to figure out a way to access it.

[13/06, 17:09] Rakesh Biswas: Afternoon session:

The incidence of rheumatic valvular heart disease has remarkably decreased and this afternoon we found both mitral and aortic badly affected in this 33M

https://youtu.be/HBlx45F-M2Q?feature=shared

@ Pg⁩ please share his chest X-ray PA view

[13/06, 17:09]cm: A lot of pleural effusion on the right with consolidation likely due to heart failure pulmonary edema @⁨huai1

[13/06, 17:27] Dhu1 Pulmonary Edema: Interesting sir, specifically since we have a CT available in this case. Should we then expect the consolidation to clear up with management appropriate to pulmonary edema soon?

[13/06, 17:27] Dhu1 Pulmonary Edema: Is this restricted only to the right lower lobe?

[13/06, 17:31]cm: Yes we should

But Hrcts can't be repeated to check that!

[13/06, 17:36] Dhu1 Pulmonary Edema: Yes quite certainly not. I will keep an eye out for more cases like these, but in this case given the distinct cardiac dysfunction pulmonary edema seems like the major culprit, leaving me confused again about why it isn't seen in both lungs.

[13/06, 19:24]cm: 👆 here's the reason perhaps

[13/06, 20:52] Dhu1 Pulmonary Edema: Not in this case I believe because there are no atelectatic factors present or local factors present.

[13/06, 21:38]cm: We don't know if they are