re: Active learning session on global CBBLE for 30M with dyspnoea and pedal edema

The active learning session below was initiated by the treating unit PG before the treating unit intern collated the patient information into his E log here: https://saikiranpatnam.blogspot.com/2020/05/medicine-case.html?m=1

[5/19, 5:13 PM] Kims Aditya Samitinjay: A 30 year old shepherd from Gopanatlapuram presented to the OPD with complaints of Dyspnea and pedal edema since 15 days. 

An able shepherd who finished schooling till Class 7 and eventually pursued his current occupation with his father, the patient had been having a fairly fulfilling life until last October when he first reported breathlessness while taking the herd atop a molehill. He remembers the event as he felt scaling this molehill was quite easy for him before but this time he felt breathless and had to rest for a while to catch up his breath. Retrospectively he says that he had a feeling of suffocation and felt relieved after a few minutes in the shade. 

The patient also reported that such events have been progressive since October and that on quite a few occasions he felt heavy pounding palpitations in the middle of his chest. He says that these palpitations too were exertional and relieved with rest. He also reported that he occaskknally felt very dizzy with near blacking out associated with profuse sweating. All feature subsided with rest. He never had overt LOC. Specifically, he did not have this with prolonged standing in the sun. No history of nausea or vomiting during these dizzy spells. Patient denies fatigue and thoroughly enjoyed going to work and spending time in the fields. 

The patient reported that from March this year he also started having dry cough without any expectoration. He also reported nocturnal wheezing, usually at around 4 am. It was never severe to wake him up from his sleep. 

With Dyspnea fast catching up and impairing his productivity, the patient stopped working for a while and visited his sister's place 15 days ago when she noticed that he was unusually becoming breathless on walking short distances. She also admitted that the patient was wheezing at around the same time he mentioned. However she noticed that it did not wake him up from his sleep. 

The patient reported that he has been having pedal edema for the last 15 days. And at this point it prompted him to consult us. 

The patient is the youngest of 2 siblings with a very concerned and caring sister. He lives with his mother who is unemployed and depends on him. His father passed away years ago and he says he was a chronic alcoholic. Apart from these symptoms, he never had urinary or bowel disturbances. He has a fairly mixed diet and has a good appetite. His main concern now though is dyspnea and pedal edema limiting his quality of life.

[5/19, 5:13 PM] Kims Aditya Samitinjay: Analysis and inputs and queries welcome.

[5/19, 5:16 PM] Vivek Poddar 3: Alcoholic Cardiomyopathy, LVF, Cardiac asthma, pedal edema due to cardiac failure!

[5/19, 5:19 PM] Vivek Poddar 3: Why profuse sweating and palpitations! Indicating over activation of sympathetic nervous system

[5/19, 5:20 PM] Vivek Poddar 3: Pedal edema could be due to primary lung cause leading to cor pulmonale or secondary to left heart failure with right ventricular failure. Alcoholic might have been responsible for Cardiomyopathy leading to LVF or atrial fibrilation?

[5/19, 5:22 PM] Vivek Poddar 3: But he remember the event when it all started, indicating acute onset?

[5/19, 5:23 PM] Vivek Poddar 3: Subsiding with rest suggesting a vascular insufficiency in the heart!

[5/19, 5:24 PM] Vivek Poddar 3: How about the JVP and cardiac and respiratory auscultatory findings?

[5/19, 5:25 PM] Vivek Poddar 3: Any other comorbid conditions?

[5/19, 5:25 PM] Vivek Poddar 3: What's his BMI?

[5/19, 5:27 PM] Kims Aditya Samitinjay: No history of PND or Orthopnea. Epidemiologically, age and short duration of progression make LHF unlikely ?

[5/19, 5:27 PM] Vivek Poddar 3: But cardiac myopathy is not unlikely?

[5/19, 5:28 PM] Kims Aditya Samitinjay: Not necessarily, I still remember the day I was very febrile and was diagnosed with 'Typhoid'. Possibly it overwhelmed him.

[5/19, 5:28 PM] Kims Aditya Samitinjay: No comorbids as such.

[5/19, 5:28 PM] Kims Aditya Samitinjay: About 22.

[5/19, 5:29 PM] Kims Aditya Samitinjay: Yes it's elevated. Will reveal those findings in a detailed monolgue.

[5/19, 7:03 PM] Rakesh Biswas: Alcoholic? 🤔

I thought that was his father?

[5/19, 7:03 PM] Rakesh Biswas: Yes happens in heart failure 👍

[5/19, 7:06 PM] Rakesh Biswas: Very well written narrative and has the potential to become a global health case report. 

However need more data to find out the etiology of his heart failure. 

Also I am not sure if a mole hill is large enough to be scaled by a human. You probably meant mound that would go for a small hill

[5/19, 7:14 PM] Vivek Poddar 3: Oh, I read he is. It was his father

[5/19, 10:17 PM] Kims Aditya Samitinjay: On examination, the patient was in no apparent distress and he was oriented to time place and person. 

The patient appeared slightly undernourished with thin and lightly underpigmented hair with a normal hairline. He appeared to have a mild conjunctival pallor with no icterus or obvious nasal abnormalities. He tongue was red with no apparent features of cyanosis or other lesions. Speech was intact was normal conversational abilities. There were no obvious deformities of the neck and chest or back. Clubbing, koilonychia or leuchonychia were absent. Lower limbs were remarkable for significant  bilateral pitting type of pedal edema which extended upto the knees.  No cervical or axillary lymphadenopathy was noted.

[5/19, 10:21 PM] Kims Aditya Samitinjay: Sorry I missed the vitals here - PR 118 bpm BP 110/70 Temp Afebrile and RR 20. Spo2 97 on room air.

[5/19, 10:22 PM] Kims Aditya Samitinjay: GRBS at 145 with FBS 114 and HbA1c 6.5.

[5/19, 10:22 PM] Vivek Poddar 3: So, is it all because of malnutrition causing anemia, shortness of breath, pedal edema (due to low albumin)?

[5/19, 10:22 PM] Kims Aditya Samitinjay: Hb 10.4 with a N/N picture. Albumin at 3.9.

[5/19, 10:24 PM] Vivek Poddar 3: though anemia can occur with normal albumin

[5/19, 10:24 PM] Vivek Poddar 3: I mean edema can*

[5/19, 10:24 PM] Vivek Poddar 3: but it is a mild anemia

[5/19, 10:24 PM] Kims Aditya Samitinjay: Yep the patient had a raised JVP. Video will be shared tomorrow morning.

[5/19, 10:25 PM] Vivek Poddar 3: How about the red cell indices?

[5/19, 10:26 PM] Kims Aditya Samitinjay: I will share pictures of his reports as soon as possible

[5/19, 10:26 PM] Rakesh Biswas: CVS examination findings?

[5/19, 10:29 PM] Kims Aditya Samitinjay: Apical impulse visible. Confirmed with palpation at 5th ICS within the MCL, I felt it was foreceful and well sustained, localising to 1 ICS. RV heave + and I felt he had a loud P2 and RVS3. I don't know how and why but I'm strongly positive he had a holosystolic murmur in the pulmonary area yesterday which seems to have disappeared today. The only therapeutic intervention given was Lasix 40.

[5/19, 10:30 PM] Rakesh Biswas: Grade of the murmur?

[5/19, 10:30 PM] Kims Aditya Samitinjay: His JVP was elevated, 11 to 12 cm and had a prominent a wave with Vy collapse.

[5/19, 10:31 PM] Kims Aditya Samitinjay: Wasn't palpable sir. So 3/6. Could palpate a heart sound at the pulmonic area though.

[5/19, 10:31 PM] Rakesh Biswas: TR likely?

[5/19, 10:32 PM] Kims Aditya Samitinjay: Possible sir. Not sure why it disappeared.

[5/19, 10:33 PM] Vivek Poddar 3: disappeared mean it never reappeared then?

[5/19, 10:35 PM] Kims Aditya Samitinjay: Well he was admitted yesterday. It was there yesterday and seems to have gone today.

[5/19, 10:36 PM] Vivek Poddar 3: He was given lasix yesterday it seems?

[5/19, 10:38 PM] Vivek Poddar 3: Reduced preload should decrease the flowthrough stenotic and regurgitant valves and thus the murmurs will decrease except for MVP and HOCM

[5/19, 10:38 PM] Kims Aditya Samitinjay: Yes one dose of 40mg at 8pm.

Paraparesis Case based questions and conversational active learning points:

Last week we had three patients of paraparesis admitted with us and our interns have shared it in their online E logs as well as videos of offline discussion around the same cases all collated in the link below for the online 8th semester students to go through this week and answer some of the case related questions and also come out with their own queries:

https://medicinedepartment.blogspot.com/2020/05/case-based-online-learning-assignment.html?m=1

Below are some of the sample online learning E logs returned by the 8th semester students that conveys their thoughts on the shared cases.

https://medcases.blogspot.com/2020/05/ive-been-given-this-case-httpssrianugna.html

https://virtualmedicalcases.blogspot.com/2020/05/the-curious-case-of-paraparesis-case-1.html

http://rishik37.blogspot.com/2020/05/gm-elog-case-2.html

https://12avirnenivaishnavi.blogspot.com/2020/05/paraparesis.html?m=1

The 8th semester UG students who didn't have offline access to these patients because of covid holidays,  were further asked to share their queries and thoughts with the PG residents and interns who were  managing the case and who had also been presenting these cases in offline sessions recorded and shared with the 8th semester through video modules of case based learning.

Following is an example of the real time interactive learning, the students had with our PG interns. It has been deidentified to protect the identity of the Students and prevent evaluator bias.

Active online learning around 23M patient of paraparesis 

"[5/23, 10:06 AM] mbbs 2016 UG1: Sir, what symptoms made us suspect TB in this case? How did we confirm the diagnosis of TB in this case?
https://vaish7.blogspot.com/2020/05/medicine.html?m=1



[5/23, 10:13 AM] PG Post Residency 1 : First let me share some discussion with another student below

"Good morning sir!
Sir, why was there no biopsy taken from the abscess sites? To check for what bacteria might've caused it?"
" Because I'm not able to visualize being able diagnose tuberculosis with the given data."
" Check out the MRI report"
" Sir. Isn't there also a possibility that during the I&D for gluteal abscess there was damage to L4 and 5 which lead to the paraparesis?"
" Very Good question. Ask our interns and PGs. Tell me if you need their numbers"
" Yes sir. Because in a few cases I've read
 And most of them also had no AFB"
" How sensitive and specific is that and would it be useful for our patient?"
" Sir. The pus from the pyocele was sent for culture sensitivity and revealed no AFB it seems sir"
" Tuberculous abscesses are only diagnosed on the basis of histo pathology"
" Okay sir. I shall ask her"
" The question is why didn't we send a biopsy of the abscess tract to get a better histopathology diagnosis"
"I have the asked for the report from the intern, and she is yet to reply."
" They also had positive tuberculin Skin test sir"
" It's already there in one of their e logs shared with you"

[5/23, 10:17 AM] mbbs 2016 UG1 : It's not very sensitive because most of us have received a BCG vaccine, which would give us a false positive
[5/23, 10:18 AM] mbbs 2016 UG1: Did we assume he has TB? There seems to be no substantial evidence to prove it.
[5/23, 10:18 AM] PG post residency 1 : Can you share some literature that says BCG vaccination gives false positive Mantoux test.

Also is being Mantoux or tuberculin positive the same as being diseased?
[5/23, 10:30 AM] mbbs 2016 UG1: I found two conflicting studies :
 https://pubmed.ncbi.nlm.nih.gov/28087302/?from_single_result=28087302&expanded_search_query=28087302
 The above study provides evidence that BCG vaccination after infancy may influence TST results beyond the 10-year period conventionally accepted by the Centers for Disease Control and Prevention (CDC), extending up to 55 years after vaccination. This suggests that BCG vaccination should be taken into account when interpreting TST results regardless of the time elapsed since vaccination.
 https://pubmed.ncbi.nlm.nih.gov/17131776/?from_single_result=17131776&expanded_search_query=17131776
 Whereas, this study claims that The effect on TST of BCG received in infancy is minimal, especially > or =10 years after vaccination. BCG received after infancy produces more frequent, more persistent and larger TST reactions.
[5/23, 4:14 PM] PG Post Residency 1: 👍👏👏

Ok now let's back to solving the problem of confirming the diagnosis of tuberculosis in the patient. What would have been the best way forward to prove tuberculosis in this patient instead of beginning the treatment empirically?
[5/23, 4:23 PM] mbbs 2016 ug1: CBNAAT
[5/23, 4:28 PM] PG Post residency 1: CBNAAT of what?
[5/23, 4:33 PM] mbbs 2016 ug1: of sputum
[5/23, 4:35 PM] mbbs 2016 ug1: Sputum smear for AFB and Chest X-ray should also be performed
[5/23, 4:50 PM] PG Post residency 1: Wasn't it performed? Please ask the interns and PGs who made the log
[5/23, 4:54 PM] mbbs 2016 ug1: Alright sir.
[5/23, 4:57 PM] mbbs 2016 ug1: And sir, how is this related to Vasculitis?
[5/23, 4:59 PM] PG POST RESIDENCY 1:
Conversation with another student "So is it ACA Vasculitis as mentioned by one of my classmates??"
[5/23, 4:59 PM] PG POST RESIDENCY 1: "I mean is the diagnosis Tubercular ACA vasculitis in the medial Homenculus area of cerebral cortex??"
[5/23, 4:59 PM] PG POST RESIDENCY 1: "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606267/
This link she mentioned also tells about cerebral vasculitis without TBM"
[5/23, 4:59 PM] PG POST RESIDENCY 1: "Yes share the interesting learning points that you gained from that article 👍"
[5/23, 5:01 PM] mbbs 2016 ug1 Thanks Sir!
[5/23, 5:30 PM] mbbs 2016 ug1: Here are a few doubts I have,
[5/23, 5:40 PM] mbbs 2016 ug1: According to the MR images shared, there seems to be no evidence that the region of the cerebral cortex supplied by the ACA is affected to conclude that it is the cause of the paraparesis.
[5/23, 6:24 PM] KIMs 2016 ug1: The Anatomical location of the UMN lesion could be anywhere - Primary Motor Cortex, Internal Capsule, Midbrain, Pons , Lateral Corticospinal Tract
[5/23, 6:29 PM] KIMs 2016 ug1: The pathology could be -
1. Damage to the brain - due to Thrombus, Hemorrhage (Stroke), Infection, Tumour (Cancer), PML
2. Injury to the brainstem or white matter of the spinal cord - due to Multiple Sclerosis, Transverse Myelitis, Trauma, Spinal Stenosis, Spinal Abscess
[5/23, 6:36 PM] KIMs 2016 ug1: How do we localise the anatomical location affected in this UMN lesion which may have caused the paraparesis? Is the only was to do so by performing an MRI of the brain and the spinal cord? How does one interpret it?
[5/23, 6:43 PM] KIMs 2016 ug1: What is the relationship between the psoas absess and "the ring enhancing lesions seen in the right and left cerebral hemispheres" on MRI?
[5/23, 7:02 PM] KIMs 2016 ug1: Mostly, The vertebral lesion could not be producing any neurological signs because according to the MRI spine report , the patient has L4, L5 Spondylodiscitis which means, most likely, the spinal cord could not have been involved as it ends at the level of L1,L2 vertebrae. Though, the cause of the Psoas Abscess and Gluteal Abscess (Both cold abscesses) can be explained by spread of AFB from the L4,L5 Spondylodiscitis as commonly seen in Tuberculous spondylodiscitis.
[5/23, 7:54 PM] pg post residency 1: 👍Yes the last paragraph is spot on
[5/23, 7:54 PM] pg post residency : The ring enhancing lesions could be tuberculoma and the psoas abscess is also due to mycobacteria
[5/23, 7:55 PM] pg post residency 1: Have you checked the report? The very few films that have been shared may not reveal all
[5/23, 7:59 PM] pg post residency 1: Yes but the first step is to localize it anatomically and the clinical possibilities were bilateral leg area of the brain and high cervical cord. Brain stem was unlikely as there was no cranial nerve involvement.

Once the localization is over then the pathology can range from vascular, demyelinating, degenerative to neoplasia
[5/23, 8:17 PM] KIMs 2016 ug1: I've only seen the images shared on the blog by Vaishnavi ma'am (intern)
[5/23, 8:21 PM] KIMs 2016 ug1: What symptoms or signs may the Tuberculoma be causing?
[5/23, 8:24 PM] pg post residency: Check the report. Or ask Vaishnavi to share the radspa link to the entire mri images with you
[5/23, 8:25 PM] pg post residency1: Good question. Currently none that we know of
[5/23, 8:33 PM] KIMs 2016 ug1: In the Brain, that would be the Precentral Gyrus in the frontal lobe. What points us towards a high cervical cord lesion?
[5/23, 8:34 PM] KIMs 2016 ug1: One possibility could be Vomiting (which was described as non-projectile by the patient but could be projectile in actuality)
[5/23, 8:38 PM] pg post residency 1: UMN signs that are above the C5 cervical cord as biceps C5 is exaggerated.

Above the high cervical cord comes the brain stem which is ruled out as there are no cranial nerve involvement and finally bilateral cortical leg area is the only location left
[5/23, 8:38 PM] pg postresidency 1: Why would the ring enhancing lesions cause vomiting?
[5/23, 8:45 PM] KIMs 2016 ug1: Due to raised ICT
[5/23, 8:47 PM] pg postresidency 1: Do ring enhancing lesions cause raised ICT without any focal neurological deficit?
[5/23, 8:47 PM] KIMs 2016 ug1: Vasculitis of the ACA explains the lesion at the bilateral cortical leg area.
But, what could be the cause for a lesion above the C5 cervical cord?
[5/23, 8:51 PM] pg postresidency 1: When someone has quadriparesis due to an apparent UMN lesion above C5 then the differentials become either high cord lesion or brain stem lesion or cortical or internal capsular lesion
[5/23, 8:51 PM] KIMs 2016 ug1: No probably not. But I don't know why.
[5/23, 9:45 PM] KIMs 2016 ug1: I still don't understand how he was diagnosed with TB, sir.
[5/23, 10:12 PM] KIMs 2016 ug1: I asked Rashmitha ma'am whether Sputum Smear for AFB and CBNAAT was done and she said that the sputum was not inducible, so it wasn't possible and that the abscess pus was negative.
[5/23, 10:17 PM] pg postresidency 1: 👍

What other disease can produce such pus everywhere and also spread to the brain?
[5/23, 10:19 PM] KIMs 2016 ug1: What about Sarcoidosis?
[5/23, 10:21 PM] Rakesh Biswas: Share a similar case reported with sarcoidosis
[5/24, 3:09 PM] KIMs 2016 ug1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669974/
[5/24, 3:09 PM] KIMs 2016 ug1: dDx : Spinal Sarcoidosis - Osseous spinal sarcoidosis: an unusual but important entity to remember

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030116/
[5/24, 3:15 PM] KIMs 2016 ug1: Other questions I had are:
1. What pathology could be responsible for a lesion at or above the C5 cervical cord? Vascular, demyelinating, degenerative, neoplasia? Was anything visible on radiology?
2. How do we rule out various pathologies after we have located the anatomical location of the lesion causing the UMN symptoms (paraparesis)? Which in this case is the bilateral leg area of the brain.
3. Why didn't we do a biopsy for histopathological diagnosis of the affected vertebrae showing spondylodiscitis (L4,L5) on MRI?
Because as I mentioned, any pathogenic organism could have caused it.
4. Why don't ring enhancing lesions cause raised ICT without any neurological deficit?
[5/24, 3:39 PM] pg post residency 1: Did this patient in the report have spinal cord or peripheral nerve involvement due to sarcoid?
[5/24, 3:50 PM] pg post residency 1 : Very good questions.

1) For that particular patient no pathology was visible in any part of the spinal cord although clinically one strong differential was high cervical cord due to the clinical neurological findings of localization.

2. Ultimate diagnosis was always made in the past by biopsy either through autopsy in case of unfortunate death of the patient or through operative biopsy. Because getting those are invasive and difficult the other option in medical decision making is to go by statistical probability of the pathology.

3) As stated above because of high statistical probability of a treatable infectious pathology known to cause similar findings in the past, most physicians avoid invasiveness and favor tolerating moderate diagnostic uncertainty over the ability to provide potential relief through easily available standard course of treatment.

4) If those ring enhancing lesions were tumors or inflammed infective lesions such as neurocysticercosis or tuberculoma (ours was possibly a non inflammed tuberculoma) they can cause raised ICT. Focal deficits are seen in ring enhancing lesions when they impinge on the pyramidal pathway. I guess our previous discussion around this was incomplete and hence the confusion. Thanks for diligently pursuing it. 👍"

Mbbs 2016 UG student 3:

2) [5/20, 8:55 AM] mbbs 2016 UG student 3: Sir in this case
https://vaish7.blogspot.com/2020/05/medicine.html?m=1, the patient didn’t have fever or any symptoms of inflammation how would we think of TB?

[5/20, 9:17 AM]: MD PG (post residency) That's the idea of differential diagnosis.

One discusses the differentials to capture something the current symptoms wouldn't allow us to think of from what is currently known.

[5/20, 8:54 AM] +91 0: https://vaish7.blogspot.com/2020/05/medicine.html?m=1

[5/20, 11:03 AM] +91 : Why haven’t we done a Lumbar puncture in the above patient sir?

[5/20, 4:40 PM] : MD PG (post residency
 Alright. How do you think it would have helped if we did the lumber puncture? What were you expecting to find in it?

[5/20, 4:40 PM] : Lymphocyte?
To confirm TB

[5/20, 4:59 PM]   : MD PG (post residency

 How many are normal in CSF?

How does TB lead to lymphocytosis in CSF?
[5/20, 5:04 PM] : Less than 5 per ml is normal in CSF
Meningeal inflammation sir.

[5/20, 5:07 PM]  MD PG (post residency:

So are you suspecting meningitis here? Does this patient of paraparesis have any sign of meningitis? What signs would you look for?

[5/20, 5:49 PM] mbbs 2016 UG: Kernigs sign

[5/20, 6:26 PM]  MD PG (post residency
: So does this patient have any signs and symptoms of meningitis to merit an LP. You can even ask the intern. I can share her number if you want. You can message her or better is ask her in her log book comment box


[5/20, 7:16 PM] : No sir.
[5/20, 7:16 PM] : Yes sir I’ll ask her.

[5/20, 8:05 PM]  MD PG (post residency
: 👍keep your questions coming. These are important to score learning points

[5/20, 8:55 PM] +91: Sir is it falx cerebri tuberculoma?

[5/20, 8:57 PM]  MD PG (post residency
: Are there descriptions of such a location being affected by mycobacteria in the past on your review of literature?

[5/20, 8:57 PM]: Yes sir

[5/20, 8:57 PM]: It says there are 3 cases reported as now.

[5/20, 8:59 PM]  MD PG (post residency:
Share those cases and check out the similarities with our patient


[5/20, 9:03 PM] mbbs 2016 UG: The patient had monoperesis because it was unilateral.

[5/20, 9:03 PM]  MD PG (post residency
: Tell me the similarities and dissimilarities and always share the links to articles as we can't share the PDFs in your log book comment box or the FAQ learning points page

[5/20, 9:04 PM]: mbbs 2016 UG: http://www.roneurosurgery.eu/atdoc/CucuA_Falx.pdf

[5/20, 9:06 PM] mbbs 2016 UG 3: Sir he had monoplegia initially
Later developed seizure which our patient didn’t.
CT revealed edema and a tumor like mass near the falx cerebri.

[5/20, 9:08 PM]  MD PG (post residency

: Was the second line similar to our current patient?

[5/20, 9:17 PM] Yes sir

[5/20, 9:17 PM]  He had meningeal enhancement and edema.

[5/20, 10:51 PM]  MD PG (post residency)
: Yes but is that same as having a tumor like mass near the falx?


[5/20, 11:11 PM] mbbs 2016 UG3: Enhancing lesion is tumor like?

[5/20, 11:13 PM]  MD PG (post residency)
: Not as seen in the mri of our patient? Check out how a tumor enhancement looks like

[5/20, 11:15 PM] mbbs 2016 UG 3: There’s a diffuse enhancement in our patient


[5/20, 11:22 PM] Rakesh Biswas: Is that what happens in tumors?

[5/20, 11:22 PM] Kims 2016: No sir.

[5/20, 11:23 PM] Rakesh Biswas: Was contrast enhancement demonstrated in our patient's mri study? Was our patient given contrast?

[5/20, 11:24 PM] Kims 2016: The blog says there was significant enhancement

[5/20, 11:27 PM] Rakesh Biswas: Please clarify this with the intern who wrote that web log

[5/21, 8:18 AM] Kims 2016: Okay sir

[5/21, 8:49 AM] Kims 2016: Sir another doubt,
When we did an Xray abdomen and it showed psoas abscess on the right why didn’t we assume it to be the reason for the lower limb weakness and did an MRI?


[5/21, 8:54 AM] Rakesh Biswas: They happened at the same time but tell me what are your thoughts on the anatomical location of his lesion that is actually causing his paraparesis?

[5/21, 8:56 AM] Kims 2016: Psoas abscess compressing the nerves of the cord.

[5/21, 8:57 AM] Kims 2016 : It can also be because of the ring enhancing lesions of the cerebrum.

[5/21, 8:57 AM] Rakesh Biswas: Which part of the cord? Where is the psoas located and how does it compress the cord?

[5/21, 8:58 AM] Kims 2016: Not the cord but the nerves arising from the cord.
L4 and L5

[5/21, 8:58 AM] Rakesh Biswas: Which is the exact location? You can't say the paraparesis is both UMN as well as LMN?

[5/21, 8:59 AM] Kims 2016: Parasaggital?

[5/21, 9:01 AM] Kims 2016: It can be both.

[5/21, 9:03 AM] Kims 2016: In ALS, Neurodegenration, Spastic paraplegia

[5/21, 9:08 AM] Rakesh Biswas: What clinical signs does he have? Does he have both UMN and LMN signs?

[5/21, 9:09 AM] Kims 2016: UMN - Hypotonia, Absent reflexes

[5/21, 9:10 AM] Rakesh Biswas: 😳

[5/21, 9:12 AM] Kims 2016: LMN sir😬 sorryy

"[5/21, 9:13 AM] Rakesh Biswas: He has hypotonia and absent reflexes? 😳🤔
[5/21, 9:13 AM] Kims 2016 : Ankle clonus was absent
[5/21, 9:15 AM] Kims 2016 : And in the examination she wrote hypotonia in lower limbs.
[5/21, 9:42 AM] Rakesh Biswas: Which patient are you talking about? This one with psoas abscess? 🤔
Can you share the link to the case you are discussing?
[5/21, 9:42 AM] Kims 2016 : https://vaish7.blogspot.com/2020/05/medicine.html?m=1
[5/21, 9:42 AM] Kims 2016: This one sir.
[5/21, 9:49 AM] Rakesh Biswas: Yes but what about the reflexes?
[5/21, 9:50 AM] Kims 2016: Reflexes were present sir.
[5/21, 9:51 AM] Rakesh Biswas: Then can it be LMN?
[5/21, 9:51 AM] Kims 2016: No sir
But the reflexes were not exaggerated also
And there was hypotonia.
[5/21, 9:54 AM] Rakesh Biswas: Can a paraparesis be due to LMN as long as reflexes are normal even if the patient has hypotonia. Please ask the intern to change the entry of the reflexes as many observers thought they were exaggerated because they could be elicited with the fingers without the hammer. Check out the discussion videos around this patient but better do that in the end because then you won't have many questions left 🙂

Keep the questions coming. This is the best way to active learning
[5/21, 9:56 AM] Kims 2016 :  It is UMN sir?
[5/21, 9:56 AM] Kims 2016: Yes sir I will ask.
[5/21, 9:57 AM] Rakesh Biswas: Where does the UMN start and where does it end and where in that path is the lesion located in this patient?
[5/21, 9:58 AM] Kims 2016 : Motor cortex to the spinal cord
[5/21, 9:58 AM] Kims 2016: Cerebral cortex?
[5/21, 10:02 AM] Rakesh Biswas: How do you explain paraparesis with the cerebral cortical lesion? Bilateral cerebral cortex? Which part of the cerebral cortex?
[5/21, 10:03 AM] Kims 2016l: ACA territory sir
Medial side
[5/21, 10:04 AM] Rakesh Biswas: Both sides? Why and how the paraparesis?
[5/21, 10:04 AM] Kims 2016: Vasculitis?
[5/21, 10:09 AM] Rakesh Biswas: Which side ACA?

How does it cause paraparesis?
[5/21, 10:10 AM] Rakesh Biswas: Cause for ACA blockage due to ACA vasculitis? How did the mycobacteria in the psoas manage to do that?
[5/21, 10:11 AM] Kims 2016: Bilateral
[5/21, 10:11 AM] Rakesh Biswas: Ok

Answer the next questions
[5/21, 10:12 AM] Kims 2016: Blood borne spread sir?
[5/21, 10:14 AM] Rakesh Biswas: Second question was how does it cause paraparesis
[5/21, 10:16 AM] Kims 2016: Because of infarction?
[5/21, 10:18 AM] Rakesh Biswas: No I meant how does affecting that area of brain cause paraparesis
[5/21, 10:18 AM] Kims 2016: It’s affecting the motor areas of cortex
[5/21, 10:20 AM] Rakesh Biswas: The motor area is large. Can you share a weblink to an image showing the different motor areas such as leg area, hand area, face etc in one single image?
[5/21, 10:20 AM] Kims 2016: Legs according to hommunculus is on the medial side.
[5/21, 10:23 AM] Rakesh Biswas: Share a coronal section of the motor homunculus
[5/21, 10:24 AM] Rakesh Biswas: And share links because one can't enter images without reference into a blog
[5/21, 10:25 AM] Rakesh Biswas: Make it a habit to share links rather than stolen images 👍
[5/21, 10:26 AM] Kims 2016: https://www.alamy.com/cortical-homunculus-illustration-image245864436.html
[5/21, 10:47 AM] Kims 2016: So isn’t it the reason sir?
[5/21, 11:12 AM] Rakesh Biswas: Yes it is. Can you find if anyone else has reported this happening in other patients of tuberculosis?
[5/21, 11:26 AM] Kims 2016: Yes sir I’ll check.
[5/21, 11:26 AM] Kims 2016 A Vaishnavi: Sir the videos that are being uploaded on YouTube are not clear.
We aren’t able to hear anything.
[5/21, 11:28 AM] Rakesh Biswas: Yes. We need some of you people here to come here and become videographers. 😅
[5/21, 11:31 AM] Kims 2016 : 😁we’ll come soon sir.
[5/21, 11:42 AM] Kims 2016: Sir the isolated cns angiitis is itself very rare and till now no proper research was done sir.
[5/21, 11:56 AM] Kims 2016: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606267/
[5/21, 12:49 PM] Kims 2016: Sir in this case
Scabies serology was negative
So can we attribute the rash to peripheral neuropathy?
[5/21, 5:00 PM] Rakesh Biswas: Quote the relevant portion that will be useful to read in the context of our current discussion
[5/21, 5:00 PM] Rakesh Biswas: But we are not thinking of isolated CNS angiitis here but tubercular CNS vasculitis?
[5/21, 5:01 PM] Rakesh Biswas: Scabies serology? 😳🤔
[5/21, 5:04 PM] Rakesh Biswas: Ask Hitesh to share the report.
[5/21, 5:04 PM] Rakesh Biswas: What about searching for tubercular CNS vasculitis
[5/21, 5:05 PM] Kims 2016: There’s one retrospective study sir
But that was as a complication oc tubercular meningitis
[5/21, 5:05 PM] Kims 2016: Okay sir.
[5/21, 8:09 PM] Rakesh Biswas: [5/21, 5:33 PM] Hitesh Kims Intern: It's not scabies serology sir
[5/21, 5:36 PM] Hitesh Kims Intern: There what I mean was as he was not having any itching we thought of immunocompromised state due to viral infection as the reason for no itching and paraperesis but retroviral serology came as negative sir
[5/21, 8:10 PM] Rakesh Biswas: There is probably no such thing as scabies serology.

How is it diagnosed?
[5/21, 8:34 PM] Kims 2016: 😬
[5/21, 8:34 PM] Kims 2016: Sir it was written serology negative
So
[5/21, 8:36 PM] Rakesh Biswas: Yes he meant retroviral serology.

So find out and tell us how is the diagnosis of scabies confirmed

[5/21, 9:51 PM] Kims 2016: Okay sir"

KIMs student 4:


[5/22, 10:46 AM] : Gud Morning Sir,
In our case of 23 yr patient with lower limb weakness
Why was an MRI of spine not done?t
It is also possible that he might have Potts paraplegia, Presence of Ankle clonus and exaggerated DTR are earliest neurological signs indicating a SC compression.
[5/22, 10:48 AM] : Also it would be better to have an Orthopedic opinion to rule out Potts paraplegia. Because if it is there and is not identified it would involve Bowel and Bladder in long term and if it's Potts paraplegia it can be managed surgically.
[5/22, 10:50 AM] : Also Gait is to be evaluated to see if there is any TB spondylitis
[5/22, 4:28 PM] Rakesh Sir KIMS: Orthopedic opinion for Potts paraplegia? 😅

Well their opinion is only asked if we want them to operate, otherwise we need to make the diagnosis for them ourselves first
[5/22, 4:30 PM] Rakesh Sir KIMS: Ask Hitesh to share with you the MR spine images.

The MRI spine lumbar vertebral involvement is mentioned in his mri report that is already in the log.

However that may not be causing his paraparesis. Can you tell why?
[5/22, 4:31 PM] Rakesh Sir KIMS: Ask Hitesh to share his gait video or at least mention what was his gait like
[5/22, 4:31 PM] : Sure sir
[5/22, 4:31 PM] : May be it's not compressing the cord
[5/22, 4:32 PM] Rakesh Sir KIMS: Ok so back to the first question
[5/22, 4:33 PM] : Sir but the lesion is definitely peripheral na Sir
[5/22, 4:34 PM] : If it's a central lesion the presentation would be far different with involvement of other structures
[5/22, 4:35 PM] : There is a chace of disc inflammation spondylodiscitis
[5/22, 4:35 PM] : But that is usually more common in immunocompromised patients
[5/22, 4:35 PM] : I think we also need to assess the patients HIV status tooo
[5/22, 4:36 PM] : To consider few other differentials
[5/22, 4:43 PM] Rakesh Sir KIMS: Yes so the most basic thing in mbbs neurology that we need to learn to distinguish is between peripheral LMN lesion and central UMN lesion.

What does his clinical features suggest?
[5/22, 4:46 PM] : Sir
From the Nervous system examination mentioned above it is evident that there is
•B/L Hypotonia, Suggestive of LMN lesions
•Hyper reflexia of Knee and Ankle reflex suggestive of lesion UMN lesion above L3,L4
• Ankle clonus, suggestive of UMN lesion above S1,S2
[5/22, 4:47 PM] : I think there is lesion just above L3,L4 in the spinal cord that reflects as UMN lesion for the levels below it.

[5/22, 4:50 PM] Rakesh Sir KIMS: Good above L3, L4 where?

[5/22, 4:59 PM] : Just above L3,L4 but not likely disturbing the L2
Because if L2 in involved in the lesion then
There should be sensory loss on antero lateral aspect of thigh upto level of knee(Lateral cutaneous nerve of thigh-L2,3)
Also loss of sensation over the medial aspect of thigh( Obturator nerve-L2,3,4)

[5/22, 5:00 PM] : As there is no sensory deficit it is likely that the sensations are preserved due to normal L2

[5/22, 5:04 PM] : Also involvement of L3,4 explain the weakness in lower limb caused due to loss of motor fibers of obturator nerve to thigh muscle

(5/22, 11:00 PM) : RB

So you mean the lesion is in the L2-3, spinal cord segment or L2 and L3 vertebra? What have they mentioned in the MRI spine report about which vertebra is involved?

Also what if I told you that his upper limb reflexes are so exaggerated that we could actually elicit the reflex with our fingers?


Student 5 kims 2016:

"[5/22, 4:12 PM] Rakesh Biswas:

"Anatomical location of the root cause could be in the Spinal cord?"

Where is the exact level in the spinal cord? Is it in the cervical, thoracic or lumbosacral segments? 🤔

[5/22, 4:19 PM] 2016 Kims: Lumbosacral segments sir

[5/22, 4:21 PM] 2016 Kims: But it could be lower thoracic and upper lumbar sir.

[5/22, 4:23 PM] 2016 Kims: I think we need more Data to confirm it sir. MRI spine should also be done
[5/22, 4:23 PM] Rakesh Biswas: What if I told you that the patient's upper limb reflexes were elicitable by me by just tapping with my fingers and even his biceps was jumping bilaterally
[5/22, 4:25 PM] 2016 Kims: Then it could be a upper motor neuron lesion sir. If it’s exaggerated then maybe it could be a UMN lesion
[5/22, 4:26 PM] 2016 Kims: His babinski sign is also positive
[5/22, 4:27 PM] 2016 Kims: But since he has hypotonia I thought it couldn’t be UMN
[5/22, 4:39 PM] Rakesh Biswas: In the stage of acute neuronal shock one can still have hypotonia in UMN
[5/22, 4:40 PM] 2016 Kims: Yes sir so how do we know that it a stage of acute neuronal shock?
[5/22, 4:49 PM] Rakesh Biswas: If the UMN findings such as hyperreflexia predominate you think of UMN with hypotonia due to acute neuronal shock.

If LMN findings such as areflexia predominates you think of hypotonia due to LMN
[5/22, 4:50 PM] 2016 Kims: Okay sir.
Thank you. So this could be a state of UMN lesion with hypotonia due to acute neuronal shock
[5/22, 4:51 PM] Rakesh Biswas: Yes and where is the UMN lesion located?
[5/22, 4:53 PM] 2016 Kims: I think it’s above the anterior horn cell in spinal cord
[5/22, 4:55 PM] 2016 Kims: Sir in the video you said it could be parasagittal meningioma but then the lesion should be in cerebral cortex for that
[5/22, 4:55 PM] 2016 Kims: And he does not have any features suggestive of cortical lesion like aphasia
[5/22, 4:56 PM] Rakesh Biswas: Where are anterior horn cells in spinal cord? 😅
[5/22, 4:57 PM] Rakesh Biswas: Are the areas of aphasia located all over the cortex? Is the leg area same as the speech area? 😅
[5/22, 4:58 PM] Rakesh Biswas: You will find anterior horn cells at every section you take of the spinal cord
[5/22, 4:58 PM] 2016 Kims: Oh yes sir. Sorry sir 😅
[5/22, 4:58 PM] 2016 Kims: I think the lesion is at the level of lower thoracic and upper lumbar vertebrae
[5/22, 4:59 PM] 2016 Kims: No sir. 😅
[5/22, 4:59 PM] 2016 Kims: It’s speech areas are brocas and wernickes
[5/22, 5:00 PM] 2016 Kims: So it could be parasaggital meningioma then?
[5/22, 5:06 PM] Rakesh Biswas: What about this then? 👆
[5/22, 5:08 PM] Rakesh Biswas: How do you explain the gluteal abscess and the mei report mentioning other things in that vertebral region?
[5/22, 5:13 PM] 2016 Kims: Sir i think that is a cold abscess.
Yeah then lesion is in lumbosacral region sir that could explain the abscess.
[5/22, 5:39 PM] Rakesh Biswas: So is the vertebral lesion producing any neurological signs?
[5/22, 7:07 PM] 2016 Kims: Yes sir I think it’s compressing upon the cord and causing the upper motor neuron signs i.e. hypotonia and exaggeration of reflexes
[5/22, 7:08 PM] 2016 Kims: Sir should I change it in my blog then ? That the reflexes are exaggerated
[5/22, 7:46 PM] Rakesh Biswas: Yes instead of deleting the previous you can add this as an edit
[5/22, 7:47 PM] Rakesh Biswas: But then where in the cord will the compression produce the paraparesis he is having?
[5/22, 8:03 PM]  2016 Kims: Okay sir. I will do that
[5/22, 8:04 PM] 2016 Kims: Sir because psoas muscle is supplied by L2,L3,L4 nerve roots so maybe the compression is over there
[5/22, 8:22 PM] Rakesh Biswas: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:02 PM] 2016 Kims: LMN sir
[5/22, 9:04 PM] Rakesh Biswas: And what are the dominant clinical signs in your patient suggestive of?
[5/22, 9:36 PM] Kims: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:36 PM] 2016 Kims: LMN sir
[5/22, 10:10 PM] Rakesh Biswas: So then the nerve root is spared ?"

Frequently asked questions around case based online learning assignments and Paraparesis Case based questions and conversational learning points

KIMS 2016 student 1 (Learning point: Format of case log discussion) :

1) Do we have to summarize the case and then answer the questions or directly start answering the questions?

Answer:

Do as in the previous format where you begin by creating a new log book post in your current weblog (complete online learning portfolio that you will use life long) for each of the three cases and clarify stating for each case your learning objectives such as:

"I've been given these three cases data here
https://medicinedepartment.blogspot.com/2020/05/case-based-online-learning-assignment.html?m=1 to solve in an attempt to understand the topic of "paraparesis."

This may develop my competency in

a) reading and comprehending clinical data related to "paraparesis" including history, clinical findings, investigations

b) come up with a diagnosis such as:

1) Anatomical location of the root cause

2) Physiological functional disability

3) Biochemical abnormalities that could be a root cause at a molecular level

4) Pathology that could reflect the root cause at a cellular level

c) a treatment plan for each of these patients of paraparesis that can have a pharmacological and non pharmacological component.

And

d) learning the scientific basis of diagnostic and therapeutic approach in terms of past collective experiences and experiments (aka evidence based medicine)

The first step to developing these competencies after reading and comprehending each patient data will be to

a) create a problem list for each patient in order of the patient's perceived priority

b) Discuss the root causes for the problem as described above in terms of anatomy, biochemistry and pathology, microbiology

and

c) discuss possible solutions to tackle these root causes from upstream (soil from which the roots begin) or downstream (to treating the stem and branches aka palliation) in terms of pharmacological (medicinal) and non pharmacological (such as prosthetics, implants) both in historical terms (past dominant treatments for the same cause and it's current evolution) as well as recent advances ( ongoing trials and innovative approaches even at a hypothetical stage).

KIMS 2016 student 2 (Learning point: How to write and represent our work in an original manner and avoid plagiarism) :

[5/22, 1:01 PM] KIMs 2016: I'm trying to fix the alignment of the text sir. There's some problem with it.

[5/22, 1:30 PM] Rakesh Biswas: But there are issues in your write up with copy pasting from uptodate.

Every statement in the text needs to cite a journal paper to support it. Not something like a blanket reference to uptodate. Uptodate people can sue for plagiarism if they see it. 🙂


[5/22, 1:31 PM] KIMs 2016: Oh no. What do you suggest I do?

[5/22, 1:31 PM] Rakesh Biswas: Overall it's very well done.
Maybe you could also just add a few sentences on how you obtained the text that were not your own original thoughts then it would be good to go

[5/22, 1:33 PM] KIMs 2016: Would that be the parts I quoted from UpToDate articles?


[5/22, 1:33 PM] Rakesh Biswas: By rules only one or two sentences can be quoted from a reference and they should be indicated by "...".

Anything more than that has to be paraphrased.

[5/22, 1:34 PM] Rakesh Biswas: Yes which ever parts you quoted from wherever that didn't originate from your original thoughts. Very difficult to keep track I know but this is how we train ourselves to do it right 👍

[5/22, 1:36 PM] KIMs 2016: Yes sir. Most of them are original. I wrote it after reading from various textbooks and video resources. I'll paraphrase the other parts which were copy pasted and redo them.

[5/22, 1:37 PM] Rakesh Biswas: It would be great if you can mention all those resources that you read in your learning and sharing journey 👍

[5/22, 1:37 PM] KIMs 2016: Okay sir I will do so

[5/22, 1:42 PM] KIMs 2016: I'm enjoying learning from real patients, it's motivating us to read up. But the entire process of reading, comprehending and interpreting the case and furthermore studying the material related to it and then penning it down using our own thoughts from our learning experience, for each case is taking a lot of time.

[5/22, 1:44 PM] Rakesh Biswas: Yes. Deep learning always takes time but is long lasting 🙂

[5/22, 3:39 PM] KIMs 2016: I just realised how so many of us are unknowingly plagiarising. Thanks for pointing it out, Sir. As you mentioned, US schools would've failed or suspended us for plagiarism. This is the first time we are learning how to write essays and research papers as it's not included in our curriculum. I hope to learn from this and follow the rules of paraphrasing and citing to avoid plagiarism in the future papers I submit.

[5/22, 3:45 PM] KIMs 2016: https://www.youtube.com/channel/UCrDcofIg9AJ3Ky3BGuMnqqw

I found this YouTube channel which has some useful videos which range from topics such as the Various types of Plagiarism, How to avoid Plagiarism, How to Paraphrase and The Review of literature.

Paraparesis Case based questions and conversational learning points:

KIMs 2016 student 3:

2) [5/20, 8:55 AM] Sir in this case
https://vaish7.blogspot.com/2020/05/medicine.html?m=1, the patient didn’t have fever or any symptoms of inflammation how would we think of TB?

[5/20, 9:17 AM]: That's the idea of differential diagnosis.

One discusses the differentials to capture something the current symptoms wouldn't allow us to think of from what is currently known.

[5/20, 8:54 AM] +91 0: https://vaish7.blogspot.com/2020/05/medicine.html?m=1

[5/20, 11:03 AM] +91 : Why haven’t we done a Lumbar puncture in the above patient sir?

[5/20, 4:40 PM] Rakesh Biswas: Alright. How do you think it would have helped if we did the lumber puncture? What were you expecting to find in it?

[5/20, 4:40 PM] : Lymphocyte?
To confirm TB

[5/20, 4:59 PM] Rakesh Biswas: How many are normal in CSF?

How does TB lead to lymphocytosis in CSF?
[5/20, 5:04 PM] : Less than 5 per ml is normal in CSF
Meningeal inflammation sir.

[5/20, 5:07 PM] Rakesh Biswas: So are you suspecting meningitis here? Does this patient of paraparesis have any sign of meningitis? What signs would you look for?

[5/20, 5:49 PM] +91: Kernigs sign

[5/20, 6:26 PM] Rakesh Biswas: So does this patient have any signs and symptoms of meningitis to merit an LP. You can even ask the intern. I can share her number if you want. You can message her or better is ask her in her log book comment box


[5/20, 7:16 PM] : No sir.
[5/20, 7:16 PM] : Yes sir I’ll ask her.

[5/20, 8:05 PM] Rakesh Biswas: 👍keep your questions coming. These are important to score learning points

[5/20, 8:55 PM] +91: Sir is it falx cerebri tuberculoma?

[5/20, 8:57 PM] Rakesh Biswas: Are there descriptions of such a location being affected by mycobacteria in the past on your review of literature?

[5/20, 8:57 PM]: Yes sir

[5/20, 8:57 PM]: It says there are 3 cases reported as now.

[5/20, 8:59 PM] Rakesh Biswas: Share those cases and check out the similarities with our patient


[5/20, 9:03 PM]: The patient had monoperesis because it was unilateral.

[5/20, 9:03 PM] Rakesh Biswas: Tell me the similarities and dissimilarities and always share the links to articles as we can't share the PDFs in your log book comment box or the FAQ learning points page

[5/20, 9:04 PM]: http://www.roneurosurgery.eu/atdoc/CucuA_Falx.pdf

[5/20, 9:06 PM] : Sir he had monoplegia initially
Later developed seizure which our patient didn’t.
CT revealed edema and a tumor like mass near the falx cerebri.

[5/20, 9:08 PM] Rakesh Biswas: Was the second line similar to our current patient?

[5/20, 9:17 PM] Yes sir

[5/20, 9:17 PM]  He had meningeal enhancement and edema.

[5/20, 10:51 PM] Rakesh Biswas: Yes but is that same as having a tumor like mass near the falx?


[5/20, 8:57 PM] Rakesh Biswas: Are there descriptions of such a location being affected by mycobacteria in the past on your review of literature?

[5/20, 8:57 PM] : Yes sir
[5/20, 8:57 PM]: It says there are 3 cases reported as now.

[5/20, 8:59 PM] Rakesh Biswas: Share those cases and check out the similarities with our patient

[5/20, 9:03 PM] Rakesh Biswas: Tell me the similarities and dissimilarities and always share the links to articles as we can't share the PDFs in your log book comment box or the FAQ learning points page

[5/20, 9:04 PM] : http://www.roneurosurgery.eu/atdoc/CucuA_Falx.pdf

[5/20, 9:06 PM] Kims 2016: Sir he had monoplegia initially
Later developed seizure which our patient didn’t.
CT revealed edema and a tumor like mass near the falx cerebri.


[5/20, 9:08 PM] Rakesh Biswas: Was the second line similar to our current patient?

[5/20, 9:17 PM] Kims 2016: Yes sir
[5/20, 9:17 PM] Kims 2016: He had meningeal enhancement and edema.

[5/20, 10:51 PM] Rakesh Biswas: Yes but is that same as having a tumor like mass near the falx?

[5/20, 11:11 PM] Kims 2016: Enhancing lesion is tumor like?

[5/20, 11:13 PM] Rakesh Biswas: Not as seen in the mri of our patient? Check out how a tumor enhancement looks like

[5/20, 11:15 PM] Kims 2016: There’s a diffuse enhancement in our patient


[5/20, 11:22 PM] Rakesh Biswas: Is that what happens in tumors?

[5/20, 11:22 PM] Kims 2016: No sir.

[5/20, 11:23 PM] Rakesh Biswas: Was contrast enhancement demonstrated in our patient's mri study? Was our patient given contrast?

[5/20, 11:24 PM] Kims 2016: The blog says there was significant enhancement

[5/20, 11:27 PM] Rakesh Biswas: Please clarify this with the intern who wrote that web log

[5/21, 8:18 AM] Kims 2016: Okay sir

[5/21, 8:49 AM] Kims 2016: Sir another doubt,
When we did an Xray abdomen and it showed psoas abscess on the right why didn’t we assume it to be the reason for the lower limb weakness and did an MRI?


[5/21, 8:54 AM] Rakesh Biswas: They happened at the same time but tell me what are your thoughts on the anatomical location of his lesion that is actually causing his paraparesis?

[5/21, 8:56 AM] Kims 2016: Psoas abscess compressing the nerves of the cord.

[5/21, 8:57 AM] Kims 2016 : It can also be because of the ring enhancing lesions of the cerebrum.

[5/21, 8:57 AM] Rakesh Biswas: Which part of the cord? Where is the psoas located and how does it compress the cord?

[5/21, 8:58 AM] Kims 2016: Not the cord but the nerves arising from the cord.
L4 and L5

[5/21, 8:58 AM] Rakesh Biswas: Which is the exact location? You can't say the paraparesis is both UMN as well as LMN?

[5/21, 8:59 AM] Kims 2016: Parasaggital?

[5/21, 9:01 AM] Kims 2016: It can be both.

[5/21, 9:03 AM] Kims 2016: In ALS, Neurodegenration, Spastic paraplegia

[5/21, 9:08 AM] Rakesh Biswas: What clinical signs does he have? Does he have both UMN and LMN signs?

[5/21, 9:09 AM] Kims 2016: UMN - Hypotonia, Absent reflexes

[5/21, 9:10 AM] Rakesh Biswas: 😳

[5/21, 9:12 AM] Kims 2016: LMN sir😬 sorryy

"[5/21, 9:13 AM] Rakesh Biswas: He has hypotonia and absent reflexes? 😳🤔
[5/21, 9:13 AM] Kims 2016 : Ankle clonus was absent
[5/21, 9:15 AM] Kims 2016 : And in the examination she wrote hypotonia in lower limbs.
[5/21, 9:42 AM] Rakesh Biswas: Which patient are you talking about? This one with psoas abscess? 🤔
Can you share the link to the case you are discussing?
[5/21, 9:42 AM] Kims 2016 : https://vaish7.blogspot.com/2020/05/medicine.html?m=1
[5/21, 9:42 AM] Kims 2016: This one sir.
[5/21, 9:49 AM] Rakesh Biswas: Yes but what about the reflexes?
[5/21, 9:50 AM] Kims 2016: Reflexes were present sir.
[5/21, 9:51 AM] Rakesh Biswas: Then can it be LMN?
[5/21, 9:51 AM] Kims 2016: No sir
But the reflexes were not exaggerated also
And there was hypotonia.
[5/21, 9:54 AM] Rakesh Biswas: Can a paraparesis be due to LMN as long as reflexes are normal even if the patient has hypotonia. Please ask the intern to change the entry of the reflexes as many observers thought they were exaggerated because they could be elicited with the fingers without the hammer. Check out the discussion videos around this patient but better do that in the end because then you won't have many questions left 🙂

Keep the questions coming. This is the best way to active learning
[5/21, 9:56 AM] Kims 2016 :  It is UMN sir?
[5/21, 9:56 AM] Kims 2016: Yes sir I will ask.
[5/21, 9:57 AM] Rakesh Biswas: Where does the UMN start and where does it end and where in that path is the lesion located in this patient?
[5/21, 9:58 AM] Kims 2016 : Motor cortex to the spinal cord
[5/21, 9:58 AM] Kims 2016: Cerebral cortex?
[5/21, 10:02 AM] Rakesh Biswas: How do you explain paraparesis with the cerebral cortical lesion? Bilateral cerebral cortex? Which part of the cerebral cortex?
[5/21, 10:03 AM] Kims 2016l: ACA territory sir
Medial side
[5/21, 10:04 AM] Rakesh Biswas: Both sides? Why and how the paraparesis?
[5/21, 10:04 AM] Kims 2016: Vasculitis?
[5/21, 10:09 AM] Rakesh Biswas: Which side ACA?

How does it cause paraparesis?
[5/21, 10:10 AM] Rakesh Biswas: Cause for ACA blockage due to ACA vasculitis? How did the mycobacteria in the psoas manage to do that?
[5/21, 10:11 AM] Kims 2016: Bilateral
[5/21, 10:11 AM] Rakesh Biswas: Ok

Answer the next questions
[5/21, 10:12 AM] Kims 2016: Blood borne spread sir?
[5/21, 10:14 AM] Rakesh Biswas: Second question was how does it cause paraparesis
[5/21, 10:16 AM] Kims 2016: Because of infarction?
[5/21, 10:18 AM] Rakesh Biswas: No I meant how does affecting that area of brain cause paraparesis
[5/21, 10:18 AM] Kims 2016: It’s affecting the motor areas of cortex
[5/21, 10:20 AM] Rakesh Biswas: The motor area is large. Can you share a weblink to an image showing the different motor areas such as leg area, hand area, face etc in one single image?
[5/21, 10:20 AM] Kims 2016: Legs according to hommunculus is on the medial side.
[5/21, 10:23 AM] Rakesh Biswas: Share a coronal section of the motor homunculus
[5/21, 10:24 AM] Rakesh Biswas: And share links because one can't enter images without reference into a blog
[5/21, 10:25 AM] Rakesh Biswas: Make it a habit to share links rather than stolen images 👍
[5/21, 10:26 AM] Kims 2016: https://www.alamy.com/cortical-homunculus-illustration-image245864436.html
[5/21, 10:47 AM] Kims 2016: So isn’t it the reason sir?
[5/21, 11:12 AM] Rakesh Biswas: Yes it is. Can you find if anyone else has reported this happening in other patients of tuberculosis?
[5/21, 11:26 AM] Kims 2016: Yes sir I’ll check.
[5/21, 11:26 AM] Kims 2016 A Vaishnavi: Sir the videos that are being uploaded on YouTube are not clear.
We aren’t able to hear anything.
[5/21, 11:28 AM] Rakesh Biswas: Yes. We need some of you people here to come here and become videographers. 😅
[5/21, 11:31 AM] Kims 2016 : 😁we’ll come soon sir.
[5/21, 11:42 AM] Kims 2016: Sir the isolated cns angiitis is itself very rare and till now no proper research was done sir.
[5/21, 11:56 AM] Kims 2016: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606267/
[5/21, 12:49 PM] Kims 2016: Sir in this case
Scabies serology was negative
So can we attribute the rash to peripheral neuropathy?
[5/21, 5:00 PM] Rakesh Biswas: Quote the relevant portion that will be useful to read in the context of our current discussion
[5/21, 5:00 PM] Rakesh Biswas: But we are not thinking of isolated CNS angiitis here but tubercular CNS vasculitis?
[5/21, 5:01 PM] Rakesh Biswas: Scabies serology? 😳🤔
[5/21, 5:04 PM] Rakesh Biswas: Ask Hitesh to share the report.
[5/21, 5:04 PM] Rakesh Biswas: What about searching for tubercular CNS vasculitis
[5/21, 5:05 PM] Kims 2016: There’s one retrospective study sir
But that was as a complication oc tubercular meningitis
[5/21, 5:05 PM] Kims 2016: Okay sir.
[5/21, 8:09 PM] Rakesh Biswas: [5/21, 5:33 PM] Hitesh Kims Intern: It's not scabies serology sir
[5/21, 5:36 PM] Hitesh Kims Intern: There what I mean was as he was not having any itching we thought of immunocompromised state due to viral infection as the reason for no itching and paraperesis but retroviral serology came as negative sir
[5/21, 8:10 PM] Rakesh Biswas: There is probably no such thing as scabies serology.

How is it diagnosed?
[5/21, 8:34 PM] Kims 2016: 😬
[5/21, 8:34 PM] Kims 2016: Sir it was written serology negative
So
[5/21, 8:36 PM] Rakesh Biswas: Yes he meant retroviral serology.

So find out and tell us how is the diagnosis of scabies confirmed

[5/21, 9:51 PM] Kims 2016: Okay sir"

KIMs student 4:


[5/22, 10:46 AM] : Gud Morning Sir,
In our case of 23 yr patient with lower limb weakness
Why was an MRI of spine not done?
It is also possible that he might have Potts paraplegia, Presence of Ankle clonus and exaggerated DTR are earliest neurological signs indicating a SC compression.
[5/22, 10:48 AM] : Also it would be better to have an Orthopedic opinion to rule out Potts paraplegia. Because if it is there and is not identified it would involve Bowel and Bladder in long term and if it's Potts paraplegia it can be managed surgically.
[5/22, 10:50 AM] : Also Gait is to be evaluated to see if there is any TB spondylitis
[5/22, 4:28 PM] Rakesh Sir KIMS: Orthopedic opinion for Potts paraplegia? 😅

Well their opinion is only asked if we want them to operate, otherwise we need to make the diagnosis for them ourselves first
[5/22, 4:30 PM] Rakesh Sir KIMS: Ask Hitesh to share with you the MR spine images.

The MRI spine lumbar vertebral involvement is mentioned in his mri report that is already in the log.

However that may not be causing his paraparesis. Can you tell why?
[5/22, 4:31 PM] Rakesh Sir KIMS: Ask Hitesh to share his gait video or at least mention what was his gait like
[5/22, 4:31 PM] : Sure sir
[5/22, 4:31 PM] : May be it's not compressing the cord
[5/22, 4:32 PM] Rakesh Sir KIMS: Ok so back to the first question
[5/22, 4:33 PM] : Sir but the lesion is definitely peripheral na Sir
[5/22, 4:34 PM] : If it's a central lesion the presentation would be far different with involvement of other structures
[5/22, 4:35 PM] : There is a chace of disc inflammation spondylodiscitis
[5/22, 4:35 PM] : But that is usually more common in immunocompromised patients
[5/22, 4:35 PM] : I think we also need to assess the patients HIV status tooo
[5/22, 4:36 PM] : To consider few other differentials
[5/22, 4:43 PM] Rakesh Sir KIMS: Yes so the most basic thing in mbbs neurology that we need to learn to distinguish is between peripheral LMN lesion and central UMN lesion.

What does his clinical features suggest?
[5/22, 4:46 PM] : Sir
From the Nervous system examination mentioned above it is evident that there is
•B/L Hypotonia, Suggestive of LMN lesions
•Hyper reflexia of Knee and Ankle reflex suggestive of lesion UMN lesion above L3,L4
• Ankle clonus, suggestive of UMN lesion above S1,S2
[5/22, 4:47 PM] : I think there is lesion just above L3,L4 in the spinal cord that reflects as UMN lesion for the levels below it.

[5/22, 4:50 PM] Rakesh Sir KIMS: Good above L3, L4 where?

[5/22, 4:59 PM] : Just above L3,L4 but not likely disturbing the L2
Because if L2 in involved in the lesion then
There should be sensory loss on antero lateral aspect of thigh upto level of knee(Lateral cutaneous nerve of thigh-L2,3)
Also loss of sensation over the medial aspect of thigh( Obturator nerve-L2,3,4)

[5/22, 5:00 PM] : As there is no sensory deficit it is likely that the sensations are preserved due to normal L2

[5/22, 5:04 PM] : Also involvement of L3,4 explain the weakness in lower limb caused due to loss of motor fibers of obturator nerve to thigh muscle

(5/22, 11:00 PM) : RB

So you mean the lesion is in the L2-3, spinal cord segment or L2 and L3 vertebra? What have they mentioned in the MRI spine report about which vertebra is involved?

Also what if I told you that his upper limb reflexes are so exaggerated that we could actually elicit the reflex with our fingers?


Student 5 kims 2016:

"[5/22, 4:12 PM] Rakesh Biswas:

"Anatomical location of the root cause could be in the Spinal cord?"

Where is the exact level in the spinal cord? Is it in the cervical, thoracic or lumbosacral segments? 🤔

[5/22, 4:19 PM] 2016 Kims: Lumbosacral segments sir

[5/22, 4:21 PM] 2016 Kims: But it could be lower thoracic and upper lumbar sir.

[5/22, 4:23 PM] 2016 Kims: I think we need more Data to confirm it sir. MRI spine should also be done
[5/22, 4:23 PM] Rakesh Biswas: What if I told you that the patient's upper limb reflexes were elicitable by me by just tapping with my fingers and even his biceps was jumping bilaterally
[5/22, 4:25 PM] 2016 Kims: Then it could be a upper motor neuron lesion sir. If it’s exaggerated then maybe it could be a UMN lesion
[5/22, 4:26 PM] 2016 Kims: His babinski sign is also positive
[5/22, 4:27 PM] 2016 Kims: But since he has hypotonia I thought it couldn’t be UMN
[5/22, 4:39 PM] Rakesh Biswas: In the stage of acute neuronal shock one can still have hypotonia in UMN
[5/22, 4:40 PM] 2016 Kims: Yes sir so how do we know that it a stage of acute neuronal shock?
[5/22, 4:49 PM] Rakesh Biswas: If the UMN findings such as hyperreflexia predominate you think of UMN with hypotonia due to acute neuronal shock.

If LMN findings such as areflexia predominates you think of hypotonia due to LMN
[5/22, 4:50 PM] 2016 Kims: Okay sir.
Thank you. So this could be a state of UMN lesion with hypotonia due to acute neuronal shock
[5/22, 4:51 PM] Rakesh Biswas: Yes and where is the UMN lesion located?
[5/22, 4:53 PM] 2016 Kims: I think it’s above the anterior horn cell in spinal cord
[5/22, 4:55 PM] 2016 Kims: Sir in the video you said it could be parasagittal meningioma but then the lesion should be in cerebral cortex for that
[5/22, 4:55 PM] 2016 Kims: And he does not have any features suggestive of cortical lesion like aphasia
[5/22, 4:56 PM] Rakesh Biswas: Where are anterior horn cells in spinal cord? 😅
[5/22, 4:57 PM] Rakesh Biswas: Are the areas of aphasia located all over the cortex? Is the leg area same as the speech area? 😅
[5/22, 4:58 PM] Rakesh Biswas: You will find anterior horn cells at every section you take of the spinal cord
[5/22, 4:58 PM] 2016 Kims: Oh yes sir. Sorry sir 😅
[5/22, 4:58 PM] 2016 Kims: I think the lesion is at the level of lower thoracic and upper lumbar vertebrae
[5/22, 4:59 PM] 2016 Kims: No sir. 😅
[5/22, 4:59 PM] 2016 Kims: It’s speech areas are brocas and wernickes
[5/22, 5:00 PM] 2016 Kims: So it could be parasaggital meningioma then?
[5/22, 5:06 PM] Rakesh Biswas: What about this then? 👆
[5/22, 5:08 PM] Rakesh Biswas: How do you explain the gluteal abscess and the mei report mentioning other things in that vertebral region?
[5/22, 5:13 PM] 2016 Kims: Sir i think that is a cold abscess.
Yeah then lesion is in lumbosacral region sir that could explain the abscess.
[5/22, 5:39 PM] Rakesh Biswas: So is the vertebral lesion producing any neurological signs?
[5/22, 7:07 PM] 2016 Kims: Yes sir I think it’s compressing upon the cord and causing the upper motor neuron signs i.e. hypotonia and exaggeration of reflexes
[5/22, 7:08 PM] 2016 Kims: Sir should I change it in my blog then ? That the reflexes are exaggerated
[5/22, 7:46 PM] Rakesh Biswas: Yes instead of deleting the previous you can add this as an edit
[5/22, 7:47 PM] Rakesh Biswas: But then where in the cord will the compression produce the paraparesis he is having?
[5/22, 8:03 PM]  2016 Kims: Okay sir. I will do that
[5/22, 8:04 PM] 2016 Kims: Sir because psoas muscle is supplied by L2,L3,L4 nerve roots so maybe the compression is over there
[5/22, 8:22 PM] Rakesh Biswas: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:02 PM] 2016 Kims: LMN sir
[5/22, 9:04 PM] Rakesh Biswas: And what are the dominant clinical signs in your patient suggestive of?
[5/22, 9:36 PM] Kims: So if the nerve root is compressed what will it look like? UMN or LMN?
[5/22, 9:36 PM] 2016 Kims: LMN sir
[5/22, 10:10 PM] Rakesh Biswas: So then the nerve root is spared ?"

Case based online learning assignment for 8th semesters this week : Three patients of paraparesis

Last week we had three patients of paraparesis admitted with us and our interns have shared it in their E logs below for the online 8th semester students to go through this week and answer some of the case related questions and also come out with their own queries:

1) Presented by Dr Anugna 2014 batch

https://hitesh116.blogspot.com/2020/05/12may-2020-elog-medicine-intern.html?m=1st

https://srianugna.blogspot.com/2020/05/hello-everyone.html

PG intern offline Case presentation and discussion 18M with paraparesis proximal to distal and calf hypertrophy: https://youtu.be/3VVH7w3rWSM


2) Presented by Dr Vaishnavi 2014 batch

https://vaish7.blogspot.com/2020/05/medicine.html?m=1

Offline intern PG discussion around 23M with paraparesis

https://youtu.be/ClopCj2KwZc


Part 2 of offline PG intern discussion around 23M with chronic gluteal abscess and paraparesis:

https://youtu.be/QhjiomY-S74

Part 3 of 23M with paraparesis case discussion

 https://youtu.be/g9CQKhxsXqY

Part 4 of Offline intern PG discussion around 23M with paraparesis

https://youtu.be/FL37cYp6ZqU


3) Presented by Dr Hitesh 2014 batch

A 18M with inability to climb and difficulty in walking

https://hitesh116.blogspot.com/2020/05/elog-13th-may-2020.html?m=1

Session video: https://youtu.be/VNq0rDdA-80

A few common questions for the 8th semester students

1) Where are the three different anatomical locations for the cause of the paraparesis for each of these patients?

2) What is the most likely pathology and etiology in that anatomical location?

3) What are the therapeutic options in such situations?

4) Please share questions that come to your mind upon going through each of the cases.

Each 8th semester student will share their answers in their own E logs. Thanks to all the 8th semester students for sharing all their 200 web based logs that will remain as their 'online learning portfolios,' and will be very useful toward their formative assessment in the coming months and years. More here:
https://medicinedepartment.blogspot.com/2020/05/integrating-medical-education-and.html?m=1

Once the 8th semesters join hospital duties they will be expected to evaluate their own patients in the wards and create their own patient online records.

Integrating Medical education and practice: Online real patient data stimulating active learning in medical students

General  Medicine online classes for Final MBBS part – II students are being  conducted through two formats.

One is a passive learning format where PPTs or lecture videos done by our faculty are shared through a schoology portal and then MCQs are provided with auto correct generation of content recall testing.

The other format is an attempt at active learning with students on social media, centered around their Elog books (Online learning portfolio) where students are provided a clinical problem to solve and then encouraged to raise questions around the case and search and discuss the answers with Faculty and other senior students.

This week we have begun our online learning session

with the UGs around

the topic of

"Patient data analysis"

with a

Target competency:

to develop an ability/competency to read and comprehend a patient's history, examination findings, investigations and analyze it in a manner to understand the patient's requirements around his/her diagnosis and treatment.

Methodology:

The students competency will be assessed by their ability to form a problem list in order of the patient's priority for which they need to get in touch with the original creator of the online patient's record and then from each problem in the list they would need to analyze the cause of the problem and come to a diagnosis and therapeutic plan for the patient that will be vetted as useful by the entire general medicine online learning ecosystem that includes, interns, Pgs, faculty locally as well as globally including the online patient himself/herself.

Below is the link to all 200 online learning logs made by the current 8th semester students:

https://detailedclinicalanalysis.blogspot.com/2020/05/online-learning-individual-patient-data.html

And here are some special sample logs from a few students who were the early birds in this online active learning session where majority of their cognitive  activity is in pm conversation with the session moderator and is reflected in the comments section of their log book.

https://decodemed.blogspot.com/2020/05/unraveling-skein.html?showComment=1589730592398&m=1#c8217929345349410897

https://shivani2401elogbookmedicine.blogspot.com/2020/05/my-medical-elog-book-may-15-2020.html?m=1

Student log book with the anonymized online patient's comments

https://anushachowdaryshivakoti150.blogspot.com/2020/05/analysis-of-case-of-42yr-old-female.html?m=1

Student log book with queries raised by the student stimulating an active learning conversation with the moderator https://muskaanmenghwani.blogspot.com/2020/05/42-year-old-female-with-multiple-health.html?m=1

This is a student log where an active learning cross consultation was obtained from another department and added to the student's log book comment box that reflects his her active conversational learning

https://rhea9895.blogspot.com/2020/05/case-of-42-year-old-female-with.html?m=1

All the interns and PGs in the department of Medicine have been informed about this exercise and the student E logs have been made available for them to participate in this active online learning activity that will be hopefully reflected in the comments section of the student's E logs following which the students shall receive formative assessment score based on a percentile once we check out the student log with the maximum number of learning points that can serve as the current highest comparator.

Maybe chat bots will soon take over the active learning and assessment part of the overall workflow?

A medicine PG resident's Web log book

Hello all. I am a resident in Medicine and my daily schedule for the week is detailed here: https://docs.google.com/document/d/1lCU31w0ir_MBsJpLTFdyD9Dt1elAq9nDuwu0hfbcZ6k/edit?usp=drivesdk&ouid=106211649452385508461

This E log book is a mandatory requirement to assess our daily attendance in terms of our mental presence and our daily learning achievements in the medicine department where every PG Resident  here shall by 8:00 PM (unless it's an admission day) provide a brief log of what they have done cognitively as well as hands on for that day from 9:00 AM to 6:00 PM.

I have been told that the daily log can be done here under the following headings 

1) Case based learning 

a) Inpatient

b) Outpatient 

c) ICU 

2) Thesis 

a) That day's thesis case data 

b) Questions around cases or even study design etc 

3) Theory knowledge acquisition for end term summative assessment:

Paper I: Basic Medical Sciences 

Paper II: Medicine and allied specialties including pediatrics, dermatology &

 psychiatry

Paper III: Tropical Medicine and Infectious Diseases

Paper IV: Recent Advances in Medicine

4) Procedures done with video evidence (with patient deidentied)

The E log book or web log book is a formative assessment tool aka internal assessment in India and in India the internal assessment as well as performance in the final exams depends on the HOD's regular formative assessment of the candidate's daily performance that builds up over the three years and this internal assessment is never expressed in the form of any number but in the form of a very very vital role the HOD plays in the candidate's learning journey and it's completion at the end of three years. 

For those not logging their daily learning activities here, the impression conveyed would be that they are not having any daily learning activity worth sharing.

So here goes my log of daily activities starting from:

Monday:

Went early for the morning rounds and found that my junior intern had still not arrived and that really made me mad as it meant that now I would have to collect all the patient reports by myself. 😡

My senior PG admitted this young boy with a chronic gluteal abscess yesterday who had developed both lower limb weakness since five days.

Case report:

23M with complaints of weakness of bilateral lower limbs since 5 days along 

with tingling and numbness 

h/o vomitings 5days back 

3-4 episodes non projectile non bilious food particles in content.

when he got up for urination,suddenly he had a fall and got up with the help of father.

gluteal abscess since 5months (operated 5 months back) 

scrotal abscess since 20 days(incision and drainage 10 days back)

PAST HISTORY 

no similar complaints in past 

auto driver

not past history of HTN/DM/ASTHMA

General examination: 

Gluteal region as in the image below:

Pallor absent

Icterus absent

No cyanosis clubbing 

lymphademopathy, Edema

Afebrile

Bp 120/80 mm hg

Pr 80 bpm

spo2 98%

Cvs s1 s2 hear no murmurs

Rs bilateral air entry + normal vesicular breath sounds heard

P/a soft, non tender

Cns 

conscious

speech-normal

cranial nerves intact.

MOTOR SYSTEM 

                         Right.         Left

Bulk:               normal.      Normal

Tone: ul.        normal.       Normal

           LL.       hypotonia    hypotonia

Power          rt.          lt

         ul.        5/5.      5/5

         LL.       2/5.      0/5

Reflexes.  

   Superficial reflexes

                       Right.           Left

Corneal.        P                   P

Conjunctival P.                  P

Abdominal.   P.                  P

Plantar          Extensor   Extensor

    Deep tendon reflexes 

                     Right.             Left

Biceps.        2+                  1+

Triceps.       2+                   1+

Supinator.    3+                   2+

Knee             3+                  2+

Ankle.           3+                  2+

jaw jerk.        1+.                1+

ankle clonus present.     absent

Primitive reflex -absent

Involuntary movements - absent 

SENSORY SYSTEM - normal

CEREBELLUM

titubation - absent

Nystagmus- absent

Intensional tremors - absent

Pendular knee jerk - absent 

Coordination test -normal

MENINGIAL SIGNS

Neck stiffness - negative

Kernigns sign - negative

Brudzinkis sign - negative

INVESTIGATIONS

HBS AG: negative

ANTIHCV ANTIBODIES: nonreactive

HIV : non reactive

HEMOGRAM : 

HB        15.5gm/dl

Platelets 2.23 lakhs/cumm

TLC         9600cells/cumm

Lymphocytes 15%         

LFT

TO.BIL.       0.82mg/dl

DI.BIL.          0.21gm/dl

SGOT.            80IU/LIT

SGPT.             10IU/LIT

ALK.PH.            192IU/LIT

TO.PRO.                7.5gm/dl

ALB.                        4gm/dl

A/G RATIO.           1.19

RFT

UREA.                  16mg/dl

CREATININE.      0.6mg/dl

URIC ACID           3.7mg/dl

CALCIUM.            9.4mg/dl

PHOS.                  4.6mg/dl

SODIUM.              136meq/lit

K+.                         3.9meq/lit

CL-.                       102 meq/lit

ESR 45 mm/1st hr

RBS 99 mg/dl


Cranial mri images:

TREATMENT :

INJ.ZOFER 4mg IV.SOS

INJ.PANTOP 40mg IV OD 

BP ,PULSE MONITORING

INJ.AUGMENTIN 1.2g IV BD

OINT.MEGAHEAL FOR LOCAL APPLICATION

SITZ BATH WITH BETADINE TID

FREQUENT CHANGE OF POSITION

I saw the above treatment penned by my senior in upper case and wondered out aloud as to why every patient who gets admitted is prescribed mandatory pantoprazole and this one had vomiting 5 days back!! This comment was frowned upon needless to say. 

        

   In the afternoon my senior presented this patient and we had an extensive discussion as to the etiology that you can see in the recorded video here 

https://youtu.be/ClopCj2KwZc

  

Procedure:

My senior PG medicine asked me to take this patient with severe anemia (web logged by our medical student here:https://classworkdecjan.blogspot.com/2016/12/60f-with-coma-e-coli-sepsis-and-upper.html?m=1) to the pathology department for a bone marrow aspiration and biopsy. Here is a video of that biopsy procedure: https://youtu.be/MeozrO1Nkyk

Theory preparation:

In the afternoon session the same day we also had a few topic discussions that I reviewed again for my theory preparation. Check out the videos here https://m.youtube.com/watch?v=yhXqgGpfIEo&list=PLvOgc9_v4PCKsIrVK4laA3_rUJOMPAYKJ

One such topic (check out the specific video here:https://www.youtube.com/watch?v=YzVI1XZ3nAI&feature=youtu.be)

was about pheochromocytoma where I learned about why in preoperative management of pheochromocytomas, alpha blockers are given prior to beta blockers.

"At low concentrations, adrenaline acts on beta2 receptors causing vasodilatation.

At higher concentration it acts on alpha 1 receptors causing vasoconstriction.

If beta blockers are given first, they act upon beta2 receptors, thus blocking them and an unapposed alpha adrenergic activity can be seen which results in HYPERTENSIVE CRISIS and cardiovascular collapse sir.

To prevent this non selective alpha blockers are given first to reduce the hypertension.

Non selective alpha blockers cause reflex tachycardia. In order to further reduce the blood pressure and to reduce the risk of tachyarrhythmias, beta blockers are added further."

Also, Labetalol(alpha plus beta blocker) has a 1:7 alpha-beta blocking activity and when it is given to a patient with pheochromocytoma, due to more beta blocking action it results in hypertensive crisis again.

So labetalol is also not given.

I read more about it here https://academic.oup.com/jcem/article/92/11/4069/2597882

Thesis project:

At the end of the day one of my batchmates from another unit mentioned that one patient has arrived at the causalty who looks like my thesis case and I am currently working on a thesis on "Etiology ,Management and outcome in patients with hyponatremia" and I have been separately logging all my thesis cases here http://allabouthyponatremia.blogspot.com/?m=1

Here is the detailed MCI guideline based rationale for our daily roster 

https://medicinedepartment.blogspot.com/2020/05/a-daily-pragmatic-learning-roster-as.html?m=1