Bobble head doll clinical complexity outcomes project

Introduction: During the seventeenth century, figurines of Buddha and other religious figures called "temple nodders" were produced in Asia.^[3] The earliest known Western reference to a bobblehead is thought to be in Nikolai Gogol's 1842 short story "The Overcoat," in which the main character's neck was described as being "like the necks of plaster cats that wag their heads.

Thanjavur dolls are a type of Indian bobblehead doll known as "Thanjavur Thalayatti Bommai" in the Tamil language, meaning "Tanjore Head-Shaking Doll." They are a native art form in the Thanjavur region of Tamil Nadu. 

CC licence: https://commons.m.wikimedia.org/wiki/File:A_Tanjore_doll.jpg#mw-jump-to-license

Project thoughts beginning from our first tryst with the patient seen in 2004 in Vydehi medical college, Bangalore although at that time we didn't even realise what his symptoms were and he googled us ten years later to show us again in another city where we documented our first observation of this syn in a reflective note as fished out from that time in an email sent on 2013 below:

Date: Thu, 10 Jan 2013, 12:35
Subject: re: Bobble head Doll history
To

I met this 39 year old man yesterday after a gap of 7 years since our first meeting in Bangalore. At the time i had simply taken his history and prescribed some non specific medications based on his history without actually witnessing the movements (which at the time was reported to be of a momentary duration). The physician-placebo effect had probably brought him back to me in Bhopal after he managed to locate me through an internet search and sent me an email.

His symptoms had gradually progressed in duration and frequency such that i could easily witness it for myself now. It was a stereotypical head movement that appeared to say no-no.He also had a badly impaired tandem walk among other positive findings. His head movements appeared to increase while lying down and this made us have to resort to a good dose of IV diazepam to sedate him during the cranial MRI (attached).

Copying this also to our neurosurgeon so that it helps to evaluate him soon by the next working day. 

There is not much evidence on how to go about the further management of such patients other than convincing reports of improvement following endoscopic third ventriculostomy in different case series. http://www.ncbi.nlm.nih.gov/pubmed/22886034

The other unique feature of our patient was the manifestation of this syndrome in adult life. The oldest patient (among the 57 patients reported till date) is 13 years http://www.neuroscience.org.np/Rana2.pdf

Also why were his symptoms increasing with lying supine? Is it because the normal third ventricular pressure increases during supine? http://www.ncbi.nlm.nih.gov/pubmed/9402598

best,

Subsequently again lost him to follow up for nearly another 7 years before he again got in touch through Facebook and our students in Hyderabad prepared the case reports below through telephonic data capture:

case report link from a student's online learning portfolio linked below: 

https://ssahamedicalcases.blogspot.com/2023/02/patient-history-pt-is-49-yrs-old-male.html?m=1

Hand written case report from another student's online learning portfolio: 

https://drsaranyaroshni.blogspot.com/2022/02/a-middle-aged-man-with-progressive.html?m=1

Video of patient 2 taken in an OPD follow up encounter in 15th October 2024:

https://youtu.be/8ZKxmeMgSLE?feature=shared

CBBLE and PaJR conversations also at the description box in the YouTube link above.

Got the content below from his PaJR description box possibly added in June 2023 during first encounter:

Sequence of events:

1993:He was born by NVD and cry after birth (+)with no H/o birth insult

He is the youngest in the family with four sisters elder than him who are apparently healthy 

2015- For the first time patient noticed involuntary movements of head and neck as insisted by his friends which were mild,he visited a hospital in Karimnagar where he was prescribed Tab Clonazepam 0.25 mg +propranolol 20 mg  and ?one more medication at night (which he was even using now)

2016- He was married to a woman with some ?spine deformity and had a kid in 2017,born by LSCS and no H/o birth insult and he is healthy now

2017-He consulted a Neurologist in Hyderabad and used medication for 6 months ,but symptoms did not subside and stopped the medication 

2018-By this time his involuntary movements of head increased and he visited a hospital in Nalgonda where he was prescribed with some medication which he almost 3-4 months ,but symptoms did not subside

2019-2020: His symptoms gradually increased despite using different medications 

2021:He Visited our hospital with pain abdomen and was diagnosed with liver abscess and the abscess was drained and he was relieved 

2022: There if further increase in head and neck movements associated with tremulous speech and movements of left upper limb and after 6 months he developed similar complaints in the right upper limb.

No involuntary movements of lower limbs till now

2023:He consulted a physician in February where he used  Vit B12 and thiamine along with some other medication after which he felt his symptoms decreased a bit

Initially he felt the symptoms relieved on taking alcohol but gradually didn’t find any difference on consumption of alcohol 

These abnormal movements are absent during rest or sleep

No H/o Loss of consciousness 

No H/o seizure activity 

No H/o giddiness,falls

Last alcohol intake was 15 days back(90ml whiskey)

Consumes around 90ml/day since 12 years

O/E:

Pt is conscious,coherent and cooperative 

Pt maintained eye contact through out the examination 

HMF

EMR summary of second patient from June 2023:

Age/Gender : 27 Years/Male
Address :
Discharge Type: Relieved
Admission Date: 06/05/2023 11:18 AM

Diagnosis

TREMOR PLUS SYNDROME
SPASTIC CEREBELLAR ATAXIA ?GENETIC CAUSE ?OTHER CAUSES
Case History and Clinical Findings
PATIENT CAME WITH C/O INVOLUNTARY MOVEMENTS OF NECK SINCE 4 YEARS INVOLUNTARY MOVEMENTS OF UPPER LIMBS SINCE 1 YEAR

HOPI
PATIENT WAS APPARENTLY NORMAL 4 YEARS BACK THEN HE DEVELOPED INVOLUNTARY MOVEMENTS OF NECK SINCE 4 YEARS WHICH WAS INSIDIOUS IN ONSET AND GRADUALLY PROGRESSIVE , INITIALLY STARTED AS FINE MOVEMENTS / TREMORS THEN GRADUALLY INCREASED IN INTENSITY
HE ALSO DEVELOPED INVOLUNTARY MOVEMENTS OF UPPER LIMBS SINCE 1 YEAR INSIDIOUS IN ONSET AND GRADUALLY PROGRESSIVE
INITIALLY LEFT UPPER LIMB THEN PROGRESSED TO RIGHT UPPER LIMB
PATIENT C/O INCREASE ININTENSITY OF INVOLUNTARY MOVEMENTS SINCE 1 WEEK NO C/O HEADACHE,SEIZURES , LOC , GIDDINESS , WEAKNESS, VISION DISTURBANCE , FEVER , VOMITINGS.
 

TREMORS ARE SEEN ONLY IN WORKING CONDITION AND RELIEVED IN RESTING STATE PAST HISTORY:
H/O LIVER ABSCESS 1 YEAR BACKDRAINED AND ADVISED FOR ALCOHOL ABSTINENCE N/K/C/O DM , HTN ,TB , EPILEPSY , HTN,CAD,CVA , THYROID.
PERSONAL HISTORY ; DIET : MIXED
APPETITE : DECREASED SLEEP : NORMAL
BOWEL AND BLADDER : REGULAR
ADDICTIONS: ALCOHOL : OCCASIONAL (STOPPED 15 DAYS BACK) NO ALLERGIES

FAMILY HISTORY :
INSIGNIFICANT


GENERAL EXAMINATION :
PATIENT IS
MODERATELY BUILT AND NOURISHED .
NO SIGNS OF ICTERUS , CYANOSIS , CLUBBING ,LYMPHADENOPATHY, EDEMA.


VITALS : TEMPERATURE:98.6 F PR - 54 BPM
BP - 100/60 MMHG RR - 21 CPM
SPO2 - 98% ON RA GRBS - 92 MG/DL

SYSTEMIC EXAMINATION : PER ABDOMEN : INSPECTION :
ABDOMEN IS SCAPHOID UMBILICUS IS CENTRAL
 

ALL QUADRANTS ARE MOVING EQUALLY WITH RESPIRATION NO SINUSES , ENGORGED VEINS, VISIBLE PULSATIONS . HERNIAL ORIFICES ARE FREE.
PALPATION :
NO LOCAL RISE OF TEMPERATURE NO TENDERNESS
LIVER AND SPLEEN - NOT PALPABLE
PERCUSSION : TYMPANIC NOTE HEARD OVER THE ABDOMEN. FLUID THRILL ABSENT
SHIFTING DULLNESS ABSENT AUSCULTATION :
BOWEL SOUNDS ARE HEARD.


CARDIOVASCULAR SYSTEM :
INSPECTION:
SHAPE OF CHEST IS ELLIPTICAL. NO RAISED JVP
NO VISIBLE PULSATIONS, SCARS , SINUSES , ENGORGED VEINS. PALPATION :
APEX BEAT - FELT AT LEFT 5TH INTERCOSTAL SPACE NO THRILLS AND PARASTERNAL HEAVES AUSCULTATION :
S1 AND S2 HEARD.


RESPIRATORY SYSTEM:
INSPECTION:
SHAPE- ELLIPTICAL B/L SYMMETRICAL
BOTH SIDES MOVING EQUALLY WITH RESPIRATION . NO SCARS, SINUSES, ENGORGED VEINS, PULSATIONS PALPATION:
TRACHEA - CENTRAL
EXPANSION OF CHEST IS SYMMETRICAL. VOCAL FREMITUS - NORMAL
 

PERCUSSION: RESONANT BILATERALLY AUSCULTATION:
BILATERAL AIR ENTRY PRESENT


CENTRAL NERVOUS SYSTEM:
PATIENT IS DROWSY E4V5M6
SPEECH- SLURRED
NO SIGNS OF MENINGEAL IRRITATION.
CRANIAL NERVES- 11 TH CRANIAL NERVE - DIFFICULTY IN SHRUGGING OF SHOULDERS SENSORY SYSTEM- NORMAL
MOTOR SYSTEM:
TONE- NORMAL
POWER- BILATERALLY 5/5 REFLEXES RIGHTLEFT BICEPS - -
TRICEPS. - - SUPINATOR - - KNEE. - - ANKLE - -
BILATERAL PLANTAR EXTENSOR CEREBELLUM EXAMINATION :
INTENTIONAL TREMORS PRESENT GAIT - NORMAL
NYSTAGMUS - ABSENT FINGER NOSE TEST - NORMAL
DYSDIADOKOKINESIA - ABSENT ROMBERGS TEST - EQUIVOCAL

COURSE IN HOSPITAL:A 26 YEAR OLD MALE CAME WITH C/O INVOLUNTARY MOVEMENTS OF NECK SINCE 4 YEARS AND INVOLUNTARY MOVEMENTS OF UPPER LIMBS SINCE 1 YEAR.MRI BRAIN SHOWED NO ABNORMALITIY.NEUROLOGY REFERRAL WAS DONE AND ADVISED MRI CERVICAL SPINE AND ADVISED CAP. BETACAP 40 MG PO/BD , TAB.VITAMIN E 400 MG PO/OD, INJ.METHYLCOBALAMIN 1500MCG IN 100ML NS FOR 1 WEEK.
 

PATIENT WAS DISCHARGED AND WAS ASKED TO REVIEW WITH MRI CERVICAL SPINE REPORT.
Investigation
ECG -
USG ABDOMEN - MILD SPLENOMEGALY ( 7-5-23) 2 D ECHO -6-5-23
NO MR /AR/TR
NO RWMA . NO AS /MS
GOOD LV SYSTOLIC FUNCTION
NO DIASTOLIC FUNCTION . NO PAH/PE/LV CLOTS HEMOGRAM:6/05/23
HB 12.2gm/dl
TLC:5700 CELLS/CUMM PLT: 2.15 LAKHS/CUMM MRI BRAIN(11/5/23)
NO ABNORMALITY DETECTED
Treatment Given(Enter only Generic Name)
IV FLUIDS @ 75 ML/HR
INJ.METHYLCOBALAMIN 1500 MCG/IV/OD IN 100 ML NS FOR 1 WEEK CAP.BETACAP TR 40MG PO/BD
TAB.TETRABENZENE 12.5 MG PO/OD TAB.EVION PO O/D
Advice at Discharge
INJ.METHYLCOBALAMIN 1500 MCG/IV/OD IN 100 ML NS FOR 1 WEEK ONCE WEEKLY FOR 4 WEEKS.
CAP.BETACAP TR 40MG PO/BD TAB.EVION PO/ OD
Follow Up
REVIEW TO GENERAL MEDICINE OPD WITH MRI CERVICAL SPINE AFTER 2 WEEKS OR REVIEW SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
 

Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE,DONOT MISS MEDICATIONS. In case
of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact: For Treatment Enquiries Patient/Attendent Declaration : - The medicines prescribed and the advice regarding preventive aspects of care ,when and how to obtain urgent care have been explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER SIGNATURE OF PG/INTERNEE SIGNATURE OF ADMINISTRATOR SIGNATURE OF FACULTY
Discharge Date Date:12/5/23 Ward:AMC
Unit:6

Video of third patient taken in OPD on April 2024 and patient lost to follow up:

https://youtu.be/BBklEbIz34g?feature=shared

Project: PaJR paper EMR integration around efficacy of intraocular antivegf in a diabetic retinopathy with cystoid edema and other comorbidities in a 35M diabetes hypertension metabolic syn alcoholism recurrent seizures 2 episodes

PaJR CBBLE transcripts October 5, 2024:

07/10, 10:41] PaJR CBBLE moderator: 35M ICU 3 unit 5 second admission with gtcs with metabolic syn and hypertension

Paper based record of second admission on October 5, 2024:

EMR summary of second admission October 5, 2024:

Age/Gender : 35 Years/Male
Address :
Discharge Type: Relieved
Admission Date: 05/10/2024 03:39 AM

Diagnosis:

1)GENERALIZED TONIC SEIZURES SECONDARY TO ?POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME,?NON COMPLIANCE TO TREATMENT 2)CELLULITIS OF LEFT FOOT SECONDARY TO THORN PRICK INJURY(RESOLVING).
3) UNCONTROLLED SUGARS(RESOLVING) ,K/C/O DIABETES MELLITUS II SINCE 4 YEARS.
4) BILATERAL EYE PROLIFERATIVE DIABETIC RETINOPATHY.
5) HYPERTENSIVE URGENCY(RESOLVED).KNOWN CASE OF HYPERTENSION SINCE 7 MONTHS.
6) KNOWN CASE OF SEIZURE DISORDER.

Case History and Clinical Findings

C/O INVOLUNTARY MOVEMENTS OF BOTH UPPER LIMBS AND LOWER LIMBS 3 HOURS BACK HOPI: PATIENT WAS Apparently ASYMTOMATIC 3 HOURS AGO AFTER WHICH HE DEVELOPED ONE EPISODEE OF SEIZURE LIKE ACTIVITY AT 12 AM ON 5/10/24 WHICH
LASTED FOR 5 MINS WITH INVOLUNTARY MOVEMENTS OF ALL LIMBS.PATIENT IS NOT ON
ANTIDIABETIC AND ANTISEIZURE MEDICATION SINCE LAST 4 DAYS. NOT ON ANTI HYPERTENSIVE MEDICATION SINCE 2 MONTHS
NO C/O FROTHING FROM MOUTH NO C/O UPROLLING OF EYES
NO C/O TONGUE BITE
 

NO C/O INVOLUNTARY MICTURITION, DEFACATION
NO C/O VOMITING, FEVER, LOOSE STOOLS,PAIN ABDOMEN NO H/O HEAD TRAUMA, FEVER, LOOS STOOLS
NO H/O PEDAL EDEMA, FACIAL PUFFINESS
H/O GTCS 1ST EPISODE IN MARCH,2024 SECONDARY TO POSTERIOR REVERINE ENCEPHALOPATHY SYNDROME WITH HYPERTENSIVE URGENCY AND GOT ADMITTTED HERE FOR 5 DAYS
H/O THORN PRICK TO LEG 10 DAYS AGO FOR WHICH HE WENT TO HOSPITAL AND DIAGNOSED AS LEFT FOOT CELLULITIS
PAST HISTORY: K/C/O HTN SINCE 6 MONTHS, NON COMPLIANCE TO MEDICATION K/C/O DMT2 SINCE 4 YEARS - NON COMPLIANCE TO MEDICATION SINCE 3DAYS N/K/C/O TB, THYROID, CVD, CAD
FAMILY HISTORY: NOT SIGNIFICANT PERSONAL HISTORY:
OCCUPATION: FARMER DIET: MIXED
APPETITE: NORMAL SLEEP: ADEQUATE
BOWEL AND BLADDER :REGULAR
ADDICTIONS: CONSUMES ALCOHOL SINCE 15 YEARS, STOPPED 6 MONTHS AGO 3 CIGARETTES PER WEEK, STOPPED 6 MONTHS AGO.
ALLERGIES: NIL GENERAL EXAMINATION:
NO PALLOR,ICTERUS,CYANOSIS,CLUBBING,LYMPHADENOPATHY,PEDAL EDEMA BP:200/120MMHG
PR:83BPM RR:19CPM SPO2:97 @ RA GRBS:HIGH
SYSTEMIC EXAMINATION: CVS:S1 S2 HEARD ,NO MURMURS RS:BAE PRESENT
CNS:
SENSORY EXAMINATION:
 

SPINOTHALAMIC-
CRUDE TOUCH- ABSENT ON RIGHT FOOT AND LEFT FOOT PAIN-ABSENT ON RIGHT FOOT AND LEFT FOOT
TEMPERATURE-ABSENT ON RIGHT FOOT AND LEFT FOOT, DECREASED ON LEFT ANTERIOR ASPECT OF LEG BELOW KNEE.
POSTERIOR COLUMN:
FINE TOUCH-ABSENT ON RIGHT FOOT AND LEFT FOOT VIBRATION- RIGHT LEFT
MEDIAL MALLEOLUS ABSENT ABSENT SHAFT OF TIBIA NORMAL DECREASED OLECRANON PROCESS NORMAL NORMAL STYLOID PROCESS NORMAL NORMAL JOINT PROPRIOCEPTION 6/10 4/10 CORTICAL :
GRAPHESTHESIA NORMAL NORMAL STEROGNOSIS NORMAL NORMAL
TWO POINT DISCRIMINATION: ABSENT ON BOTH FOOT AND ANTERIOR ASPECT OF LEFT LEG BELOW KNEE AND DECREASED ON RIGHT THIGH.
MOTOR EXAMINATION: RIGHT LEFT TONE : UL NORMAL NORMAL
LL NORMAL NORMAL POWER:UL 5/5 5/5
LL 5/5 5/5 REFLEXES:B +2 +2
T +2 +2
S +1 +1
K +2 +2
A +1 +2 P F F
P/A:SOFT,NT
SURGERY REFERRAL WAS DONE ON 5/10/24 IN VIEW OF THORN PRICK INJURY TO LEFT FOOT ? CELLULITIS
ADVISED CBP,USG,ESR,CRP.
 

DIAGNOSIS- SOFT TISSUE INJURY SECONDARY TO TRAUMA WITH DECREASED CELLULITIS OF LEFT LOWER LIMB
ADVISED LEFT LOWER LIMB ELEVATION
OPHTHALMOLOFY REFERRAL WAS DONE IN VIEW OF DIABETIC RETINOPATHY IMPRESSION: BILATERAL EYE PROLIFERATIVE DIABETIC RETINOPATHY CHANGES+ ADVISED: FILLING PRP AND ANTI VEGF
Investigation
BLOOD GROUPING AND RH TYPE : O POSITIVEHBsAg-RAPID 04-10-2024 04:57:PM Negative HIV 1/2 RAPID TEST 4/10/2024 3:46 PM - Negative
ANTI HCV ANTIBODIES 4/10/2024 3:46 PM - Negative
Anti HCV Antibodies - RAPID 04-10-2024 04:57:PM Non Reactive HEMOGRAM 5/10/24 5:08 AM
HAEMOGLOBIN 10.9 gm/dl TOTAL COUNT 17,300 cells/cumm NEUTROPHILS 82 % LYMPHOCYTES 08 % EOSINOPHILS 01 %MONOCYTES 9 % BASOPHILS 00 %PLATELET
COUNT 32,6SMEAR Normocytic normochromic
BLOOD SUGAR RANDOM 5/10/24 6:21 AM - 487 MG/DL BLEEDING AND CLOTTING TIME : 2 MIN 30 SEC CLOTTING TIME : 5 MIN 00 SEC
COMPLETE URINE EXAMINATION (CUE) 04-10-2024 03:46:PMCOLOUR Pale yellowAPPEARANCE ClearREACTION AcidicSP.GRAVITY 1.010ALBUMIN ++SUGAR ++++BILE SALTS NilBILE PIGMENTS NilPUS CELLS 2-4EPITHELIAL CELLS 2-3RED BLOOD CELLS NilCRYSTALS NilCASTS NilAMORPHOUS DEPOSITS AbsentOTHERS Nil

SERUM CREATININE: 1.3 MG/DL
SERUM ELECTROLYTES 5/10/24 6:21 AM
SODIUM: 135 mmol/L
POTASSIUM: 4.1 mmol/L
CHLORIDE: 98 mmol/L CALCIUM IONIZED 1.15 mmol/L
LIVER FUNCTION TEST (LFT) 05-10-2024 05:20:PMTotal Bilurubin 0.53 mg/dl 1-0 mg/dlDirect Bilurubin 0.19 mg/dl 0.2-0.0 mg/dlSGOT(AST) 13 IU/L 35-0 IU/LSGPT(ALT) 19 IU/L 45-0 IU/LALKALINE PHOSPHATASE 312 IU/LTOTAL PROTEINS 6.7 gm/dl ALBUMIN 3.00 gm/dl A/G RATIO 0.79HBA1C: 6.8%
ESR DONE 5/10/24 11:52 AM: 60 MM/1ST HOUR USG ABDOMEN PELVIS DONE ON 05/10/24:
 

IMPRESSION: NO SONOLOGICAL ABNORMALITY SEEN USG LEFT LOWER LIMB (FOOT):
FINDINGS: E/O SUBCUTANEOUS EDEMATOUS CHANGES NOTED IN DORSUM ON FOOT NO E/O ANY COLLECTIONS NOTED
EXAMINED MUSCLES APPEAR NORMAL UNDERLYING VASCULAR BUNDLESAPPEAR NORMAL
IMPRESSION: SUBCUTANEOUS EDEMA OF DORSUM OF LEFT FOOT ECG: NORMAL SINUS RHYTHM
MRI: NOT WILLING ON 6/10/24
HAEMOGLOBIN 10.6 gm/dlTOTAL COUNT 13,600 cells/cummNEUTROPHILS 68%LYMPHOCYTES 24%EOSINOPHILS 02%MONOCYTES 06%BASOPHILS 00%PCV30.5vol %M C V 80.8flM C H28.1pgM C H C 34.7%RDW-CV 13.2%RDW-SD 42.5flRBC COUNT 3.78
millions/cummPLATELET COUNT 3.92 lakhs/cu.mm SERUM ELECTROLYTES: 7/10/24
SODIUM-138 MMOL/L
POTASSIUM-3.4mmol/l CHLORIDE-103 mmol/l CALCIUM IONISED-1.27 mmol/l 24 HOUR UPCR:0.50
24 HOUR URINE PROTEIN:986 MG/DAY
24 HOUR URINE CREATININE:1.95 GM/DAY
24 HOUR URINE VOLUME -2900 ML


Treatment Given(Enter only Generic Name)
1. IV FLUIDS-0.9%NS AND RL @ 75 ML/HR
2. INJ PIPTAZ 4.5 GM/IV/TID 3.INJ MIXTARD SC/BD 70/30
4. INJ PAN 40 MG IV/OD/7AM/BBF
5. INJ LEVETIRACETAM 500 MG/PO/BD
6. TAB PCM 650 MG PO/SOS 7.TAB TELMA 40 MG PO/OD 8.TAB CILINDIPINE 10 MG PO/OD 9.TAB CHYMERAL FORTE PO/BD
 

10.LEFT LOWER LIMB ELEVATION.


Advice at Discharge
TAB GLIMY MV2 PO/TWICE DAILY TO CONTINUE 8AM -8PM
TAB DAPAGLIFLOZIN 10 MG PO/ONCE DAILY TO CONTINUE 1PM TAB CHYMORAL FORTE PO/THRICE DAILY X 5 DAYS 8AM-2PM-8PM TAB CILINDIPINE 20 MG PO/ONCE DAILY NIGHT-8PM TO CONTINUE TAB NICARDIA 20MG PO/ONCE DAILY AT 2 PM TO CONTINUE
TAB TELMA-80 MG PO/ONCE DAILY TO CONTINUE 8AM
TAB LEVETIRACETAM 500 MG/PO/TWICE DAILY 8AM -8PM TO CONTINUE TAB BENFOTHIAMINE 100 MG PO/TWICE DAILY X 7 DAYS 8AM-8PM
TAB ALDACTONE 25 MG PO/ONCE DAILY AT 8 AM TO CONTINUE TAB CLAVAM 625 MG PO/THRICE DAILY FOR 5 DAYS 8AM-2PM-8PM TAB PAN 40 MG PO/ONCE DAILY/7AM/BBF X 5 DAYS
TAB PCM 650 MG PO/SOS STRICT DIABETIC DIET HOME BP MONITORING

Follow Up
REVIEW TO GM OPD AFTER 1 WEEK WITH FBS,PLBS,SR CREAT AND HOME BP RECORDINGS
REVIEW TO OPHTHALMOLOGY OPD I/V/O PRP,ANTI VEGF
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE,DONOT MISS MEDICATIONS. In case
of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:  For Treatment Enquiries Patient/Attendent Declaration : - The medicines prescribed and the advice regarding preventive aspects of care ,when and how to obtain urgent care have been explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER


SIGNATURE OF PG/INTERNEE
 



SIGNATURE OF ADMINISTRATOR


SIGNATURE OF FACULTY
Discharge Date Date:8/10/2024 Ward:AMC Unit:GM V

EMR summary of first admission March 2024:

Age/Gender : 32 Years/Male
Address :
Discharge Type: Relieved
Admission Date: 08/03/2024 05:59 AM
Diagnosis
GTCS SECONDARY TO HYPERTENSIVE POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME WITH HYPERTENSIVE URGENCY ALSO POSSIBLY ALCOHOL Withdrawal DIABETES MELLITUS SINCE 6 YRS WITH DIABETIC NEPHROPATHY AND PROLIFERATIVE
DIABETIC RETINOPATHY
DENOVO HYPERTENSION [RESISTANT HYPERTENSION]

Case History and Clinical Findings

PATIENT WAS BROUGHT TO CASUALITY WITH H/O INVOLUNTARY MOVEMENTS MULTIPLE TIMES SINCE 2 DAYS
HOPI
PATIENT WAS APPRENTLY ASYMPTOMATIC 2 DAYS AGO THEN HE DEVELOPED ONE EPISODE OF SEIZURE LIKE ACTIVITY AT 11 PM ON 6/3/24 .ONE EPISODE AT 9PM ON 7/3/24,4 EPISODES WITH 5 MINUTES INTERVAL AT 12 AM ON 7/3/24 EACH EPISODE LASTING FOR 5- 10 MINUTES WITH INVOLUNTARY MOVEMENTS OF ALL FOUR LIMBS.FROATHING FROM MOUTH PRESENT,UPROLLING OF EYEBALLS PRESENT
TONGUE BITE ABSENT
INVOLUNTARY MICTURITION,Defecation ABSENT
H/O VOMITING FOR 2 DAYS ,3 EPISODES PER DAY,FOOD AS CONTENT,NON BILIOUS NO H/O HEAD TRAUMA,FEVER,LOOSE STOOLS
PAST HISTORY;
K/C/O DM SINCE 6 YEARS ON REGULAR MEDICATION ON TAB.GLICLAZIDE 60MG PO/OD N/K/C/O HTN,EPILEPSY,CAD,CVA,ASTHAMA,THYROID
 

GENERAL EXAMINATION PT IS C/C/C
PR - 104BPM
BP - 180 / 100 MMHG RR - 20 CPM
TEMP - 98 F
GRBS - 312 MG /DL CVS - S1 S2 PRESENT
RS - BAE PRESENT , NVBS P/A - SOFT , NON TENDER
PSYCHIATRY REFERRAL ON 8/3/24 I/V/O ALCOHOL WITHDRAWL ADVICED -
PT AND ATTENDERS PSYCHOEDUCATED PT COUNSELLED
INJ LORAZEPAM 1/2 AMP IM /SOS IF PT IRRITABLE OR SLEEPLESS RELAXATION AND DIVERSION TECHNIQUES EXPLAINED
CNS - NO FND
OPTHALMOLOGY REFFERAL ON 9/3/24 I/V/O RETINOPATHY
RE ? MODERATE TO SEVERE DIABETIC RETINOPATHIC CHANGES LE ?PROLIFERATIVE DIABETIC RETINOPATHY
ADVISED
B SCAN BUT PT NOT WILLING
Investigation
SERUM ELECTROLYTES (Na, K, C l) 08-03-2024 06:07:AMSODIUM 132 mEq/L 145-136 mEq/LPOTASSIUM 4.5 mEq/L 5.1-3.5 mEq/LCHLORIDE 105 mEq/L 98-107 mEq/L
ABG 08-03-2024 06:07:AMPH 7.37PCO2 37.8PO2 115HCO3 21.7St.HCO3 22.3BEB -2.5BEecf -
2.7TCO2 40.6O2 Sat 95.5O2 Count 24.4BLOOD UREA 08-03-2024 07:06:AM 34 mg/dl 42-12 mg/dl SERUM CREATININE 08-03-2024 07:06:AM 1.1 mg/dl 1.3-0.9 mg/dlLIVER FUNCTION TEST (LFT)
08-03-2024 07:06:AMTotal Bilurubin 0.60 mg/dl 1-0 mg/dlDirect Bilurubin 0.19 mg/dl 0.2-0.0
mg/dlSGOT(AST) 18 IU/L 35-0 IU/LSGPT(ALT) 20 IU/L 45-0 IU/LALKALINE PHOSPHATASE 220
IU/L 128-53 IU/LTOTAL PROTEINS 7.1 gm/dl 8.3-6.4 gm/dlALBUMIN 3.9 gm/dl 5.2-3.5 gm/dlA/G
RATIO 1.24
HBsAg-RAPID 08-03-2024 07:06:AM NegativeAnti HCV Antibodies - RAPID 08-03-2024 07:06:AM
Non Reactive
 

POST LUNCH BLOOD SUGAR 08-03-2024 07:07:AM 408 mg/dl 140-0 mg/dlSERUM ELECTROLYTES (Na, K, C l) 09-03-2024 08:00:AMSODIUM 136 mEq/L 145-136 mEq/LPOTASSIUM 3.9 mEq/L 5.1-3.5 mEq/LCHLORIDE 101 mEq/L 98-107 mEq/L
URINE FOR KETONE BODIES -NEGATIVE CBP[8/3/2024]
HB - 15.4
TC - 15,000
RBC - 5.15
PLT - 1.56 CBP[12/3/2024] HB -14.4
TC-10,900 PLT - 1.75
SPOT UPCR -1.88
24 HR URINE PROTEIN-660MG/DAY
24 HR URINE CREATININE- 0.79 G/DAY
RATIO- 0.83


T3- 0.83ng/ml T4-12.09mcg/dl
TSH-1.01micro iu/ml LIPID PROFILE
TOTAL CHOLESTEROL- 274
TRIGLYCERIDES 293 MG/DL
HDL 59.6 MG/DL
LDL 140 MG/DL
VLDL 58.6 MG/DL 2D ECHO IMPRESSION - EF - 60%
TRIVIAL MR +/TR+ , NO PAH
NO RWMA , CONCENTRIC LVH + GOOD LV SYSTOLIC FUNCTION GRADE 1 DIASTOLIC DYSFUNCTION
 

IVC 1.0CMS ,COLLAPSING NO PE / CLOTS
USG ON 9/3 /24
IMPRESSION - GRADE 1 FATTY LIVER
MRI BRAIN - NO ABNORMALITY DETECTED
Treatment Given(Enter only Generic Name)
INJ .LEVIPIL 500 MG IV BD
INJ . THIAMINE 200 MG IN 100 ML NS IV TID INJ.HAI S/C TID
INJ NPH S/C BD
INJ LABETOLOL 10MG/HR TAPERED ACC TO BP T NICARDIA 20MG PO TID
T LABETOLOL 100MG PO SOS T.TELMA 40 MG PO OD
T LASIX 40MG PO BD
T OLKEM TRIO [CILNIDIPINE 10MG +CHLORTHALIDONE 12.5MG+ OLMESARTAN 40MG]PO OD
Advice at Discharge
T.TELMA 40 MG PO /OD 8AM -X-X CONTINUE T.PRAZOSIN 2.5 MG PO/TID 1-1-1 FOR 15 DAYS T.ALDACTONE 25 MG PO /OD 1-X-1 FOR 15 DAYS TAB AMLODIPINE 5MG PO HS X-X-1 FOR 15 DAYS T.BENFOMET PLUS PO BD 1-0-1 FOR 1 MONTH T.LEVIPIL 500 MG PO BD 1-0-1 FOR 1 MONTH
INJ. HUMAN ACTRAPID INSULIN S/C TID 16 U- 16U -16U INJ . NPH S/C BD 14U -X-14U
Follow Up
REVIEW TO GM OPD AFTER 1 WEEK OR SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
 

AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE,DONOT MISS MEDICATIONS. In case
of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact: For Treatment Enquiries Patient/Attendent Declaration : - The medicines prescribed and the advice regarding preventive aspects of care ,when and how to obtain urgent care have been explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER SIGNATURE OF PG/INTERNEE SIGNATURE OF ADMINISTRATOR SIGNATURE OF FACULTY
Discharge Date Date:13/3/2024 Ward:AMC
Unit:4

[07/10, 10:44] : ICU 3 unit 5

Reviewing older PAPER based archived clinical encounter records even before his first admission with us in March 2024:

[07/10, 15:11]: 35M icu 3 with progressive loss of vision and on OCT right eye showed cystoid edema for which intravitreal anti vegf was administered on June 2023.

[07/10, 15:17] : @⁨Meta AI⁩ what is the efficacy of anti vegf in diabetic retinopathy with cystoid edema. Please substantiate your statements with proper scientific randomised controlled trial data in a PICO format taking care to share the absolute values and not just percentages in terms of disease parameters, interventions and outcomes.

[07/10, 15:17] Meta AI: A very specific and technical question!

Anti-VEGF (Anti-Vascular Endothelial Growth Factor) therapy has been shown to be effective in treating diabetic retinopathy (DR) with cystoid edema. Here's a summary of the efficacy in PICO format:

*P* (Population): Patients with diabetic retinopathy (DR) and cystoid edema.

*I* (Intervention): Anti-VEGF therapy (e.g., ranibizumab, bevacizumab, or aflibercept).

*C* (Comparison): Sham injection or laser photocoagulation.

*O* (Outcomes):

- *Primary outcome:* Change in central retinal thickness (CRT) from baseline to 24 weeks.

- *Secondary outcomes:* Change in best-corrected visual acuity (BCVA), diabetic retinopathy severity score (DRSS), and presence of cystoid edema.

*Randomized Controlled Trial (RCT) data:*

- RISE and RIDE studies (2011): Ranibizumab vs. sham injection.

    - CRT change at 24 weeks: -127.4 μm (ranibizumab) vs. +12.8 μm (sham).

    - BCVA change at 24 weeks: +7.7 letters (ranibizumab) vs. -0.4 letters (sham).

- RESOLVE study (2012): Ranibizumab vs. laser photocoagulation.

    - CRT change at 12 weeks: -142.6 μm (ranibizumab) vs. -64.8 μm (laser).

    - BCVA change at 12 weeks: +8.4 letters (ranibizumab) vs. +1.2 letters (laser).

- VIVID and VISTA studies (2015): Aflibercept vs. laser photocoagulation.

    - CRT change at 24 weeks: -169.1 μm (aflibercept) vs. -73.4 μm (laser).

    - BCVA change at 24 weeks: +10.3 letters (aflibercept) vs. +2.2 letters (laser).

*Absolute values:*

- CRT (central retinal thickness): -127.4 μm to -169.1 μm reduction with anti-VEGF therapy.

- BCVA (best-corrected visual acuity): +7.7 to +10.3 letters improvement with anti-VEGF therapy.

*Conclusion:* Anti-VEGF therapy significantly reduces central retinal thickness and improves visual acuity in patients with diabetic retinopathy and cystoid edema, compared to sham injection or laser photocoagulation.

Please note that these results are based on a summary of specific RCTs and may not represent the entirety of available evidence.

[07/10, 15:28] : @⁨Meta AI⁩ please elaborate on BCVA and explain how +7.7 to +10.3 letters improvement is significant?

[07/10, 15:28] Meta AI: _BCVA_ (Best-Corrected Visual Acuity) is a measure of the sharpest vision a person can achieve with glasses or contact lenses. It's usually measured using an eye chart (like the Snellen chart) and expressed in units called "letters" or "lines."

In the context of clinical trials for diabetic retinopathy, BCVA is a crucial outcome measure. An improvement in BCVA means that patients can see more clearly and perform daily tasks with greater ease.

Now, let's break down the significance of the +7.7 to +10.3 letters improvement:

- In clinical trials, a change of 5-10 letters is considered a meaningful improvement in BCVA. This is because it represents a noticeable difference in everyday vision.

- The +7.7 to +10.3 letters improvement seen in the anti-VEGF trials indicates that patients experienced a significant gain in visual acuity, allowing them to read smaller print, recognize faces more easily, and perform tasks with greater confidence.

- To put this into perspective:

    - 7.7 letters is equivalent to going from 20/40 to 20/25 vision (a noticeable improvement).

    - 10.3 letters is equivalent to going from 20/40 to 20/20 vision (near-normal vision).

These improvements are significant because they:

1. Enhance patients' quality of life.

2. Allow for greater independence.

3. Reduce the risk of further vision loss.

In summary, the +7.7 to +10.3 letters improvement in BCVA represents a substantial and clinically meaningful gain in visual acuity, making a positive impact on patients' daily lives.

[07/10, 15:39] : Our 35M’s vision didn’t improve after ranizumab costing 20,000/- and so he changed his doctors and went to ... where they administered platelet rich plasma again costing 20,000 for each session and after he spent 100,000 and didn’t see any improvement in his vision

[07/10, 20:26] : 35M ICU 3, at this time last year 2023 walked a stretch of distance barefoot as per protocol in Shabari malai and developed cellulitis following which he returned and got admitted in a nursing home in Miryalguda for which he claims to have spent 10,00,000!

[07/10, 20:28]: @⁨Meta AI⁩ what is the efficacy of platelet rich plasma PRP in diabetic retinopathy with cystoid edema? 

Please substantiate your statements with proper scientific randomised controlled trial data in a PICO format taking care to share the absolute values and not just percentages in terms of disease parameters, interventions and outcomes.

[07/10, 20:28] Meta AI: The efficacy of Platelet-Rich Plasma (PRP) in diabetic retinopathy (DR) with cystoid edema is still being researched. Here's a summary of available Randomized Controlled Trial (RCT) data in PICO format:

*P* (Population): Patients with diabetic retinopathy (DR) and cystoid edema.

*I* (Intervention): Intravitreal injection of Platelet-Rich Plasma (PRP).

*C* (Comparison): Sham injection or standard treatment (e.g., anti-VEGF).

*O* (Outcomes):

- Primary outcome: Change in central retinal thickness (CRT) from baseline to 12-24 weeks.

- Secondary outcomes: Change in best-corrected visual acuity (BCVA), diabetic retinopathy severity score (DRSS), and presence of cystoid edema.

*RCT data:*

- *Study 1:* Ghazi et al. (2018) - PRP vs. sham injection.

    - CRT change at 12 weeks: -45.6 μm (PRP) vs. -10.8 μm (sham).

    - BCVA change at 12 weeks: +2.5 letters (PRP) vs. -1.3 letters (sham).

- *Study 2:* Kulkarni et al. (2020) - PRP vs. anti-VEGF (ranibizumab).

    - CRT change at 24 weeks: -70.8 μm (PRP) vs. -124.9 μm (ranibizumab).

    - BCVA change at 24 weeks: +4.2 letters (PRP) vs. +7.1 letters (ranibizumab).

- *Study 3:* Lee et al. (2022) - PRP vs. standard treatment (laser photocoagulation).

    - CRT change at 24 weeks: -55.1 μm (PRP) vs. -30.6 μm (standard treatment).

    - BCVA change at 24 weeks: +3.5 letters (PRP) vs. +1.9 letters (standard treatment).

*Absolute values:*

- CRT reduction: 45.6-70.8 μm with PRP (less effective than anti-VEGF).

- BCVA improvement: 2.5-4.2 letters with PRP (less effective than anti-VEGF).

*Conclusion:* While PRP shows some promise in reducing CRT and improving BCVA, the current evidence suggests:

1. PRP is less effective than anti-VEGF therapy.

2. PRP may be considered as an adjunct or alternative therapy for patients who are non-responsive or intolerant to anti-VEGF.

*Limitations:*

1. Small sample sizes.

2. Variable PRP preparation methods.

3. Limited follow-up duration.

More large-scale, well-designed RCTs are needed to fully assess the efficacy and safety of PRP in diabetic retinopathy with cystoid edema.

Would you like me to provide information on ongoing trials or potential benefits/risks of PRP therapy?

UDLCO: AI LLMs and their current collaborative stance inspite of competing rival human creators?

UDLCO summary: AI LLMs in their routine responses are always courteous albeit they can start confabulating (aka hallucinations popularly but perhaps not the appropriate term) and mislead. In the sample taken from our morning PaJR session with one of our patients and meta AI, we notice a positive note of collaboration in their courteous stance that is again very unlike competing humans for now. At this juncture it's difficult to say how long our honeymoon with AI shall last before it quickly learns all our human follies!

Conversational PaJR transcripts on the morning of 9th October between different PaJR users, patient advocate, PaJR moderator and meta AI centered around the requirements of a 30 year old type 1 diabetic:

[09/10, 23:59] Patient DM1 MP Advocate 2: 6:30 pm drink 1 cup black tea without sugar 

7 pm insulin lantus 8.5 unit 

7:50 pm sugar 52

Trembling and shivering so I ate 1 sweet,3 chocolate and rice with bottle gourd curry and brinjal fry

[10/10, 08:34] Patient DM1 MP Advocate 2: Good morning sir 

10/10/24

8:30 am fasting sugar 146

[10/10, 10:41] PaJR moderator: How do we explain this episode of hypoglycemia at 7:50 AM yesterday, in terms of precipitating cause @⁨Meta AI⁩ ?

[08/10, 09:01] Patient DM1 MP Advocate 2: Good morning sir 

8/10/24

8:45 am fasting sugar 187

[08/10, 17:06] Patient DM1 MP Advocate 2: 9 am drink 1 cup black tea without sugar 

10:25 am before breakfast sugar 230

10:30 am 

Sprouts 

12:30 pm after breakfast sugar 235

2:55 pm before lunch sugar 166

3 pm 

Rice with cabbage fry and lentil 

5 pm after lunch sugar 143

[08/10, 23:53] Patient DM1 MP Advocate 2: 5:15 pm drink 1 cup black tea without sugar 

7 pm insulin lantus 8.5 unit 

9:25 pm before dinner sugar 140

9:30 pm 

2 roti with lentil and cabbage fry 

11:30 pm after dinner sugar 214

[09/10, 06:38] Patient DM1 MP Advocate 2: Good morning sir 

9/10/24

6:30 am fasting sugar 143

[09/10, 15:37] Patient DM1 MP Advocate 2: 8:30 am drink 1 cup black tea without sugar 

9:55 am before breakfast sugar 186

10 am 

Besan chila

12 pm after breakfast sugar 175

1:25 pm before lunch sugar 163

1:30 pm 

Khichdi, mix veg and kheer ( Prasad)

3:30 pm after lunch sugar 180

[09/10, 23:59] Patient DM1 MP Advocate 2: 6:30 pm drink 1 cup black tea without sugar 

7 pm insulin lantus 8.5 unit 

7:50 pm sugar 52

Trembling and shivering so I ate 1 sweet,3 chocolate and rice with bottle gourd curry and brinjal fry

[10/10, 08:34] Patient DM1 MP Advocate 2: Good morning sir 

10/10/24

8:30 am fasting sugar 146

[10/10, 10:41] Meta AI: The episode of hypoglycemia (low blood sugar) at 7:50 AM yesterday can be analyzed based on the provided data.

Precipitating causes:

1. Insulin dose: 8.5 units of Lantus insulin taken at 7 PM the previous evening. Lantus has a peak effect in 10-16 hours, which aligns with the hypoglycemic episode.

2. Timing of last meal: Dinner was at 9:30 PM, and the next meal wasn't until breakfast at 10 AM, resulting in a relatively long fasting period.

3. Physical activity: No significant physical activity mentioned.

4. Food intake: No significant carbohydrate intake between dinner and the hypoglycemic episode.

Contributing factors:

1. Possible insulin stacking: Taking 8.5 units of Lantus insulin at the same time each evening may have accumulated in the patient's system.

2. Inadequate carbohydrate intake before bedtime or at breakfast.

Recommendations:

1. Monitor blood glucose levels more frequently.

2. Adjust insulin dosing regimen or timing.

3. Ensure adequate carbohydrate intake before bedtime and at breakfast.

4. Consider a snack before bedtime or a late-evening snack.

Consult a healthcare professional for personalized guidance.

Please provide additional context or information, if needed.

[10/10, 10:43] PaJR moderator: @⁨Meta AI⁩ in error I mentioned 7:50AM. That was supposed to mean 7:50 PM, which is when the patient experienced hypoglycemia

[10/10, 10:43] Meta AI: Given the corrected time of hypoglycemia (7:50 PM), let's re-analyze the data:

Precipitating causes:

1. Insulin dose: 8.5 units of Lantus insulin taken at 7 PM, which is 50 minutes before the hypoglycemic episode. Lantus has a peak effect in 10-16 hours, but the patient experienced hypoglycemia within a shorter timeframe.

2. Recent food intake: Dinner was at 9:30 PM the previous night, and the patient had black tea without sugar at 5:15 PM.

Contributing factors:

1. Timing of insulin administration: Taking Lantus insulin at 7 PM may have coincided with a natural dip in blood glucose levels before dinner.

2. Inadequate carbohydrate intake between 5:15 PM tea and 7:50 PM hypoglycemia.

3. Potential insulin stacking or sensitivity.

Recommendations:

1. Consider adjusting insulin dosing timing to closer to dinner (e.g., 9 PM).

2. Ensure adequate carbohydrate intake between 5 PM and dinner.

3. Monitor blood glucose levels more frequently, especially before and after dinner.

4. Consult a healthcare professional to reassess insulin regimen and adjust as needed.

Additional questions:

1. What is the patient's typical physical activity level?

2. Has the patient experienced hypoglycemia at this time of day previously?

3. Are there any other medications or health conditions that could impact blood glucose levels?

[10/10, 10:49] PaJR moderator: @⁨Meta AI⁩ thanks for the valuable inputs.

Wish you could read the patient's entire data from few months, painstakingly archived in the URLed web based EHR content here:

 https://2patienthealthreport.blogspot.com/2024/06/patienthealthreport.html?m=1

Updated till 5th October. @⁨Patient DM1 MP Advocate 2⁩ can you update it till today?

I guess till meta AI learns to read URLs we can share the URL with Notebook LM for more insights from longer past data trends?

[10/10, 10:49] Meta AI: I'm glad I could provide helpful insights.

Unfortunately, I'm currently unable to access external URLs or scrape data from websites, including the patient's EHR data. However, I can offer suggestions:

*Short-term solution:*

1. Continue sharing relevant data snippets, and I'll provide analysis and recommendations.

2. Consider copying and pasting specific data periods or events for more detailed analysis.

*Long-term solution:*

1. Notebook LM: Share the URL with Notebook LM, as you mentioned, to leverage its capabilities.

2. Data export: Export the patient's EHR data in a machine-readable format (e.g., CSV, JSON).

3. Secure data sharing: Explore secure, HIPAA-compliant platforms for sharing and analyzing patient data.

*Future development:*

As AI capabilities advance, I may be able to:

1. Access and parse data from URLs.

2. Integrate with EHR systems.

3. Analyze larger datasets.

Until then, I'm here to assist with data analysis and insights based on the information you provide.

To update the data till today, please share:

1. Blood glucose readings.

2. Insulin dosages and timing.

3. Relevant medical events or changes.

4. Any new medications or lifestyle changes.

I'll continue providing valuable inputs.

Creative commons license: https://commons.m.wikimedia.org/wiki/File:RAG_schema.svg#mw-jump-to-license

UDLCO: Case based learning and a case study of the 2024 Nobel in medicine using critical realist pedagogy!

UDLCO conversational transcripts: 

[08/10, 06:48] medical education faculty: Good morning, could any one share literature clearly differentiating CBD and CBL

[08/10, 07:11] +60 ASM : The following video may help in understanding the concept and conduct of CBL

https://youtu.be/piaoHLMpTx8

[08/10, 07:49]  Prof Meu: Case-Based Discussion (CBD) and Case-Based Learning (CBL) are educational strategies used in medical and healthcare education. Both methods use cases to initiate/facilitate learning. However there are distinct differences regarding the purpose, outcome and process.

CBD focusses on analyzing a patient's case to develop critical thinking and decision-making skills while CBL focusses on  integrating knowledge, skills, and attitudes through real-life scenarios.

CBD is  Instructor-led, small group discussions with the objectives of

  developing diagnostic and management skills and enhance clinical reasoning while CBL is self-directed, and problem-based learning.

    Both foster collaboration and communication amongst learners and improve critical thinking skills.

In CBL, learners identify learning issues and address them.

3. Objectives: CBD targets specific clinical skills, whereas CBL aims to develop broader competencies.

4. Learner engagement: CBD involves group discussions, while CBL encourages individual or small group work.

CBD is a more structured, instructor-led approach focusing on clinical skills, while CBL is a self-directed, problem-based strategy emphasizing integrated learning and lifelong skills.

😁

[08/10, 07:49] SG : You can get more details, just ask Meta or Gemini..😜

[08/10, 07:53] +91: Yup

[08/10, 08:08]Physiology Prof Meu: 😆 One Health...one miRNA...

[08/10, 08:09] +91J: m bole to? 😂

[08/10, 08:13] b: And..

One skill..One miRNA..

One disease...one miRNA....

[08/10, 08:33] CBBLE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4013251/

👆This historical review article says, "miRNAs were discovered in 1993 by Lee and colleagues in the nematode Caenorhabditis elegans and Ambros was the last author and Lee is cited in 4 more papers in the same review article while Ambros is not. Wonder what happened to Lee!

The review article is dated 2013 and appears to have been written by an Indian who also cites his own work around miRNA in modulating fetal lung development in reference 13.

Ambros is again cited in reference 2, this time as a first author around his work on annotation of miRNA.

More about Ambros here:

https://www.nobelprize.org/prizes/medicine/2024/press-release/

[08/10, 08:51] VS: What should we make of it..?

[08/10, 08:57] CBBLE: It's a morning medical education exercise to activate thinking caps! Part of a critical realist methodology for medical education delivery!

[08/10, 09:31]K : Good morning madam. The basic difference between CBL and CBD is that while the former is a pedogogical/instructional tool (active learning) , the latter is a structured WPBA tool (formative). Though I could find (as of now) a peer reviewed article that discretely defines the difference between two, I am sharing two resources

[08/10, 09:34] CBBLE: 👆As per this, there doesn't need to be any difference and CBD is a subset or part of CBL

[08/10, 09:36] CBBLE: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5736264/

[08/10, 09:36] CBBLE: CBL would cover all the domains addressed in the image here 👇

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

While CBD could be restricted to the outermost domain

[08/10, 09:38] AD: CBD is a WPBA tool. Didn’t we all use it in summative exams also during Covid pandemic?

[08/10, 09:41] K: https://www.bjmp.org/content/critical-analysis-case-based-discussions

[08/10, 09:41] VS: In research articles, the first author is usually the student who did all the bench work and the last author is the senior professor, which is why Rosalind Lee is the first author..

Reference 2 in the article is a convention paper, where Victor Ambros came up with a system to name microRNAs. There is no original research there. It is only a suggested system for naming something new, which the field agreed to adopt…

Also it turns out, they married each other 😀👇🏾

[08/10, 09:42]VS : She continues to work with him in the lab https://www.umassmed.edu/ambroslab/LabMembersOnly/senior-scientist/

[08/10, 09:44] CBBLE: Full marks in our assessment of your active learning using a critical realist pedagogy! 🙂🙏

[08/10, 09:46] CBBLE: Good point AD!

Yes CBD is a subset of CBL and often used for summative assessment while CBL is an overall picture that only a longitudinal formative assessment can provide

[08/10, 09:46]: https://www.bmj.com/careers/article/wpba-assessments-what-are-wbpas-in-medicine-

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

Creative commons license:

https://commons.m.wikimedia.org/wiki/File:MiRNA.svg#mw-jump-to-license

Critical realist heutagogy and the theatre of oppressed in medical education: past celebrations and present failures

In his book, the pedagogy of oppressed, Freire calls traditional pedagogy the "banking model of education" because it treats the student as an empty vessel to be filled with knowledge, like a piggy bank. He argues that pedagogy should instead treat the learner as a co-creator of knowledge.

This was subsequently incorporated in the work of Augusto Boal in "theatre of oppressed" that is a form of "simulated education" where the audience learners (spect-actors) get to learn with the teachers (professional actors).

We often find simulations as an easy way of delivering medical education too and there are currently many tools and tactics to deliver these and yet most medical practitioners and practicing teachers tend to engage more with the primary beneficiaries of medical education (patients) in real time and perhaps even need their students and spect-actors to actually lend them a hand (as in a hands on approach to co-creating knowledge) and thus actually benefiting the primary beneficiaries of medical education, even creating a scope to correlate student and teacher learning outcomes with patient illness outcomes.

Co-creating emancipatory knowledge in real time:

We look back decades before "critical pedagogy" was founded and peer into the life of an Indian hands on Marxist anarchist revolutionary, Bhagat Singh, who for some time in his short existence of 20 years had been exploiting the power of drama as a means to inspire the revolt against the British, purchasing a magic lantern to show slides that enlivened his talks about revolutionaries. 

In 1929, he proposed a dramatic act to the HSRA intended to gain massive publicity for their aims. Influenced by Auguste Vaillant, a French anarchist who had bombed the Chamber of Deputies in Paris,^[36] Singh's plan was to explode a bomb inside the Central Legislative Assembly. The actual intention was for the perpetrators to allow themselves to be arrested so that they could use court appearances as a stage to publicise their cause. The Supreme Court of India established a museum to display landmarks in the history of India's judicial system, displaying records of some historic trials. The first exhibition that was organised was the Trial of Bhagat Singh.

https://en.m.wikipedia.org/wiki/Bhagat_Singh

https://consciousnotebooksequel.blogspot.com/2024/10/wiki-udlco-ultimate-role-play-in.html?m=1

Much has happened in the years since then with further evolution of critical pedagogy embracing critical realism that allows healthcare learners to 1) understanding complex outcomes, (2) optimizing interventions, and (3) researching biopsychosocial pathways. Such questions are central to evidence-based practice, chronic disease management, and population health.

https://en.m.wikipedia.org/wiki/Critical_realism_(philosophy_of_the_social_sciences)

https://pubmed.ncbi.nlm.nih.gov/37335625/

While we don't have a ©️ on the very useful figure of critical realist view of stratified reality shared by Hoddy et al : Source: https://www.researchgate.net/publication/342246458_Critical_realism_and_constructivism_merging_research_paradigms_for_a_deeper_qualitative_study/figures?lo=1, Full text: https://fenix.iseg.ulisboa.pt/downloadFile/281608120804971/Critical%20realism%20and%20GT%20Hoddy%202019.pdf, 

we would like to add our own diagram as a positive contribution to expand on their viewpoint from a medical cognition lens and the essence of it is all about the individual patient's and physician's cognition at the centre of the concentric circles corresponding to Hoddy's domain of the 'empirical' as in perceptions, experiences and observations of 'individual cognition' while the surrounding concentric circle forms a ring of 'actual collective cognition' that tries to tie together all knowledge elements into an 'ontology' many of which are unknown and form the connecting link to the next ring which is Hoddy's domain of the 'real' that contains all the structures and mechanisms that generate events that again feed back cyclically into the central concentric circle of individual perception of empirical events surrounded by the ring of collective cognitive interpretation of 'actual' events.

In our CBBLE and PaJR groups we witness daily in real time, a co creation of user driven learning community ontologies powered by Web 2.0 critical realist heutagogy through team based learning between multiple stakeholders such as health professional learners, faculty, patients and their relatives that is increasingly supported by Web 3.0 technology where all these stakeholders co create as online system users, with a username, something that has been labelled in the past user driven healthcare.

Ref 35: https://pubmed.ncbi.nlm.nih.gov/19018905/ and Ref 36: Biswas, R. & Martin, C. M. (Eds.). (2011). User-Driven Healthcare and Narrative Medicine: Utilizing Collaborative Social Networks and Technologies. IGI Global. https://doi.org/10.4018/978-1-60960-097-6

https://www.igi-global.com/book/user-driven-healthcare-narrative-medicine/41908#:~:text=User%2DDriven%20Healthcare%20and%20Narrative%20Medicine:%20Utilizing%20Collaborative,problems%20in%20healthcare%2C%20utilizing%20real%20life%20examples.

This co creation has enabled healthcare educator practitioners to not only remain focused on real patient care centred learning outcomes but develop realist ontologies for medical education and practice such as "real patient OSCEs" that retain whole patient clinical complexity rather than reduce it to smaller parts in order to optimize clinical complexity.

https://medicinedepartment.blogspot.com/2024/01/medical-cognition-cpd-jan-25-2024theme.html?m=1

Source: https://www.researchgate.net/publication/342246458_Critical_realism_and_constructivism_merging_research_paradigms_for_a_deeper_qualitative_study/figures?lo=1

Full text: https://fenix.iseg.ulisboa.pt/downloadFile/281608120804971/Critical%20realism%20and%20GT%20Hoddy%202019.pdf

Present failure:

"Many if not most students come to the university in order to gain access to and eventual enfranchisement in 'the establishment,' not to critique and reject its privileges."

Students want to gain, rather than to critique, positions of privilege, as encouraged by critical pedagogues."

https://en.m.wikipedia.org/wiki/Critical_pedagogy

Updated terminology:

[06/11, 09:50] Kmcq: Heutagogy!

Pedagogy is outdated

[06/11, 09:52]: It's a heutagogist's strategy of calling heutagogy as pedagogy but yes I realise it would be better to name it heutagogy

@⁨Meta AI⁩ how's heutagogy different from pedagogy?

[06/11, 09:53] Meta AI: Heutagogy and pedagogy are two distinct approaches to learning and teaching:

*Pedagogy:*

1. Teacher-centered

2. Focus on transmitting knowledge

3. Emphasis on instructor's expertise

4. Learners receive information passively

5. Assessment-focused

*Heutagogy:*

1. Learner-centered

2. Focus on self-directed learning

3. Emphasis on learner's autonomy

4. Encourages critical thinking, reflection, and meta-cognition

5. Flexibility and adaptability

Key differences:

1. Control: Pedagogy (teacher) vs. Heutagogy (learner)

2. Focus: Knowledge transmission (pedagogy) vs. Learning process (heutagogy)

3. Role of teacher: Expert (pedagogy) vs. Facilitator/Mentor (heutagogy)

Heutagogy fosters:

1. Self-directed learning

2. Personalized learning paths

3. Collaboration

4. Real-world applications

5. Reflection and meta-cognition

In heutagogy, learners take ownership of their learning, and teachers guide and support.

*Evolution of learning approaches:*

1. Pedagogy → Andragogy (adult learning) → Heutagogy (self-determined learning)

*Implications for education:*

1. Shift from standardized to personalized learning

2. Emphasis on developing critical thinking, creativity, and problem-solving skills

3. Integration of technology-enhanced learning

4. Redefining teacher roles and responsibilities

Collective cognition feedback Update:

[08/11, 08:51]drnr : It may be difficult for medical teachers to emulate Bhagat Singh's dramatisation: to allow or kill a patient for explaining the natural history of the disease, and then face the fury of the family, the MCI and the never ending judicial proceedings!

The medical student may not be left with many teachers, unless Hezbollah takes over medical education ((strictly for boys (pun intended))!

[08/11, 08:55]rb: That was an extreme case!😅

[08/11, 08:56]rb: But because of some Western Bhagat Singh's who cleverly designed the randomized controlled trial post pencillin, we can still reap it's benefits

[08/11, 08:59]drnr: You could always have a new GCP, with a slave act enabled

[08/11, 09:07]rb: The existing ones are just that! Slave acts! Yes that's the term to best describe most guideline based medicine vs true evidence based medicine 👏👏

[08/11, 09:10] rb: This makes me reimagine the randomized controlled trial participant as Bhagat Singh on trial (and to be true to medical ethics and patient autonomy, the patient has had a good role in it's design) although it's difficult to predict the random outcome for any of the participants in the trial as that's what equipoise should be all about! The patient Bhagat Singh just stands there, brave and strong ready to meet whatever the dice ordains!