THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HER SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[7.49 pm, 26/01/2026] PPM 1: @PPM3 this is also to take into account the PaJR workflow and hence some explicit role clarifications while sharing the event data here.
While her current admission with our local point of care team was 14th January 2026, she was also admitted here at the same point of care with a different local team in November 2025
Here's her EMR summary from then:
Admission Date: 13/11/2025 01:05 PM
Discharge Date: 15/11/2025 10:20 AM
Diagnosis
LEFT PLANTAR FOOT ABSCESS,
HOSPITAL ACQUIRED PNEUMONIA, AKI,
Septic SHOCK(RESOLVED)
HFREF(EF:39%), ACUTE DECOMPENSATED HEART FAILURE WITH CARDIOGENIC
SHOCK(RESOLVED)
T2DM 10 yrs
S/P 1 PINT PRBC TRANSFUSION DONE
Case History and Clinical Findings
C/O SHORTNESS OF BREATH SINCE TODAY MORNING DECREASED URINE OUTPUT Since
YESTERDAY NIGHT. SWELLING OF RT FOOT SINCE 1 WEEK
HOPI: PATIENT WAS APPRENTLY NORMAL 1 WEEK BACK THEN SHE GOT INJURED ON RT
FOOT BY A NAIL FOLLOWING WHICH SHE DEVELOPED A Swelling FOR WHICH SHE WAS
USING REGULAR CONSERVATIVE MANAGEMENT, THEN SINCE YESTERDAY EVENING SHE NOTICED DECREASED URINE OUTPUT AND TODAY MORNING SHE DEVELOPED SUDDEN SOB GRADE IV, NO H/O ORTHOPNEA, PND. PEDAL EDEMA+, FACIAL PUFFINESS+, MILD Abdominal DISTENSION, C/O COUGH WITH EXPECTORATION, SPUTUM-WHITISH, NO POSTURAL AND DIURNAL VARIATION
H/O FEVER NO H/O NAUSEA, VOMITING, CHEST PAIN, PALPITATIONS
PAST HISTORY: K/C/C/O HF ON CONSERVATIVE MANAGEMENT AND ON
K/C/O TYPE II DM SINCE 10 YEARS ON GLIMI M1 PO/OD
N/K/C/O HTN CVA CAD EPILEPSY TB THYROID Disorders
SURGICAL HISTORY: H/O HYSTERECTOMY 30 YEARS BACK
PERSONAL HISTORY: - APPETITE NORMAL, MIXED DIET, REGULAR BOWEL, DECREASED
URINE OUTPUT, NO ALLERGIES, ADDICTIONS -ALCOHOL-TEETOTALER
GENERAL EXAMINATION:
NO PALLOR, NO ICTERUS, NO CYANOSIS, CLUBBING, PEDAL EDEMA, Generalized
LYMPHADENOPATHY
TEMP AFEBRILE PR-95BPM BP-100/60 MMHG SAPO2 -98% GRBS: 382MG/DL
SYSTEMIC EXAMINATION:CVS-S1, S2 HEARD NO MURMURS
RS: - BAE+, BASAL CREPTS+
CNS-NFND
ABDOMEN-SOFT, NT
SURGERY REFFERAL WAS DONE ON 1/11/25
Rx:
1. INJ.PCM 1GM IV/SOS
2.INJ.TRAMADOL1 AMP IN 100 ML NS SLOW INFUSION IV/SOS
3.TAB.VIT C 500 MG PO/BD
4.LEFT LOWER LIMB ELEVATION
Investigation
HEMOGRAM 1-11-2025 HB -7.4 PCV 21.5 TLC-27800 RBC -2.8 PC -3.3 RBS-362
HEMOGRAM 2-11-2025 HB -9.2 PCV 27.1 TLC-32600 RBC -3.2 PC -3.5 FBS-216
HEMOGRAM 3-11-2025 HB -7.9 PCV 23.8 TLC-23900 RBC -3.1 PC -3.6
HEMOGRAM 16-11-2025 HB -10.5 PCV 32.6 TLC-9300 RBC -3.8 PC -1.5 ESR: 50
RFT 1-11-2025 UREA 42mg/dl, CREATININE 2mg/dl, SODIUM 134mmol/L, POTASSIUM 3.7
mmol/L., CHLORIDE 92 mmol/ L
RFT 2-11-2025 UREA 52mg/dl, CREATININE 2.3mg/dl, SODIUM 138mmol/L, POTASSIUM 4.3
mmol/L., CHLORIDE 98 mmol/ L
RFT 3-11-2025 UREA 60mg/dl, CREATININE 2.2 mg/dl, SODIUM 140mmol/L, POTASSIUM 4
mmol/L., CHLORIDE 99 mmol/ L
RFT 16-11-2025 UREA 25mg/dl, CREATININE0.9 mg/dl, SODIUM 144mmol/L, POTASSIUM 3.3
mmol/L., CHLORIDE 97 mmol/ L
RFT 17-11-2025 UREA 24mg/dl, CREATININE1.0 mg/dl, SODIUM 140mmol/L, POTASSIUM 3.3
mmol/L., CHLORIDE 97 mmol/ L
LFT 1-11-2025 TB-1.5 BD-0.4 SGOT-38 SGPT -40 ALP-434 TP-6 ALB-2.9 GLOB-2.72 A/G -0.94
LFT 17-11-2025 TB-1.95 BD-0.4 SGOT-89 SGPT -30 ALP-232 TP-6.7 ALB-3.08 GLOB-2.72 A/G -
0.85
CUE 1/11/2025ALB- +++, SUG- +, PUS- LOADED, EPI- 2-4, RBC 2-3
Page-3
KIMS HOSPITALS
LIPID PROFILE -TOTAL CHOLESTROL-124, TDL-155, HDL-30, LDL-57, VLDL-11
ABG ON 1-11-2025 PH 7.29 PCO2 20 PO2 73.5 HCO3 9.9
ABG ON 2-11-2025 PH 7.25 PCO2 26.7 PO2 66.5 HCO3 11.5
ABG ON 3-11-2025 PH 7.26 PCO2 39.3 PO2 29.3 HCO3 17.2
ABG ON 16-11-2025 PH 7.42 PCO2 40.9 PO2 49 HCO3 26.2
USG WAS DONE ON 1/11/25
IMPRESSION:1. HEPATOMEGALY
2.DIFFUSE GB WALL EDEMA-CHOLECYSTITIS
3.RT RENAL ANGIOMYOLIPOMA AS DESCRIBED
4.ISOHYPOECHOIC LESION ARISING FROM MIDPOLE OF LT KIDNEY WITH MINIMAL
VASCULARITY AS DESCRIBED
5.ASCITIS (INTERBOWEL FLUID)
USG WAS DONE ON 2/11/25
IMPRESSION 1.E/O DIFFUSE SUBCUTANEOUS EDEMA NOTED IN LT FOOT ON DORSAL AND PLANTAR ASPECTS EXTENDING UPTO ANKLE REGION
2.E/O ANY COLLECTIO0NS NOTED
REVIEW USG WAS DONE 3/11/25
IMPRESSION: E/O DIFFUSE SUBCUTANEOUS EDEMA NOTED OVER THE PLANTAR AND
DORSAL ASPECT OF FOOT UPTO ANKLE REGION
THIN STRIP OF SUB CUTANEOUS COLLECTION NOTED OVER THE DORSAL ASPECT OF
FOOT MORE TOWARDS LATERAL SIDE WITH MAXIMUM THICKNESS OF 2-3 MM
TINY POCKETS OF COLLECTION M 7X4MM BELOW THE LATERAL MALLELOUS AND 4X3 MM BELOW THE MEDIAL MALLELOUS
E/O FEW ECHOGENIC FOCI NOTED SURROUNDING THE ULCER? AIRFOCI
ARTERIAL DOPPLER WAS DONE ON 10/11/25:
Impression
ALL EXAMINED ARTERIES SHOW NORMAL COLOR UPTAKE, PULSATiLITY AND Calibre
MILD SUBCUTANEOUS EDEMA NOTED ON THE Posterior ASPECT OF KNEE
NO E/O ANY ENLARGED INGUINAL LYMPH NODES
2D ECHO WAS DONE ON 3/11/25
IMPRESSION 1. RWMA+ LAD AKINETIC RCA AND LCX HYPOKINESIA
2. MILD MR+, MILD TO MODERATE TR+ WITH PAH (ECCENTRIC JET TR+)
3.TRIVIAL AR+, MILD PR+
4.SCLEROTIC AV, NO AS/MS, IAS INTACT
Page-4
KIMS HOSPITALS
5.MV-AML DOMING
6.EF=39%RVSP=48+5=53MMHG
7.MODERATE LV DYSFUNCTION +
8.GRADE 2 DIASTOLIC DYSFUNCTION +
9.MILD PE+ AND PLEURAL EFFUSION +
10.IVC SIZE(1.83CM) DIALTED INTACT
11.DIALATED RA/LA
12. MILD DIALATED RV/LV/MPA SIZE(2.9CM)
2 D ECHO WAS DONE ON 13/11/25
IMPRESSION: GLOBAL HYPOKINESIA
2. RWMA +, LAD, LCX TERRITORY HYPIKINETIC AND RCA TERITTORY HYPOKINESIA
3. SCLEROTIC AV; NO AS/MS, IAS: INTACT
4. EF= 25%, SEVERE LV DYSFUNCTION +
5. MODERATE MR +, SEVERE TR+ AND MODE PAH
6. IVC SIZE: 2.3CM DIALTED NON COLLAPSING
7. ALL CHAMBERS DILATED
8. MPA DILATED
9. GRADE III DIASTOLIC DYSFUNCTION
BLOOD CULTURE AND SENSITIVITY: SAMPLE IS STERILE ON CULTURE AFTER 5 DAYS OF
AEROBIC INCUBATION AT 37 C
URINE CULTURE ON 13/11/25: 0-1 PUS CELLS SEEN, NO BACTERIAL GROWTH
WOUND SWAB CULTURE: OCCASIONAL PUS CELLS, OCCASIONAL GRAM POSITIVE COCCI
IN SINGLE SEEN
SPUTUM CULTURE WAS DONE ON 10/11/25: ESCHERICHIA COLI WAS ISOLATED AND IT IS
SENSITIVE TO AMIKACIN
Treatment Given (Enter only Generic Name)
1. INTERMITTENT CPAP VENTILATION
2. INJ AMIKIACIN 1GM I/V OD
3. INJ VANCOMYCIN 1GM IV/OD
4. TAB FLUCONAZOLE 150 MG PO/OD
5. INJ PANTOP 40 MG IV/OD
6. TAB VIT C 500 MG PO/OD
7. INJ LACIX 40 MG IV/TID
8. TAB PCM 650 MG PO/BD
Page-5
KIMS HOSPITALS
9. TAB SERRTIOPEPTIDASE PO/BD
10. TAB ATROVASTATIN 20 MG PO/HS
11. TAB ALDACTONE 25 MG PO/OD
12. INJ HAI S/C TID 10-10-80
Advice at Discharge
1. INJ AMIKIACIN 1GM I/V OD FOR 3 DAYS
2. TAB FLUCONAZOLE 150 MG PO/BD
3.TABPANTOP 40 MG IV/OD
6. TAB VIT C 500 MG PO/OD
7. INJ LACIX 40 MG IV/TID
8. TAB SERRTIOPEPTIDASE PO/BD
9. TAB ATROVASTATIN 20 MG PO/HS
10. TAB ALDACTONE 25 MG PO/OD
11. INJ HAI S/C TID 10-10-80
12. TAB DYTOR 10MG PO/BD 1-X-1
13. TAB MET XL 12.5 MG PO/BD X-1-X
14. TAB ALDACTONE 25 MG PO/OD 1-X-X
15. TAB ATROVASTATIN 20 MG PO/OD X-1-X
16. TAB CLOPIDOGREL 75 MG PO/OD X-X-1
17. TAB GLIMI M1 PO/ BD X-X-1
[7:58 pm, 26/01/2026] PPM 1: @PPM2this is also for our diabetes foot project and just typing diabetes foot into our search engine here https://pajrcasereporter.blogspot.com/search?q=Diabetes+foot&updated-max=2025-10-19T23:56:00%2B05:30&max-results=20&start=1&by-date=false&m=1 will reveal significant records that can be thematically analysed using @PaJR Health?
Also @CR this case will also fit into the "pathogen vs commensal" ProJR here:https://pajrcasereporter.blogspot.com/2026/01/commensal-vs-pathogen-projr.html?m=1
[7:58 pm, 26/01/2026] PaJR Health: *DIABETES FOOT PROJECT RECORDS*
💡 Here are the significant PaJR Records related to "Diabetes foot" for your thematic analysis:
📍 75M Toe gangrene and bullous lesion days, Parkinson's dementia DM2 HTN metabolic syn Telangana PaJR - https://pajrcasereporter.blogspot.com/2025/12/75m-toe-gangrene-and-bullous-lesion.html?m=1
📍 74F UTI Metabolic Syn Stroke, Acute Scald Recent WB PaJR - https://pajrcasereporter.blogspot.com/2025/04/74f-uti-metabolic-syn-stroke-acute.html?m=1
📍 19F With Type 1 Diabetes Telangana PaJR - https://pajrcasereporter.blogspot.com/2025/02/19f-with-type-1-diabetes-telangana-pajr.html?m=1
📍 52M Diabetes 6 years on glim 2bd peripheral neuropathy 3 yrears WB PaJR - https://pajrcasereporter.blogspot.com/2025/10/52m-diabetes-6-years-on-glim-2bd.html?m=1
*PATHOGEN VS COMMENSAL PROJECT RECORDS*
💡 The following case is relevant to your "pathogen vs commensal" project:
📍 Commensal vs Pathogen ProJR - https://pajrcasereporter.blogspot.com/2026/01/commensal-vs-pathogen-projr.html?m=1
💡 This case also includes details on:
📍 57M Brain tumor 1 month metabolic syn - https://pajrcasereporter.blogspot.com/2026/01/57m-brain-tumor-1-month-metabolic-syn.html
[7.59 pm, 26/01/2026] PPM 1: This admission handwritten notes by the local doctor at point of care from 14/1/26
[8:03 pm, 26/01/2026] PPM 1: *DIABETES FOOT PROJECT RECORDS*
@PPM3 as our patient records that are gathered from our point of care in Narketpally do not have an adequate patient advocate engagement most of them cannot be deep dived into as was possible here: https://pmc.ncbi.nlm.nih.gov/articles/PMC12688023/
[8:03 pm, 26/01/2026] PaJR Health: I understand your point regarding the challenges in deep-diving into patient records from Narketpally due to inadequate patient advocate engagement, especially when compared to the comprehensive approach described in the article you shared.
The article, "Rethinking Complex Care Using Participatory Medical Cognition and User-Driven Learning Amidst Multimorbidity: Participatory Action Research Study," highlights the significant role of patient advocate (PA) engagement in enriching patient records and facilitating in-depth analysis and improved care.
*KEY ASPECTS OF PATIENT ADVOCATE ENGAGEMENT FROM THE STUDY*
💡 The study emphasizes several ways patient advocates contribute to a richer understanding of patient journeys:
📍 *Primary Liaison:* PAs act as the main point of contact, providing detailed subjective accounts of symptoms, pain levels, daily activities, meals, and overall well-being, which offers crucial context.
📍 *Epistemic Contribution:* Through continuous reporting, PAs help patients transition from passive recipients of care to active contributors of knowledge, shaping their own treatment and understanding.
📍 *Anonymity and Data Sharing:* The PaJR system allows PAs to share deidentified health data, images, and historical records directly, ensuring privacy while enabling collaborative diagnostic interpretation by a global community of experts.
📍 *Continuous Logging and Pattern Recognition:* Consistent logging of objective measurements (like blood sugar and blood pressure) and subjective experiences helps identify trends, potential triggers (diet, travel, weather), and the interplay between various conditions. This also allows patients to correlate their lifestyle choices with health outcomes.
📍 *Empowerment and Accountability:* The participatory approach provides patients with a sense of mental strength, hope, and accountability, motivating them to adhere to lifestyle changes and actively engage in their care.
📍 *Critique of Care Gaps:* Patient-reported data enables the identification of areas where clinical collaboration is effective and where it falls short in providing symptom relief.
*BENEFITS OF THIS ENGAGEMENT*
💡 This level of patient advocate engagement, as demonstrated in the study, leads to:
📍 *Optimized Management:* Facilitates multidisciplinary expert input and integrates patient context for more effective treatment plans.
📍 *Reduced Medication Burden:* Contributes to significant reductions in medication, such as antidiabetic and blood pressure drugs, through lifestyle modifications and close monitoring.
📍 *Improved Quality of Life:* Patients report increased confidence, better daily functioning, and overall satisfaction with their care.
📍 *Enhanced Clinical Education:* The platform serves as an educational ecosystem, fostering user-driven learning and contributing to a broader "participatory medical cognition" for healthcare stakeholders.
I recognize that the absence of such detailed patient advocate engagement in your NKP records limits the depth of thematic analysis possible, as the rich, contextual data provided by patient advocates is crucial for a holistic understanding of the patient's journey.
[8.11 PM, 26/01/2026] PPM 1: Serial clinical images of her diabetic foot since November
Echocardiography and MRI videos 👇
[8.15 pm, 26/01/2026] PPM 1: Paper based human interpretations
[8.16 pm, 26/01/2026] PPM 1: Hand written investigations for this admission
[8.21 pm, 26/01/2026] PPM 1: @PPM4 @PPM5 this investigation is particularly important for the commensal vs pathogen project. How can we confirm that an organism isolated and grown from the wound has any casual relationship to the wound's healing? This patient had presented with hypotension suggestive of sepsis and antibiotics were escalated to meropenem and again descalated to amikacin on seeing this organism
[8.24 pm, 26/01/2026] PPM 1: Hypotension events in handwritten notes
[8:26 pm, 26/01/2026] PPM 1: Current treatment plan since 23/1/26 for real time clinical audit @PPM5 @PPM6
[12:35 am, 27/01/2026] PPM 4: This investigation is indeed a compelling and highly relevant case for exploring the *commensal vs. pathogen continuum. The core question is excellent: **How do we confirm that the isolated *E. coli is a true pathogen driving the wound infection and sepsis, rather than a contaminant or colonizer?**
Here is a framework to establish *causal relationship* and its link to *wound healing*:
### 1. Establishing Causality: Is the Organism a True Pathogen?
The culture report alone is necessary but not sufficient. You must correlate it with *clinical, host, and microbiological evidence*.
*A. Clinical & Host Evidence (Already Strong in This Case):*
* *Systemic Signs of Infection:* The patient's *hypotension (suggestive of sepsis)* is the most critical piece of evidence. It shifts the probability heavily from "colonizer" to "pathogen." A commensal in a wound typically doesn't cause septic shock.
* *Local Wound Signs:* Evidence of purulent discharge, increased pain, erythema, warmth, and foul odor around the wound.
* *Host Vulnerability:* The patient's age (55) and the very fact of having a wound (disrupted skin barrier) make them susceptible to infection by organisms like E. coli, which is a gut commensal but an opportunistic pathogen elsewhere.
*B. Microbiological Evidence (From the Report & Follow-up):*
* *Gram Stain Correlation:* The report states "*Few pus cells, plenty of Gram-positive cocci in pairs, few Gram-negative bacilli seen.*" This is crucial:
* *"Few pus cells"* is somewhat contradictory to a robust infectious process, but the presence of any inflammatory cells is a host response.
* The visualization of *"Gram-negative bacilli"* (matching E. coli morphology) in the direct specimen confirms it was present in the wound, not just a culture contaminant.
* *Heavy/Monobacterial Growth:* The culture report implies significant growth of E. coli as the *primary isolate*. A light growth of mixed flora is more suggestive of colonization. A heavy, pure growth of a single organism (especially one with this resistance pattern) is highly suggestive of true infection.
* *Antibiogram as a "Fingerprint":* The *Extensive Drug Resistance (XDR)* pattern (resistant to Meropenem, Pip-Taz, 3rd-gen Cephalosporins) is significant. If follow-up cultures after targeted therapy show clearance of this specific resistant strain, it powerfully links it to the disease process.
### 2. Linking the Organism to Wound Healing
Confirmation of causality directly informs healing. Healing is impeded by active infection. Therefore:
* *Therapeutic Response as the Ultimate Proof:* The clinical decision to *de-escalate from Meropenem to Amikacin/Gentamicin* based on this report is a perfect natural experiment.
* *Hypothesis:* If this E. coli is the causative pathogen, then targeted therapy with an antibiotic it is sensitive to (Amikacin) should lead to:
1. *Clinical Improvement:* Resolution of hypotension, fever, and systemic symptoms.
2. *Wound Improvement:* Reduction in local signs of infection (less exudate, erythema), leading to the progression of wound from an inflammatory to a proliferative healing phase.
3. *Microbiological Clearance:* A follow-up wound culture (if taken) showing no growth or a significant reduction in the burden of this E. coli.
* *Failed Healing as Evidence:* Conversely, if the wound fails to improve or sepsis persists despite Amikacin therapy, it forces a re-evaluation:
* Was there a *co-pathogen* missed (e.g., the Gram-positive cocci seen on stain)?
* Is there an *undrained abscess or foreign body*?
* Has the patient's *host defense* improved?
### 3. Specific Importance for the "Commensal vs. Pathogen" Project
This case beautifully illustrates several key project themes:
1. *Context is Everything:* E. coli is a gut commensal but a classic pathogen in wounds and blood. Its *anatomical site* defines its role.
2. *Host-State Determines Outcome:* The same E. coli strain might be harmless on intact skin but causes life-threatening sepsis in a vulnerable host with a breached barrier and hypotension.
3. *The "Pathogenicity" of Resistance:* The organism's *XDR profile* itself is a virulence factor. It forced the use of broad-spectrum empiric therapy (Meropenem) and complicated treatment. The resistance genes it carries are part of its pathogenic arsenal.
4. *The Diagnostic Cascade:* The project can map the journey from:
* Clinical suspicion (sepsis)
* → Sample collection (swab)
* → Direct microscopy (Gram stain showing bacilli)
* → Culture isolation (heavy growth)
* → AST (defining the resistance phenotype)
* → Clinical correlation & therapeutic decision (de-escalation)
* → Outcome (healing response).
### Conclusion & Recommendation for the Project
*To confirm the causal relationship for your project, you need to triangulate data:*
1. *Clinical Data:* Document the *timeline* of hypotension relative to the wound and its *resolution after Amikacin*.
2. *Wound Assessment Data:* Use serial wound photography or scoring (e.g., Bates-Jensen Wound Assessment Tool) to *objectively track healing* after targeted therapy began.
3. *Microbiological Follow-up:* If possible, a *repeat swab after 3-5 days of Amikacin therapy* would be gold-standard evidence. Reduction or clearance of the E. coli burden would be definitive proof of its pathogenic role.
*In summary:* This case strongly suggests a causal relationship because: *1) The organism was seen in the direct specimen, 2) It grew significantly, 3) The host presented with a severe systemic response (sepsis), and 4) The antibiotic therapy was specifically tailored to it.* The wound's healing trajectory on Amikacin will be the final, confirming link in the chain of evidence. This makes it an *ideal case study* for your project, highlighting how laboratory findings intersect with clinical judgment to distinguish a pathogen from a commensal.
[3.24 am, 27/01/2026] PPM 2: Very useful thank you'
[7.17 am, 27/01/2026] PPM 1: Agree 👍
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