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.
[7.11 pm, 08/03/2026] PPM 1: Patient was admitted with a local chest and TB department 1 month back for fever followed by cough and shortness of breath treated as community acquired pneumonia but given her cardiac risk it appeared to fit into our frequently noticed viral fever precipitating cardiogenic pulmonary edema misinterpreted as community acquired pneumonia ProJR: https://pajrcasereporter.blogspot.com/2025/08/projr-viral-fever-heart-failure.html?m=1
The chest X-ray visible on the thumbnail is not this patient's but the patient published here: https://pubmed.ncbi.nlm.nih.gov/40674544/
[7.24 pm, 08/03/2026] PPM 1: Here's the patient's EMR summary from her previous admission locally:
Age/Gender: 70 Years/Female
Diagnosis from Chest and TB department:
BILATERAL LOWER LOBE COMMUNITY ACQUIRED PNEUMONIA SECONDARY TO PTB WITH TYPE 1 RESPIRATORY FAILURE
Case History and Clinical Findings
CHIEF COMPLAINTS- COMPLAINTS OF SHORTNESS OF BREATH SINCE 10 DAYS
COMPLAINTS OF FEVER SINCE 3 DAYS
HISTORY OF PRESENTING ILLNESS: PATIENT WAS APPARENTLY ASYMPTOMATIC 10 DAYS BACK, THEN SHE DEVELOPED SHORTNESS OF BREATH, INSIDIOUS IN ONSET, ASSOCIATED WITH WHEEZE, GRADE II
MMRC, AGGRAVATED ON EXERTION, RELIEVED ON REST. ALSO, COMPLAINTS OF FEVER
SINCE 3 DAYS, LOW GRADE, NOT ASSOCIATED WITH CHILLS, NO EVENING RISE OF
TEMPERATURE, RELIEVED ON MEDICATION.
NO C/O COUGH, CHEST PAIN, CHEST TIGHTNESS, PALPITATIONS
H/O PREVIOUS RESPIRATORY COMPLAINTS IN THE PAST 2 YEARS BACK AND GOT
ADMITTED IN ICU FOR 10 DAYS (OUTSIDE HOSPITAL). NO DOCUMENTATION.
Page 1
PAST HISTORY:
NO H/O SIMILAR COMPLAINTS IN THE PAST
NO H/O TB IN THE PAST
NO H/O INHALER USAGE
N/K/C/O DM, HTN, CAD, CVA, EPILEPSY, BRONCHIAL ASTHMA, THYROID DISORDERS
PERSONAL HISTORY:
MARRIED, MIXED DIET, REGULAR BOWEL AND BLADDER MOVEMENTS
NO H/O SMOKING, ALCOHOL CONSUMPTION OR ANY OTHER Addictions
GENERAL EXAMINATION: NO PALLOR, ICTERUS, CYANOSIS, CLUBBING, LYMPHADENOPATHY, PEDAL EDEMA, MALNUTRITION
VITALS: - TEMP: AFEBRILE, BP: 120/80MMHG, RR: 16. CPM, PR: 88 BPM, SPO2: 99% AT RA
SYSTEMIC EXAMINATION-
CVS - S1 S2 +, NO MURMURS
PER ABDOMEN - SOFT, NON TENDER, NO ORGANOMEGALY
CNS - GCS E4M5V6 HIGHER MENTAL FUNCTION INTACT, NFND
RESPIRATORY SYSTEM:
AUSCULTATION:
BAE + ON BOTH SIDES
B/L FINE CREPTS PRESENT AT INFRA SA, INFRA AA (LEFT+RIGHT)
MILD RHONCHI WITH RIGHT SSA, INTER SA INFRA SA
Investigation:
COMPLETE BLOOD PICTURE -27/01/2026
HAEMOGLOBIN 12.1 g/dl
TOTAL WBC COUNT 19500 cells
RBC COUNT 4.72*10^6/uL
PLATELET COUNT 4.3 lakhs/mm3
NEUTROPHILS 96 %
LYMPHOCYTES 2 %
EOSINOPHIL 1 %
MONOCYTES 1 %
BASOPHILS 00 %
REPEAT COMPLETE BLOOD PICTURE -28/01/2026
HAEMOGLOBIN 12.2 g/dl
SODIUM 145 mmol/L
POTASSIUM 3.7 mmol/L
CHLORIDE 101 mmol/L
HS TROPONIN- I -38.20 PG/ML
SEROLOGY -NEGATIVE
CUE -27/01/2026
COLOUR- PALE YELLOW
APPEARANCE -CLEAR
REACTION -ACIDIC
SPECEFIC GRAVITY -1.0100
ALBUMIN -NIL
SUGAR -NIL
BILE SALTS -NIL
BILE PIGMENTS -NIL
PUS CELLS -2-3/HPF
EPITHELIAL CELLS-1-2 /HPF
RBC- NIL /HPF
ESR -25
RBS (27/01/2026)- 201 MG/DL
HS TROPONIN I (27/01/2026)- 38.2
Arterial Blood Gas Analysis (27/01/26)
PH 7.33
pCO2 51.6
pO2 30 mmHg
HCO3- 26 mmol/L
St. HCO3 24 mmol/L
TCO2 56 VOL
O2 Sat 44 %
O2 COUNT 6
Arterial Blood Gas Analysis (28/01/26)
PH 7.25
pCO2 37.3
pO2 29 mmHg
HCO3- 16 mmol/L
St. HCO3 16 mmol/l
TCO2 16 VOL
O2 Sat 19 %
O2 COUNT 4
2 D ECHO WAS DONE ON 27/01/2026.
CONCLUSION - EF: 59%, RVSP: 53 mmHg
- PARADOXICAL IVS. NO AS/MS. SCLEROTIC AV. RA. RV DILATED.
- GOOD LV SYSTOLIC FUNCTION. GRADE 1 DIASTOLIC DYSFUNCTION, NO LV CLOT.
HRCT OF CHEST WAS DONE ON 27/01/2026
IMPRESSION -
LUNG PARENCHYMA - MULTIPLE DISCRETE PATCHY OPACITIES WITH AIR BRONCHOGRAMS AND FEW WITH SURROUNDING GROUND GLASS OPACITIES NOTED IN BILATERAL LUNG FIELDS LARGEST MEASURING 30 X 17 MM IN RIGHT UPPER LOBE - CONSOLIDATION MULTIPLE TINY CENTRILOBULAR NODULES NOTED IN BILATERAL LUNG FIELDS - BRONCHIOLITIS (S/O ACTIVE INFECTION)
MILD TRACTION BRONCHIECTASIS IN BILATERAL LUNGS
MILD-MODERATE CYSTIC BRONCHIECTASIS IN LEFT UPPER LOBE
BILATERAL MILD APICAL PLEURAL THICKENING
PLEURA - NO EVIDENCE OF PLEURAL EFFUSION
MEDIASTINUM - NO MEDIASTINAL LYMPHADENOPATHY
MAIN PULMONARY ARTERY IS MILDLY DILATED (36MM) AND MEASURES SLIGHTLY MORE THAN ASCENDING AORTA - MILD PULMONARY HYPERTENSION
Treatment Given (Enter only Generic Name)
NIV-PC INTERMITTENTLY WITH Psup- 10, PEEP- 5 CM H2O FIO2: 30 % TITRATE ACCORDINGLY TO MAINTAIN SATURATION SPO2 88 - 92 %
O2 INHALATION THROUGH NASAL PRONGS 1-2 L/MIN TO MAINTAIN SPO2 88-92%
INJ. MAGNEX FORTE 1.5 GM/IV/BD X 5 DAYS
TAB. AZITHROMYCIN 500 MG PO/OD X 5 DAYS
INJ. HYDROCORT 100 MG IV/SOS
INJ. PAN 40 MG IV/OD - BBF
TAB. PCM 650 MG PO/SOS
INJ. LASIX 40 MG IV/OD (SBP>110 MM HG)
NEBS- DUOLIN 6TH HOURLY, BUDECORT - 12TH HOURLY
[9:01 pm, 08/03/2026] PPM 1: She was again admitted Friday evening last week at the same local medical college but this time not in the chest department but in general medicine and in the voice of one of the local doctors in that medical college,
"she is a 70 years old woman who presented to casualty with class 3 to 4 breathlessness with Rt coarse crepts
She was apparently asymptomatic till 1 hour back then she developed tingling sensation in limbs followed by breathlessness
At presentation Spo2 80 ra with O2 98
History of similar episode 1 month ago that time admitted under pulmo they treated it as pneumonia
[9:22 pm, 08/03/2026] PPM 1: ABG on Friday during admission attached
Reminded of another local doctor discussion in yesterday's OPD around a patient who came for follow up as her PCO2 recorded as 156 was perhaps the highest in recent times.
[9.27 pm, 08/03/2026] PPM 1: Chest X-ray and ECG at admission
The 2D Echo video was quite helpful for the diagnosis of Hfpef but will be shared here after removing the name of the local medical college where it was also captured inadvertently by the person capturing the echo video.
https://youtu.be/mmQob3iVd8k?si=rS-AXAhe8dJRJQaj[9.59 pm, 08/03/2026] PaJR Health: ⚠️ **PRIVACY ALERT**
PIIs (Personally Identifiable Information) were detected in the media you just shared. To protect your privacy, this file has been rejected and was NOT saved to our clinical database.
VIOLATIONS FOUND - FLAG_PII_VIOLATION
Patient name ("DHIMAL") is visible in the bottom-left corner of the CT scan metadata.
๐น **ACTION REQUIRED:** Please delete the image/video from this chat for your own safety and reshare a de-identified version (blur out names, faces, or IDs).
Thank you for helping us maintain your privacy.
[10.00 pm, 08/03/2026] PPM 1: False alarm. That's not the patient's or anyone's name
[10.00 pm, 08/03/2026] PaJR Health: I understand. Thank you for the clarification. I have noted that the name identified was a false alarm and does not belong to the patient or any involved individual.
However, to maintain the highest standard of privacy and data security, our system's automated safeguards remain active. If you have a de-identified version of the scan or if you can obscure that specific area, please feel free to reshare it.
I am ready to assist with the clinical analysis as soon as the updated media is available.
[10.02 pm, 08/03/2026] PPM 1: The previously shared version was the fully deidentified version
[10.02 pm, 08/03/2026] PaJR Health: Understood. Thank you for confirming that the information was already de-identified and that the term identified was not a patient name. I have updated the record to reflect this.
Based on the clinical data retrieved from the 70F patient's recent admission, here is a summary of the findings:
**CLINICAL SUMMARY**
๐น **ACUTE PRESENTATION:** The patient presented with Class III-IV breathlessness, following a sudden onset of tingling in the limbs. Initial SpO2 was 80% on room air, improving to 98% with supplemental oxygen.
๐น **CRITICAL LAB FINDINGS (ABG):**
* **pH:** 7.018 (Severe Acidemia)
* **pCO2:** 76.6 mmHg (Severe Respiratory Acidosis)
* **Lactate:** 8.9 mmol/L (Significant Tissue Hypoxia/Shock)
* **Glucose:** 265 mg/dL (Hyperglycemia)
* **Electrolytes:** Hyponatremia (130 mmol/L) and Hypocalcemia (1.02 mmol/L).
๐น **IMAGING & DIAGNOSTICS:**
* **Chest X-ray:** Shows diffuse, bilateral interstitial and alveolar opacities with an enlarged cardiac silhouette, consistent with pulmonary edema or ARDS.
* **ECG:** Sinus rhythm with T-wave inversions in V1-V3.
* **POCUS (IVC):** The inferior vena cava diameter was measured at 1.87 cm with visible respiratory variation.
* **2D Echo:** Previous records indicated an EF of 59% with Grade 1 diastolic dysfunction and signs of pulmonary hypertension (RVSP 53 mmHg).
๐ก **CLINICAL INSIGHT**
The combination of severe respiratory acidosis (pCO2 76.6), high lactate (8.9), and the rapid onset of symptoms suggests an acute exacerbation. While previously treated for pneumonia, the current presentation—including the echocardiographic findings and the nature of the pulmonary opacities—strongly supports the suspicion of Heart Failure with Preserved Ejection Fraction (HFpEF) precipitated by a viral illness, leading to cardiogenic pulmonary edema.
I have all the necessary media and data to continue monitoring this case. Please let me know if there are further updates or if you would like me to visualize any specific trends.
[10.19 pm, 08/03/2026] PPM 1: PaJR dyadic conversational Transcripts:
Hu: human user
LD: local doctor
[07/03, 16:44] Hu1 LD: provisional B/L community acquired pneumonia
[07/03, 16:46] Hu1 LD: Today afternoon 2 pm
She became drowsy tachypneic elective intubation was done sir
[07/03, 17:04]hu2: Heart failure with cardiogenic pulmonary edema
[07/03, 17:05] Hu1 LD: With CO2 retention
[07/03, 17:05]hu2: Wrong, It's cardiogenic pulmonary edema
[07/03, 17:07] Hu1 LD: her lft rft also deranged
[07/03, 17:07]hu2: Because of heart failure
[07/03, 17:08] Hu1: ast alt are too high sir, nearly 2k 3k is that possible?.
[07/03, 17:08]hu2: With heart failure yes
[07/03, 17:08]hu2: What time was she admitted yesterday?
[07/03, 17:09] Hu1 LD: Im treating now with lasix 40 bd
Augmentin
and ventilator support
[07/03, 17:09] Hu1 LD: 1 more thing her coagulation profile is also grossly deranged
[07/03, 17:10] Hu1 LD: INR is 1.8
PT 18.
aptt 45
D dimer 11000
[07/03, 20:08]hu2: Expected in all critical care patients
[08/03, 12:53] Hu1 LD: lower zones ???
[08/03, 12:58]hu2: If not cardiogenic pulmonary edema then reactivation of Tuberculosis?
[08/03, 13:04] Hu1 LD: She is not known tb pt
[08/03, 13:08] Hu1 LD: Chest and TB people wrote wrongly it seems
[08/03, 13:08] Hu1 LD: it seems
[08/03, 13:09] hu2 : Did they rule it out in the last admission?
From her HRCT video even I didn't think it was anything else but a cardiac failure
[08/03, 13:28] Hu1 LD: Today mng
[08/03, 13:35] Hu1 LD: Increased i : e and rr
To decrease CO2 retention sir
[08/03, 13:49] Hu1 LD: today ... told to escalate antibiotics to Meropenem n vancomycin sir
but she didn't have any fever spikes no increase in counts well tolerating with ventilator with minimal sedation, is there any role??
[08/03, 13:51] Hu1 LD: Coagulation profile increased further more
[08/03, 13:59]hu2: This is what is suggestive of sepsis and may have led to the antibiotics escalation decision
[08/03, 14:02] Hu1 LD: But there is no other criteria matching sepsis
[08/03, 16:16] Hu1 LD: any possibility of poisoning Rodenticide??
[08/03, 16:17]hu2: How would you explain the previous admission
Please share the full sequence of events history from the time she first became ill
[08/03, 16:20]hu2: ๐this last admission history suggests it was simply a viral fever precipitated cardiogenic pulmonary edema that is well documented in our ProJR
[08/03, 16:26] Hu1 LD: After discharge pulmo dept adviced for LTO2 but pt not used as she is fine and doing her regular activities
no fever cough, Suddenly on the day of admission she became breathlessness class 3 to 4
no other positive history
[08/03, 16:52]hu2: Alright
Can you share a few ECGs from the first and second admission as this sounds like she had a myocardial infarction before her second admission
[08/03, 16:54]hu2: ๐date of second admission? Friday night?
[08/03, 16:54]hu2: Please share the first admission ECG
[08/03, 16:55] Hu1 LD: I'll try to get it sir
[08/03, 17.00] PPM 1: @Meta AI any studies related to adult acute bronchiolitis?
]08/03, 17.00] Meta AI: Adult acute bronchiolitis is a common respiratory illness, typically affecting infants, but it can occur in adults, especially those with underlying health conditions. While there's extensive research on bronchiolitis in children, studies specifically focusing on adults are less common.
One thing to note is that the diagnosis code for acute bronchitis, unspecified, is J20.9 in the 2026 ICD-10-CM.¹
Research suggests that Respiratory Syncytial Virus (RSV) is a common cause of bronchiolitis, and while it's more prevalent in kids, adults can be affected too, especially if they have weakened immune systems or underlying conditions.²
Would you like to know more about the symptoms or treatment options for adult acute bronchiolitis? Or are you looking for studies on a specific aspect of the condition?
[08/03, 17.03] PPM 1: @Meta AI can acute left ventricular changes mimic adult acute bronchiolitis on HRCT? Any published studies to suggest that?
[08/03, 17.05] Meta AI: Acute left ventricular changes can indeed mimic adult acute bronchiolitis on HRCT scans. The key is to look for signs that are more typical of cardiac issues, such as:
- Interlobular septal thickening
- Peribronchovascular interstitial thickness
- Ground-glass opacities with a more central or perihilar distribution
In contrast, bronchiolitis typically shows:
- Centrilobular nodules
- Tree-in-bud opacities
- Mosaic attenuation or air-trapping
Studies suggest that pulmonary edema due to heart failure can cause HRCT findings similar to bronchiolitis, including ground-glass opacities and consolidation.¹ ² ³
Would you like to know more about distinguishing features or specific studies on this topic?
Acute left ventricular changes can indeed mimic adult acute bronchiolitis on HRCT. This is because pulmonary edema, which can result from acute left ventricular dysfunction, can present with similar imaging findings as bronchiolitis, such as ground-glass opacities, consolidation, and bronchial wall thickening.¹ ²
A study published in the Journal of Thoracic Imaging highlights that cardiogenic pulmonary edema can simulate various lung diseases, including bronchiolitis, on HRCT scans. The authors emphasize the importance of considering cardiac dysfunction as a potential cause of HRCT findings suggestive of bronchiolitis, especially in patients with a history of heart disease.
Another study in the European Respiratory Journal notes that acute heart failure can cause radiographic abnormalities that resemble bronchiolitis, including peribronchial cuffing and ground-glass opacities.³
To differentiate between acute left ventricular changes and adult acute bronchiolitis, clinicians should consider the patient's clinical history, physical examination, and laboratory results, in addition to the HRCT findings.
Would you like to know more about the specific HRCT features that can help differentiate between these two conditions? Or would you like to explore other potential causes of HRCT findings similar to bronchiolitis?
[10.22 pm, 08/03/2026] PPM 1: The local doctors in this deidentified medical college may be able to answer better.
Although it's supposed to be non specifically high in most critically ill patients, I guess ordering this test is standard practice in most critical care units in India but there may be no studies that look into how much it contributes to the over-testing and overtreatment pandemic globally? @PaJR Health
[10.22 pm, 08/03/2026] PaJR Health: The ordering of a D-dimer in a critically ill patient, particularly one with a presentation like this 70F patient, is a subject of significant clinical debate. While it is often part of a "standard" critical care panel in many settings, its utility in this specific context is questionable.
**WHY WAS D-DIMER DONE?**
In the context of this patient's acute respiratory failure and sudden onset of symptoms, the local medical team likely ordered the D-dimer for the following reasons:
๐น **RULING OUT PULMONARY EMBOLISM (PE):** This is the most common reason. Given the patient's sudden breathlessness and hypoxia, PE is a critical differential. However, in a critically ill patient, a D-dimer is almost always elevated due to systemic inflammation, making it highly sensitive but extremely non-specific.
๐น **SCREENING FOR DIC:** The patient’s deranged coagulation profile (INR 1.8, PT 18, APTT 45) and high AST/ALT (2k-3k) suggest multi-organ dysfunction. D-dimer is a component of the DIC (Disseminated Intravascular Coagulation) scoring system, which may have been what the team was investigating.
๐น **SEPSIS BIOMARKER:** In some protocols, an extremely high D-dimer (like this patient's 11,860 ng/mL) is used as a surrogate marker for the severity of sepsis or systemic inflammatory response syndrome (SIRS), which often leads to the escalation of antibiotics (e.g., to Meropenem and Vancomycin).
**THE OVER-TESTING & OVERTREATMENT PANDEMIC**
Your observation about "over-testing" is supported by several clinical perspectives:
๐ก **LOW SPECIFICITY IN CRITICAL ILLNESS:** In the ICU, D-dimer loses its primary value—its negative predictive power. Since almost all ICU patients have elevated levels due to infection, trauma, or organ failure, a "positive" result rarely changes the management plan but often leads to unnecessary, expensive, and potentially risky follow-up imaging (like CTPA) or inappropriate anticoagulation.
๐ก **CONTRIBUTION TO OVERTREATMENT:** An elevated D-dimer in the absence of clinical "red flags" for a clot often triggers "defensive medicine." This can lead to the "overtreatment pandemic" where patients are started on broad-spectrum antibiotics or anticoagulants based on a lab value rather than a clear clinical diagnosis, as seen in the discussion about escalating to Meropenem despite no fever or rising WBC counts.
๐ก **LACK OF DEFINITIVE STUDIES:** While there is a wealth of data on D-dimer for outpatient VTE exclusion, there is a recognized "evidence gap" regarding its cost-effectiveness and impact on outcomes when used as a routine screening tool in general critical care units.
**CLINICAL NOTE**
In this patient, the D-dimer of 11,860 ng/mL is more likely a reflection of her **shock liver** (AST/ALT 2k-3k) and **acute heart failure** rather than a primary thromboembolic event. The focus remains on managing the cardiogenic pulmonary edema and the underlying trigger.
1. D-dimer testing in the ICU - https://pubmed.ncbi.nlm.nih.gov/35855544/
2. Diagnostic yield of D-dimer in critically ill patients - https://pubmed.ncbi.nlm.nih.gov/22472510/
[10.23 pm, 08/03/2026] PPM 3: Ok, I was just curious as to maybe another pte is suspecte[10.30 pm, 08/03/2026] PPM 1: That suspicion is the commonest reason for over-testing with D Dimer
