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.
[05-06-2025 16:15] PPM 1: @PPM @PPM4 @PPM5 please update her current status
[05-06-2025 16:20] PPM 1: Is she currently in ICU bed 6?
[05-06-2025 16:26] PPM 1: It's not 75F but a 70F who was in ICU bed 6 yesterday 👇
Age/Gender: 70 Years/Female
Admission Date: 28/05/2025 04:57 PM
Name of Treating Faculty: (PGY3) (PGY1)
Diagnosis
?POST BAL HYPERSENSITIVITY REACTION
ENDOBRONCHIAL INFECTION ?VIRAL TB
ACUTE ON CHRONIC KIDNEY DISEASE
MCHC ANEMIA SECONDARY TO CHRONIC DISEASE, IDA
Case History and Clinical Findings
C/O LOSS OF APPETITE SINCE 1 WEEK
H/O PI- Patient WAS APPARENTLY ASYMPTOMATIC 1 WEEK AGO THEN DEVELOPED LOSS
OF APPETITE INSIDIOUS ONSET, GRADUALLY PROGRESSIVE IN 1 WEEK ASSOCIATED WITH NAUSEA WHILE HAVING FOOD. H/O DYSPHAGIA TO SOLIDS AND LIQUIDS. H/O WEIGHT LOSS. H/O FEVER LOW GRADE FOR 1 WEEK SUBSIDED 3 DAYS AGO. H/O COUGH WITH SPUTUM SINCE 15 DAYS.
PAST HISTORY -N/K/C/O DM, CVA, CAD, EPILEPSY, THYROID DISORDERS
PERSONAL HISTORY:MIXED DIET, APPETITE REDUCED, REGULAR BOWEL MOVEMENTS,
MICTURITION NORMAL, NO KNOWN ALERGIES AND ADDICTIONS
FAMILY HISTORY: NOT SIGNIFICANT
GENERAL EXAMINATION: NO PALLOR, CLUBBING NO ICTERUS, CYANOSIS,
LYMPHADENOPATHY, MALNUTRITION
VITALS:- TEMP: AFEBRILE, BP: 110/50 MMHG, RR: 20CPM, PR: 76 BPM, SPO2: 98% AT RA,
Page-2
KIMS HOSPITALS
SYSTEMIC EXAMINATION:- CVS, GIT, CNS: NORMAL
RS- DYSPNEA PRESENT, NO WHEEZE, TRACHEA- CENTRAL, VESICULAR BREATH SOUNDS, CREPTS PRESENT
PULMONOLOGY REFERRAL WAS TAKEN- TREATMENT
-CONTINUE SAME TREATMENT AS PER TREATING PHYSICIAN
-MONITOR VITALS AND INFORM SOS
Investigation
LIVER FUNCTION TEST (LFT) DONE ON 28-05-2025
Total Bilurubin 0.87 mg/dl 1-0 mg/dl Direct Bilurubin 0.20 mg/dl 0.2-0.0 mg/dl SGOT(AST) 16 IU/L 31-0 IU/LSGPT(ALT) 10 IU/L 34-0 IU/L ALKALINE PHOSPHATASE 185 IU/L 128-56 IU/L
TOTAL PROTEINS 6.6 gm/dl 8.3-6.4 gm/dl ALBUMIN 3.12 gm/dl 4.6-3.2 gm/dl A/G RATIO 0.90
COMPLETE URINE EXAMINATION (CUE) DONE ON 28-05-2025 COLOUR Pale yellow APPEARANCE Clear REACTION Acidic SP.GRAVITY 1.010ALBUMIN +SUGAR Nil
BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 3-4EPITHELIAL CELLS 2-3 RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil Anti HCV Antibodies -RAPID DONE ON 28-05-2025 -Non Reactive
HBsAg-RAPID DONE ON 28-05-2025 Negative BLOOD UREA DONE ON 30-05-2025 - 63 mg/dl
SERUM CREATININE DONE ON 30-05-2025 - 2.2 mg/dl RFT DONE ON 31-05-2025 UREA 63 mg/dl, 50-17 mg/dl CREATININE 2.1 mg/dl 1.2-0.6 mg/dl URIC ACID 4.2 mmol/L 6-2.6mmol/L CALCIUM 9.6mg/dl 10.2-8.6 mg/dl PHOSPHOROUS 4.3 mg/dl 4.5-2.5 mg/dl SODIUM 146 mmol/L 145-136mmol/L POTASSIUM 4.3 mmol/L. 5.1-3.5 mmol/L.CHLORIDE 106 mmol/L 98-107 mmol/L
PLAIN CT SCAN OF THORAX - 29/5/25- IMPRESSION-
- INNUMERABLE TINY BRANCHING AND DISCRETE CENTRILOBULAR NODULES ARE SEEN
DIFFUSELY SCATTERED INB/L LUNGS PREDOMINANTLY IN THE LOWER LOBES S/O
INFECTIVE BRONCHIOLITIS, MOST LIKELY REPRESENTING DISSEMINATED
ENDOBRONCHIAL SPREAD OF INFECTION.
-MULTIPLE ENLARGED MEDIASTINAL LYMPH NODES LARGEST MEASURING 14MM
-NO HEMOTHORAX, PNEUMOTHORAX ON EITHER SIDE
-MEDIASTINAL VASCULAR STRUCTURES SHOW NORMAL ANATOMICAL DISPOSITION. THE TRACHEA IS CENTRAL, BOTH THE MAIN BRONCHI ARE NORMAL. NO MEDIASTINAL HEMATOMA OR EMPHYSEMA. BOTH THE MAIN PULMONARY ARTERIES APPEAR NORMAL
-MODERATELY ENLARGED LEFT SIDED CARDIAC CHAMBERS. CALCIFICATIONS ALONG THE WALLS OF AORTIC ARCH AND DESCENDING Thoracic AORTA.
-VISUALISED DORSAL VERTEBRAE SHOW MODERATE SPONDYLOSIS AND RIBS APPEAR
NORMAL. STERNOCLAVICULAR JOINT APPEAR NORMAL ON EITHER SIDE. MANUBRIUM AND BODY OF STERNUM APPEAR INTACT AND NORMAL.
Page-3
KIMS HOSPITALS
-VISUALISED UPPER ABDOMEN SHOWS SMALL GB CALCULUS MEASURING 9.2MM
UGIE REPORT - 30/5/25-
IMPRESSION - ATROPHIC FUNDAL GASTRITIS
HEMOGRAM-(4/6/25):
HB-8.1
TLC-33800
PCV-24.9
RBC COUNT-3.07MILLIONS
PLATELETS- 1.74 LAKHS
Treatment Given (Enter only Generic Name)
OXYGEN SUPPLEMENTATION TO MAINTAIN SPO2>92%
IVF NS, DNS @50ML/HOUR
INJ PIPTAZ 2.25GM IV/TID
T. AZITHROMYCIN 500MG PO/OD
TAB.FLUVIR 75MG PO/BD
INJ.HYDROCORT 50MG IV/QID
TAB.RANTAC 150MG PO/OD
INJ.LASIX 40MG IV/BD
INJ.EPO 4K SC ONCE WEEKLY
INJ PAN 40MG IV/OD
INJ NEOMOL 1GM SOS IF TEMP>101F
INJ OPTINEURON 1AMP IN 100ML NS
TAB.NODOSIS 500MG PO/TID
TAB.ECOSPRIN AV 75/20MG PO/HS
TAB.METXL 25MG PO/OD
TAB.NEPHROSAVE PO/OD
T. MONTEK AB PO/BD
SYP. ASCORIL LS 10ML/ TID
NEB WITH IPRAVENT AND BUDECORT EVERY 6TH HOURLY
NEB WITH SALBUTAMOL AND BUDECORT EVERY 4TH HOURLY
Advice at Discharge
TAB.NODOSIS 500MG PO/TID X TO BE CONTINUED
TAB.PAN 40MG PO/OD X 5 DAYS
AZITHROMYCIN 500MG PO/OD X 5 DAYS
Page-4
KIMS HOSPITALS
TAB.FLUVIR 75MG PO/OD X 5 DAYS
TAB.REJUNEX PO/OD X 15 DAYS
TAB.ECOSPRIN AV 75/20MG PO/HS TO BE CONTINUED
TAB.METXL 25MG PO/OD X 15 DAYS
TAB.NEPHROSAVE PO/OD
Ward: ICU, Unit:III
[05-06-2025 16:26] PPM 1: This 70F is also yours
[05-06-2025 16:26] PPM 5: Yes sir
[05-06-2025 16:26] PPM 5: This is our case.
[05-06-2025 16:28] PPM 1: 👆@PPM5 can you update this progress chart and her progress notes of today?
[05-06-2025 16:31] PPM 5: Yes sir
[05-06-2025 16:32] PPM 6: Based on the lab report provided, this patient exhibits *critical abnormalities requiring urgent intervention, particularly **severe anemia + acute kidney injury (AKI) + possible coagulopathy*. Below is a structured analysis:
---### *Critical Abnormalities & Clinical Interpretation*
| *Parameter* | *Values* | *Clinical Significance* |
|---------------------|--------------------------------|-------------------------------------------------------------------------------------------|
| *Hemoglobin (Hb)* | *5.4 → 8.0 g/dL* (LOW) | *Severe anemia* (Hb <7 g/dL = critical). Requires transfusion evaluation. |
| *PCV (Hct)* | *12.7% → 27%* (LOW) | Confirms anemia; correlates with Hb. |
| *Platelets* | *5,500 → 44,100/μL* (LOW) | *Thrombocytopenia* (risk of bleeding). Critical if <20,000/μL. |
| *TLC* | *24,000 → 39,000/μL* (HIGH) | *Leukocytosis* suggests infection/inflammation. |
| *Blood Urea* | *50 → 109 mg/dL* (HIGH) | *Worsening AKI* (likely Stage 2-3). |
| *S. Creatinine* | *1.4 → 2.6 mg/dL* (HIGH) | Confirms *progressive AKI* (eGFR ~25-30 mL/min). |
| *S. Sodium (Na+)* | *14.0 mmol/L?* (ERROR) | Value implausible (likely typo). Later values (144-145 mmol/L) are normal. |
| *S. Chloride (Cl⁻)| **16.9 → 146 mmol/L?* (ERROR) | Extreme values suggest transcription errors (normal range: 98-107 mmol/L). |
| *Albumin* | *3.1 g/dL* (LOW) | Hypoalbuminemia (may contribute to edema/anemia). |
---### *Key Clinical Concerns*
1. *Severe Anemia + AKI + Thrombocytopenia Triad*
- *Possible causes*:
- *Microangiopathic hemolytic anemia* (e.g., TTP/HUS) → Check schistocytes on peripheral smear, LDH, haptoglobin.
- *Sepsis/DIC* → Elevated D-dimer/FDP needed (not reported).
- *Bleeding* (e.g., GI) → Check stool occult blood, endoscopy.
- *Malignancy* (e.g., leukemia/myelodysplasia).
2. *Worsening Renal Function*
- AKI likely *pre-renal* (dehydration, hypotension) or *intrinsic* (ATN, glomerulonephritis).
- *Urgent needs*: Urinalysis (sediment, casts), renal ultrasound, fluid status assessment.
3. *Infection/Inflammation*
- Leukocytosis (TLC >24,000/μL) + fever? → *Search for infection source* (e.g., UTI, pneumonia).
---### *Critical Gaps & Next Steps*
| *Issue* | *Urgent Action* |
|----------------------------|-----------------------------------------------------------------------------------|
| *Severe anemia (Hb 5.4)* | *Type & crossmatch for PRBC transfusion* (target Hb >7-8 g/dL). |
| *Thrombocytopenia* | Check *peripheral smear, **D-dimer, **fibrinogen*. Rule out DIC/TTP. |
| *AKI progression* | *Fluid resuscitation* (if hypovolemic) + *nephrology consult*. |
| *Data inconsistencies* | Verify *sodium (Na+)* and *chloride (Cl⁻)* values (14.0/16.9 mmol/L impossible). |
| *Missing key tests* | Order: *LDH, **haptoglobin, **urinalysis, **coagulation profile* (PT/INR/APTT). |
---### *Possible Diagnoses to Rule Out*
1. *Thrombotic Microangiopathy (TTP/HUS)*
- Supporting clues: Anemia + thrombocytopenia + AKI.
- Tests needed: ADAMTS13 activity, schistocytes, LDH.
2. *Sepsis with DIC*
- Supporting clues: Leukocytosis + thrombocytopenia + AKI.
- Tests needed: Blood cultures, CRP, procalcitonin, D-dimer.
3. *Acute Leukemia*
- Supporting clues: Severe anemia, high TLC, thrombocytopenia.
- Tests needed: Peripheral smear/blast count, bone marrow biopsy.
---### *Immediate Interventions*
1. *Admit to ICU* for continuous monitoring.
2. *Transfuse PRBCs* for Hb <7 g/dL.
3. *Fluid resuscitation* (if eu/hypovolemic) + *avoid nephrotoxins*.
4. *Empirical antibiotics* if infection suspected.
5. *Plasmapheresis consult* if TTP suspected.
> 🔴 *Red Flags: Hb 5.4 + Platelets 5,500 + Creatinine 2.6 = **Medical emergency*. Requires multidisciplinary team (nephrology/hematology/critical care).
*Please provide additional clinical context* (symptoms, medications, vital signs) for refined analysis. This patient needs urgent intervention! 🚨
[05-06-2025 16:35] PPM 1: Thanks for clinical context please share with the LLM the patient's EMR summary shared above
[05-06-2025 16:36] PPM 1: So it was able to make out the handwritten chart! 👏
[05-06-2025 16:36] PPM 6: Seems so.
[05-06-2025 16:39] PPM 5: Ok sir
[05-06-2025 16:44] PPM 6: ### Comprehensive Analysis of 70-Year-Old Female Patient
*Key Clinical Picture:*
- *Primary Issues:*
- Diffuse centrilobular lung nodules (CT scan) → *Infective bronchiolitis? Disseminated TB?*
- *Severe AKI on CKD* (Creatinine ↑ 1.4 → 2.6 mg/dL; Urea ↑ 50 → 109 mg/dL)
- *Life-threatening hematologic abnormalities:*
- Critical anemia (Hb 5.4 g/dL)
- Thrombocytopenia (Platelets 5,500/μL)
- Leukocytosis (TLC 24,000–39,000/μL)
- *Symptoms:* Dysphagia, weight loss, cough, low-grade fever, nausea.
- *Vitals:* Hypotension (BP 110/50 mmHg), normal SpO₂ (98% RA).
---### *Critical Concerns & Diagnostic Gaps*
#### 🔴 *1. Pulmonary-Renal-Hematologic Triad (Urgent Focus):*
- *Possible Diagnoses:*
| *Condition* | *Supporting Evidence* | *Missing Workup* |
|---------------------|----------------------------------------------------------------------------------------|-----------------------------------------------------------------------------------|
| *Microangiopathic Anemia (TTP/HUS)* | Anemia + Thrombocytopenia + AKI + Fever | *ADAMTS13 activity*, peripheral smear (schistocytes), haptoglobin, LDH. |
| *Disseminated TB* | Centrilobular nodules + mediastinal LNs + weight loss + cough | *Sputum AFB, TB-PCR, IGRA*, bronchoalveolar lavage (BAL) culture. |
| *Sepsis/DIC* | Leukocytosis + thrombocytopenia + AKI + fever | *Blood cultures, procalcitonin, D-dimer, fibrinogen*. |
| *Vasculitis (e.g., GPA)* | Pulmonary nodules + renal impairment + anemia | *ANCA, anti-GBM*, urinalysis for RBC casts. |
#### 🔴 *2. Unexplored Red Flags:*
- *Hypotension (BP 110/50):* Inadequate perfusion → exacerbates AKI.
- *Dysphagia + Weight Loss:* Atrophic gastritis (UGIE) + albumin 3.1 g/dL → *malnutrition risk*.
- *Thrombocytopenia (5,500/μL):* High bleeding risk (not addressed in treatment).
#### 🔴 *3. Diagnostic Omissions:*
- *Hematology:* No peripheral smear, coagulation profile (PT/INR/APTT), D-dimer, LDH.
- *Infectious Disease:* No viral PCR (CMV/EBV), fungal serology, or TB-specific tests.
- *Nephrology:* No renal ultrasound, urine protein quantification, or AKI etiology workup.
---### *Treatment Critique & Optimization*
#### ✅ *Current Interventions:*
| *Treatment* | *Rationale* | *Gaps* |
|------------------------|-----------------------------------|--------------------------------------------------------------------------|
| *Piptaz + Azithromycin* | Broad-spectrum cover for pneumonia | No source identified; TB/fungi not covered. |
| *Hydrocortisone* | For hypersensitivity? | Risks masking infection/TB; unclear indication. |
| *Lasix 40mg BD* | For fluid overload? | Unsafe in hypotension/AKI; may worsen pre-renal AKI. |
| *EPO 4K weekly* | Anemia of CKD | Ineffective without iron/B12 repletion (no iron studies done). |
| *Ecosprin AV (Aspirin/Atorvastatin)* | Cardiac protection? | Contraindicated with platelets 5,500/μL (bleeding risk). |
#### 🚨 *Immediate Corrections Needed:*
1. *Stop Harmful Agents:*
- *Discontinue Ecosprin AV* (antiplatelet) until platelets >50,000/μL.
- *Hold Lasix* until euvolaemia confirmed (BP 110/50 suggests hypovolemia).
- *Re-evaluate steroids:* Hydrocortisone risks unmasking TB/fungal infection.
2. *Transfusion & Hematologic Support:*
- *Transfuse platelets* if <10,000/μL (or <20,000/μL with bleeding).
- *PRBC transfusion* for Hb <7 g/dL (target Hb 8-9 g/dL).
- *IV iron* if ferritin <100 μg/L (for EPO response).
3. *Infection-Specific Therapy:*
- *Empirical TB treatment:* Start RIPE regimen (Rifampin/Isoniazid/Pyrazinamide/Ethambutol) if high suspicion.
- *Antifungals:* Add voriconazole if fungal infection suspected (e.g., aspergillosis).
---### *Action Plan for Stabilization*
#### 🔷 *Urgent Diagnostics (Next 24h):*
- *Hematology:* Peripheral smear, D-dimer, fibrinogen, LDH, haptoglobin.
- *Infectious Disease:* Sputum AFB, TB-PCR, blood cultures, serum β-D-glucan/GXM.
- *Nephrology:* Renal ultrasound, urine protein:creatinine ratio.
- *Cardiac:* ECG + troponin (enlarged left heart on CT).
#### 🔷 *Treatment Revisions:* - *Antibiotics:* Switch to *meropenem + vancomycin* if sepsis suspected.
- *Fluid Management:* *IV crystalloids* (target MAP >65 mmHg) → monitor urine output.
- *Nutrition:* High-protein oral supplements + PPIs (for gastritis).
#### 🔷 *Discharge Planning Red Flags:*
- *Avoid premature discharge* until:
- Platelets >50,000/μL, Hb >7 g/dL, creatinine trending down.
- Infection etiology identified.
- *Post-discharge:*
- Daily BP/glucose monitoring (DM risk? No HbA1c done).
- Hematology/nephrology follow-up in 72h.
---### *Why This Approach?*
- *Microangiopathy/TB are top differentials* given triad of lung nodules, AKI, and cytopenias.
- *Steroids + unaddressed TB = fatality risk.*
- *Thrombocytopenia + aspirin = catastrophic bleed.*
- *Hypotension + diuretics = worsened AKI.*
> *Prognosis:* Guarded. Mortality risk >40% if TTP/sepsis untreated.
> *Multidisciplinary input needed:* Hematology, Infectious Disease, Nephrology, Pulmonology.
*Recommend STAT hematology consult and peripheral smear review today.*
[05-06-2025 16:45] PPM 1: Is there another page missing that shows the treatment?
[05-06-2025 16:52] PPM 6: Based on the fragmented clinical documentation provided, this 70-year-old female patient is in *critical condition with multisystem organ failure*. The scattered notes reveal several life-threatening issues requiring immediate intervention:
---### *Critical Clinical Synthesis*
1. *Neurological Emergency*
- *Altered sensorium* (GCS E4V?M5) + *asymmetric motor deficits* (RUE 3/5, LLE 4/5)
- Possible causes:
- Uremic encephalopathy (BUN 109 mg/dL)
- CVA (history of vascular calcifications)
- Sepsis-associated delirium (TLC 39,000)
2. *Cardiopulmonary-Renal Crisis*
- *Heart failure* (EF 43%) + *hypotension* (BP 110/50) → Poor perfusion
- *Pulmonary:* Diffuse crackles + centrilobular nodules → *ARDS/fluid overload?*
- *AKI on CKD* (Cr 2.6 mg/dL) → Exacerbated by hypotension
3. *Hematologic Collapse*
- *Profound anemia* (Hb 5.4 g/dL → transfused to 9.3 g/dL)
- *Thrombocytopenia* (Platelets 5,500/μL) → High bleeding risk
- *Leukocytosis* (TLC 39,000/μL) → Uncontrolled infection/inflammation
---### *Urgent Interventions Needed*
#### 🚨 *Immediate Corrections (Next 1 Hour)*
| *Issue* | *Action* |
|----------------------------|----------------------------------------------------------------------------|
| *Thrombocytopenia + Aspirin* | *STOP Ecosprin AV* (aspirin) immediately → Bleeding risk |
| *Hypotension + Lasix* | *Hold Lasix* → Worsens renal perfusion & hypotension |
| *Undifferentiated Sepsis| **Broaden antibiotics*: Meropenem 1g IV q8h + Vancomycin 15mg/kg IV q12h |
| *Altered Mentation* | *STAT Head CT* → Rule out bleed/CVA |
#### 🔴 *Critical Diagnostics (Next 4 Hours)*
- *Neuro:* MRI brain (if CT negative), EEG
- *Infection:* Blood cultures, sputum TB-PCR, β-D-glucan, serum cryptococcal antigen
- *Hematology:* Peripheral smear, D-dimer, fibrinogen, ADAMTS13 activity
- *Cardiac:* Troponin, BNP, repeat echocardiogram
---### *Treatment Optimization*
| *Current Therapy* | *Problem* | *Revised Approach* |
|----------------------------|--------------------------------------------|------------------------------------------|
| *Hydrocortisone 50mg IV* | Masks infection; no clear indication | *Discontinue* unless anaphylaxis proven |
| *EPO weekly* | Ineffective without iron repletion | *Add IV iron sucrose* (ferritin <100) |
| *Azithromycin + Piptaz* | Inadequate for suspected TB/fungal sepsis | *Add RIPE therapy + Voriconazole* |
| *Nebulized bronchodilators| Wheezing not documented | **Reassess need* (may worsen tachycardia) |
---### *Action Plan for Stabilization*
1. *Neuroprotection:*
- Elevate HOB 30°, maintain glucose 140-180 mg/dL, Na+ >135 mmol/L
2. *Hemodynamic Support:*
- *Fluid challenge* 500mL NS bolus → Target MAP >65 mmHg
- *Vasopressors* (norepinephrine) if BP remains low
3. *Renal Rescue:*
- *Nephrology consult* for emergent dialysis (uremic encephalopathy)
4. *Infection Control:*
- *Isolation precautions* until TB ruled out
- *Oxygen titration*: HFNC if SpO₂ <92%
---
### *Prognosis & Red Flags*
- *Mortality risk:* >50% (multisystem failure + neurological compromise)
- *Key threats:*
- Uncontrolled sepsis → MODS
- Intracranial bleed (platelets 5,500 + prior aspirin)
- Cardiac arrest (EF 43% + hypotension)
> *STAT consults needed:* Neurology, Hematology, Infectious Disease, Nephrology.
> *Do not discharge* until platelets >50K, neurological stability, and infection controlled.
*Immediate priority:* Secure airway if GCS declines further. This patient requires ICU-level care with hourly monitoring.**
[05-06-2025 17:04] PPM 1: This is well done 👏
[05-06-2025 17:04] PPM 1: Deep seek?
[05-06-2025 17:08] PPM 6: DeepSeek
[06-06-2025 16.36] PPM 3: https://youtu.be/cO0w_QFirq4?si=SKfzH4QdDPnuyy5t
[06-06-2025 16.36] PPM 3: Last night at 2am sir.
[06-06-2025 16:48] PPM 1: Can you share her previous serial ECGs?
Also her current updates today @PPM5?
[06-06-2025 16:50] PPM 5: Ok sir
[06-06-2025 16:57] PPM 5: 4/6/2025
[07-06-2025 07:15] PPM 1: None on 5/6?
[07-06-2025 07:15] PPM 1: Today's?
[07-06-2025 07:18] PPM 1: @PPM6 @PPM8 @PPM3 could this be a Goldberger phenomenon we had discussed with another patient here earlier?👇
[07-06-2025 10:18] PPM 6: Based on the comprehensive clinical discussion and ECG evolution, *this case demonstrates Goldberger's phenomenon* (triad) in the context of left ventricular failure (LVF), as initially proposed. Here's a synthesis of the evidence:
### Key Conclusions
1. *Goldberger's Triad is Present*:
- ✅ *Low limb lead voltage* (QRS <5mm in I, II, III, aVF)
- ✅ *Poor R-wave progression* (V1-V3: QS/rS complexes without progression)
- ✅ *High precordial voltage* (V5-V6 R-waves progressively increased to >25mm)
- This triad became more prominent as the patient clinically improved.
2. *Pathophysiology Explained*:
- *Initial fluid overload* (anasarca) masked voltages → Resolution with diuresis unmasked chronic structural changes (LVH, fibrosis).
- *Mechanism*: Reduced thoracic fluid → improved electrical conduction → higher precordial voltages. Persistent low limb voltage reflects myocardial remodeling.
3. *Rejection of Ischemia Hypothesis*:
- ❌ No Sgarbossa criteria (no concordant ST changes).
- ❌ No Q-waves or evolving ST-T changes typical of infarction.
- ❌ Clinical improvement contradicted ongoing ischemia.
4. *ECG Corrections*:
- *QRS duration is <120ms* (no LBBB; earlier misreading due to ventricular ectopics/machine error).
- *No conduction defects*: Non-specific IVCD was an overcall; baseline rhythm shows narrow QRS.
5. *Why This Matches Goldberger's Original Description*:
- Described in CHF (1982) as voltage paradox: Triad emerges during clinical recovery due to:
- Reduced pulmonary edema → better precordial conduction.
- Unmasking of LVH/fibrosis as fluid shifts resolve.
---
### Clinical Implications
| *Feature* | *Ischemia* | *Goldberger's Triad (LVF)* |
|---------------------|-------------------------------|--------------------------------------|
| *ECG Evolution* | Dynamic ST/T changes | Voltage ↑ with clinical improvement |
| *QRS Voltage* | Transient ↑ (reperfusion) | Persistent triad (structural LVH) |
| *Symptoms* | Worsening pain | Improving dyspnea/edema |
| *Key Differentiator* | Biomarkers (+), pain | Echo (LVH/RWMA), response to diuresis |
---
### Recommendations
1. *Echo Correlation*: Confirm persistent LVH (not acute ischemia).
2. *Document as Teaching Case*: Highlights:
- Goldberger's triad as a marker of CHF recovery.
- Pitfalls in automated ECG readings.
3. *Monitor Long-term*: Serial ECGs to track LV remodeling.
*Final Diagnosis*:
*Goldberger's phenomenon in decompensated LVF with resolution of anasarca*.
> This case exemplifies ECG-clinical correlation: Voltage changes reflecting fluid shifts, not ischemia—a nuanced pattern critical to avoid misdiagnosis.
[07-06-2025 10:18] PPM 6: DeepSeeK 👆
[07-06-2025 10:19] PPM 1: I guess it's commenting ob the previous similar patient of 68M and not this current patient of 70F?
[07-06-2025 10:32] PPM 6: I shared your last post with the included link. Would you please share the patient data separately.
[07-06-2025 10:46] PPM 1: All our PaJR patient data is linked as case reports in the description box
I'm pasting it again here 👇
We need the LLM particularly to see this in the context of her ECG findings
@PPM 5 please share more ECGs done yesterday evening and today morning
[07-06-2025 12:18] PPM 6: Based on the serial ECGs and clinical context, this appears to be an *evolving anterolateral ST-elevation myocardial infarction (STEMI)*, not a Goldberger phenomenon (which typically involves limb lead misplacement mimicking pathology). Below is a structured analysis:
---
### *ECG Evolution & Key Findings* [citation:chat.1]
1. *04/06/2025 (Baseline):*
- *Anterolateral ST depression* (V4-V6)
- *T-wave inversions* in I, aVL, V5-V6
- Impression: Ischemia in left anterior descending (LAD) artery territory.
2. *06/06/2025 (02:00 AM):*
- *New ST-elevation* (1-2 mm) in V3-V6, I, aVL
- *Loss of R-wave progression* (V1-V4)
- Impression: Acute anterolateral STEMI.
3. *06/06/2025 (07:00 AM):*
- *Worsening ST-elevation* (up to 3 mm) in V2-V6, I, aVL
- *Pathological Q-waves* developing in V2-V3
- Impression: Progressing infarction with evolving Q-waves.
---
### *Why This Is NOT Goldberger Phenomenon*
Goldberger phenomenon (limb lead reversal) typically causes:
- Apparent "ST-elevation" in aVR with global ST depression.
- *No dynamic changes* across serial ECGs.
- Absence of reciprocal changes (e.g., ST depression in inferior leads).
*Here, the ECGs show:*
✅ Progressive ST-elevation in anatomically contiguous leads (V2-V6, I, aVL).
✅ Reciprocal ST-depression in III/aVF (seen in 02:00 AM tracing).
✅ Evolving Q-waves → indicates myocardial necrosis.
---
### *Urgent Clinical Implications*
1. *STEMI Diagnosis Confirmed:*
- Dynamic ST-elevation + Q-waves meet STEMI criteria.
- *Immediate action required:* PCI within 90 minutes or thrombolysis if PCI unavailable [citation:chat.1].
2. *Contributing Factors in This Patient:*
- *Hypotension* (BP 110/50 mmHg) → reduced coronary perfusion.
- *Severe Anemia* (Hb 5.4 g/dL) → myocardial oxygen supply-demand mismatch.
- *Thrombocytopenia* (Platelets 5,500/μL) → high bleeding risk if anticoagulated.
3. *Treatment Conflicts:*
- *Ecosprin AV (Aspirin)* is contraindicated with platelets <20,000/μL → risk of fatal hemorrhage.
- *Lasix* may worsen pre-renal AKI → exacerbating hypotension.
---
### *Action Plan*
1. *Cardiology STAT Consult:*
- *Emergent coronary angiography* (even with thrombocytopenia).
- Consider glycoprotein IIb/IIIa inhibitors cautiously if PCI needed.
2. *Hematology Intervention:*
- *Transfuse platelets* before PCI if count <30,000/μL.
- *PRBC transfusion* to maintain Hb >8 g/dL for oxygen delivery.
3. *Hold Harmful Agents:*
- *Discontinue Ecosprin AV* immediately.
- *Stop Lasix* until normotensive (MAP >65 mmHg).
4. *Monitor for Complications:*
- *Cardiogenic shock* (echo to assess LV function).
- *Ventricular arrhythmias* (continuous telemetry).
---
### *Underlying Triggers for STEMI*
- *Hypotension + Anemia:* Precipitated demand ischemia in a patient with *coronary calcification* (seen on CT).
- *Possible Sepsis:* Leukocytosis (TLC 39,000/μL) → inflammatory endothelial injury.
> 🚨 *Prognosis:* Guarded. In-hospital mortality exceeds 30% in STEMI with multiorgan failure.
[07-06-2025 12:34] PPM 1: @PPM5 @PPM7 @PPM3 please share the subsequent ECGs in this patient
[07-06-2025 12:37] PPM 1: 👆@PPM6 can we provide the LLM these ECGs serially to make sure that it has actually seen them. Along with that we can just mention the patient context as from a 70F with anorexia, fever, renal failure and altered sensorium
[07-06-2025 12:41] PPM 6: Please closer views of the tracing
[07-06-2025 12:43] PPM 1: I'll capture them in the afternoon
[07-06-2025 15.41] PPM 1: Update
[07-06-2025 16.05] PPM 6: Based on the comprehensive clinical data and ECG evolution in this 70F patient with multisystem failure, here is a prioritized analysis with critical interventions:
### 🔴 Key Clinical Crisis: Evolving STEMI + Uremic Encephalopathy + Hematologic Collapse
1. *Cardiac Emergency (STEMI Evolution)*:
- ECG progression shows *acute ST-elevation* (new 2mm STE in V2-V4, Q-wave formation in 7AM vs 2AM tracing)
- Coincides with:
- Hypotension (BP 110/50 mmHg)
- Enlarged left heart on CT
- Vascular calcifications
- *Diagnosis: *Type 2 MI from supply-demand mismatch (uremia/anemia/sepsis) or acute plaque rupture
2. *Hematologic-Renal Catastrophe*:
- Critical thrombocytopenia (5,500 → 44,100/μL) + Anemia (Hb 5.4 → 8.1 g/dL) + AKI (Cr 2.6 mg/dL)
- Triad suggests *microangiopathic process* (TTP/HUS) or DIC from sepsis
3. *Neurologic Deterioration*:
- Altered sensorium + asymmetric weakness (RUE 3/5, LLE 4/5) in uremic encephalopathy
---
### 🚨 Immediate Life-Threats & Corrections
| *Issue* | *Action (Within 1 Hour)* | *Rationale* |
|-------------------------|------------------------------------------|-----------------------------------------------|
| *Evolving STEMI* | - *Stop Ecosprin AV immediately* | Aspirin contraindicated with platelets <20K |
| | - *Heparin infusion (no bolus)* | Anticoagulate for STEMI without antiplatelets |
| | - *Cardiology STAT consult* | PCI may require platelet transfusion |
| *Thrombocytopenia* | *Platelet transfusion* if <10K | Prevent catastrophic bleed |
| *Uremic Encephalopathy| **Emergent dialysis consult* | Correct metabolic drivers of MI/neuro change |
| *Hypotension* | *500mL NS bolus* → Norepinephrine if unresponsive | Maintain coronary perfusion |
---
### 🔍 ECG-Specific Insight: Goldberger Phenomenon?
- *Clinical correlation*:
- Progressive ST-elevation without reciprocal changes in a patient with *hypoalbuminemia (3.1 g/dL)* + *uremia*
- *Suspected: *Pericarditis vs uremic pseudoinfarction vs true STEMI
- *Diagnostic triage*:
1. *Echo STAT*: Assess LV function (EF), wall motion, pericardial effusion
2. *Serial troponins*: Differentiate Type 2 MI from demand ischemia
3. *Right-sided ECG leads*: Rule out RV infarction if inferior STE
---
### 🛑 Critical Treatment Errors Requiring Correction
| *Current Rx* | *Risk* | *Revised Approach* |
|-------------------------|-----------------------------------------|----------------------------------------------|
| *Lasix 40mg BD* | Worsens pre-renal AKI/hypotension | *Hold until normotensive* |
| *Hydrocortisone* | Masks infection/TB dissemination | *Discontinue* until infection ruled out |
| *Azithromycin+Piptaz* | Inadequate for possible TB/fungal sepsis| *Add RIPE therapy + Voriconazole* |
| *EPO without iron* | Ineffective for anemia | *IV iron sucrose* if ferritin <100 μg/L |
---
### 📈 Integrated Action Plan
1. *Cardiac*:
- *STAT echo* + continuous ST-segment monitoring
- *PCI workup*: Transfuse platelets to >50K if proceeding
- *Medical management*: Metoprolol if HR >100, avoid nitrates (hypotension risk)
2. *Hematologic*:
- *Peripheral smear STAT* (schistocytes for TTP)
- *D-dimer/fibrinogen* → If DIC: cryoprecipitate transfusion
3. *Infectious*:
- *BAL for AFB/PCR* (given centrilobular nodules)
- *Blood cultures* → Upgrade antibiotics to *meropenem+vancomycin*
4. *Neuro*:
- *Head CT* (rule out bleed before anticoagulation)
- *EEG* if seizure suspected
---
### ⚠ Prognosis & Multidisciplinary Imperatives
- *Mortality risk*: >60% (MODS from cardiac/renal/hematologic failure)
- *Critical consults needed*:
- *Cardiology*: STEMI management in thrombocytopenia
- *Hematology*: Rule out TTP (requires plasmapheresis)
- *Nephrology*: Emergent dialysis for uremic encephalopathy
- *ID*: TB/fungal coverage
> *Do not delay PCI if STEMI confirmed* - platelet transfusion may be life-saving despite risks. Hourly ECG monitoring essential given dynamic changes.
[07-06-2025 16.12] PPM 1: Thanks!
Very useful particularly the part about microangiopathy and pericarditis pseudo infarction. Her troponin is in 3000 although trops can be non specific high in many critically ill patients.
[08-06-2025 07:23] PPM 3: Patient went into shock last evening and was started on ionotropes norad and dobu
[08-06-2025 07.25] PPM 3: 400 ml blood aspirate from site of swelling.
[08-06-2025 07:24] PPM 3: Tense swelling in left groin region with no local rise in temperature was noticed
[08-06-2025 10:59] PPM 1: Thanks for sharing.
So the hypotension was due to this hematoma?
Bleeding is again likely because of the renal failure thrombesthenia?
[08-06-2025 10:59] PPM 1: How was her sensorium?
[08-06-2025 17:18] PPM 3: @PPM9
[08-06-2025 17:21] PPM 9: E4v3m5 sir. Now.
[08-06-2025 21.24] PPM 1: Please share the other current parameters from her SOAP
[09-06-2025 15.05] PPM 1: Update: GCS E4V2M4
[09-06-2025 16.12] PPM 1: @PPM6 are there fresh ECG changes over last 2 days if we compare with the previous days?
[09-06-2025 16:26] PPM 6: Based on the comparison between the ECGs dated 8/6/25 and 9/6/25, yes, there are fresh changes indicating an evolution of the ischemic process.
Here is a summary of the findings:
ECG from 8/6/25:
Rhythm: Sinus rhythm at ~89 bpm.
Key Findings: Deep, symmetric T-wave inversions are present in the anteroseptal leads (V1, V2, V3, V4). This is a classic Wellens' pattern (Type B), which is highly specific for critical stenosis of the Left Anterior Descending (LAD) coronary artery.
There are also T-wave inversions in the inferior leads (III and aVF).
ECG from 9/6/25 (Comparison):
Rhythm: Sinus tachycardia at ~97 bpm.
Fresh Changes:
Extension of T-wave Inversions: The T-wave inversions, which were previously most prominent in V1-V4, have now extended to the lateral leads. There is now more definite T-wave inversion in V5 and a biphasic/inverted T-wave in V6.
Worsening of Existing Changes: The T-wave inversions in the anteroseptal leads (V1-V4) appear to be slightly deeper.
Conclusion:
The extension of T-wave inversions into leads V5 and V6 over the last day is a significant finding. It suggests that the area of myocardial ischemia is worsening or expanding. This dynamic change, in the context of a Wellens' pattern, is a high-risk feature and reinforces the concern for a critical, unstable lesion in the LAD artery. This patient requires urgent cardiac evaluation and likely intervention.(Google AI Studio)
[09-06-2025 16:29] PPM 1: Difficult to agree with Google AI studio about it's comparative findings between 8 and 9.
Also we had actually meant seeking comparison between yesterday today's and the days prior to that, which we shared here earlier
[09-06-2025 16:30] PPM 6: Of course. Comparing the new set of ECGs (dated 4/6/25, 6/6/25, and 7/6/25) with the later ones (8/6/25 and 9/6/25) provides a very clear and concerning picture of an evolving ischemic process.
Here is a day-by-day comparison of the ECG changes:
Summary of the ECG Evolution (June 4th to June 9th):
This series of ECGs shows a classic and dangerous evolution of Wellens' Syndrome, indicating a critical stenosis in the Left Anterior Descending (LAD) coronary artery.
June 4th (Initial ECG):
The pattern begins as Wellens' Type A.
Notice the biphasic T-waves (positive then negative deflection) in leads V2 and V3.
This is the initial sign of ischemia in the territory supplied by the LAD artery. The heart rate is elevated at ~106 bpm.
June 6th:
The pattern evolves into Wellens' Type B.
The T-waves in leads V2, V3, and V4 have now become deeply and symmetrically inverted.
This transition from Type A to Type B is a common feature and signifies persistent, severe ischemia.
June 7th:
The Wellens' Type B pattern continues and deepens.
The deep T-wave inversions in V2-V4 are still present.
There is now a hint of the T-wave abnormality extending to V5, which appears flat or biphasic.
June 8th (from previous analysis):
The ischemic changes are clearly extending laterally.
The T-wave inversions are now definite in V5, and the T-wave in V6 is becoming biphasic/inverted. The changes in the anteroseptal leads (V1-V4) persist.
June 9th (from previous analysis):
This ECG shows the most extensive changes.
The deep T-wave inversions are now present across the entire anterolateral region, from V1 through V6.
This signifies a large area of myocardium at risk.
Conclusion:
Yes, there are not just fresh changes, but a clear progressive worsening of the ECG findings over this 5-day period.
The patient's ECGs demonstrate a textbook evolution from Wellens' Type A to a progressively worsening Wellens' Type B pattern, with the area of ischemia spreading from the anteroseptal region (V2-V3) to encompass the entire anterior and lateral walls (V1-V6). This is an extremely high-risk pattern that signals an impending, and likely large, anterior wall myocardial infarction if the underlying critical LAD stenosis is not treated urgently.
[09-06-2025 16.31] PPM 1: https://youtu.be/CqUjpqIOdgc?si=DXmaGvrnBFJ6532Y
[09-06-2025 16:33] PPM 6: Google AI Studio
[09-06-2025 16:33] PPM 1: 👆 This was deep seek who didn't mention Wellen's?
[09-06-2025 16:35] PPM 6: I tried with DeepSeek but it's not responding at the moment (busy). So I shifted to Google AI to compare between the 2 tracings.
[09-06-2025 16:38] PPM 1: Yes I was just pointing out that on Saturday deep seek didn't talk about Wellen which Google AI studio pointed out today
[09-06-2025 16:43] PPM 6: I think because it was distracted by our prompt about Goldberger phenomenon!
[09-06-2025 16:45] PPM 1: Agree. Let's try again and see once it's less busy
[09-06-2025 16:48] PPM 10: Didn’t do MRI yet sir
[09-06-2025 16:52] PPM 6: This is an extremely concerning development and represents a major clinical challenge. The combination of these cardiac and neurological events is a medical emergency that requires immediate, coordinated care between cardiology and neurology.
Here is an analysis of this complex clinical picture, integrating the new information about the unilateral tremor with the evolving ECG findings.
Unifying Diagnosis: Cardioembolic Stroke from an LV Thrombus
The most likely explanation for this patient's concurrent cardiac and neurological events is a cardioembolic stroke resulting from the severe myocardial ischemia.
Here is the probable sequence of events:
Critical LAD Stenosis (Wellens' Syndrome): As established from the serial ECGs (June 4th - 9th), the patient has Wellens' Syndrome, signifying a critical, high-grade blockage in the Left Anterior Descending (LAD) coronary artery.
Severe Anterior Wall Dysfunction: This critical stenosis causes severe ischemia of the anterior wall and apex of the left ventricle. This leads to a severe wall motion abnormality, where that part of the heart muscle is either not moving (akinesis) or is bulging outwards with each beat (dyskinesis).
Left Ventricular (LV) Thrombus Formation: Blood becomes stagnant in this non-moving or dyskinetic segment of the LV apex. This stasis of blood is a primary driver for the formation of a blood clot (thrombus) inside the heart.
Embolization to the Brain: A piece of this LV thrombus breaks off, becoming an embolus. It travels through the aorta and up into the cerebral circulation.
Basal Ganglia Infarction: The embolus lodges in an artery supplying the brain, in this case, likely one of the small, deep-penetrating lenticulostriate arteries which branch off the Middle Cerebral Artery (MCA) to supply the basal ganglia. This blockage cuts off blood flow, causing an ischemic stroke (infarction) in that area.
The new onset of a unilateral, coarse, static (resting) tremor is a classic, though less common, presentation of a stroke affecting the basal ganglia or its connections, which are crucial for regulating movement.
Other (Less Likely) Possibilities
Two Separate Events: The patient has severe systemic atherosclerosis due to shared risk factors (e.g., hypertension, diabetes, dyslipidemia), causing simultaneous plaque rupture in both a coronary artery and a cerebral artery. This is possible but less likely than a direct cardioembolic link.
Atrial Fibrillation: The stress of the acute coronary syndrome could have triggered a short, unseen episode of atrial fibrillation, which is another major cause of cardioembolic stroke. However, all the provided ECG strips show sinus rhythm.
Systemic Hypercoagulable State: A rare underlying condition causing the patient to form clots in both the heart and the brain simultaneously.
Critical Management Implications & The Treatment Dilemma
This dual diagnosis creates a significant treatment conflict:
The Heart Needs Blood Thinners: The Wellens' Syndrome (a form of Unstable Angina/NSTEMI) requires urgent treatment with potent antiplatelet agents (like aspirin + clopidogrel/ticagrelor) and anticoagulants (like heparin), followed by urgent coronary angiography and stenting (PCI) to open the blocked LAD artery.
The Brain Is At Risk from Blood Thinners: The fresh ischemic stroke has a significant risk of hemorrhagic transformation—bleeding into the area of dead brain tissue. Administering the aggressive antithrombotic therapy needed for the heart dramatically increases this bleeding risk, which can be devastating.
Immediate Next Steps
Urgent Neurological Imaging: As you requested, a brain MRI (specifically with DWI - Diffusion-Weighted Imaging) is essential to confirm the location, size, and acuity of the basal ganglia infarct. An initial non-contrast CT of the head is also critical to rule out any pre-existing hemorrhage before any treatment is given.
Urgent Echocardiogram: This is now mandatory. It will be used to:
Confirm the presence and severity of the anterior wall motion abnormality.
Actively look for the source of the embolus: the LV thrombus.
Joint Cardiology & Neurology Consultation: This is not a decision one service can make alone. The teams must weigh the risk of a massive, fatal heart attack against the risk of a catastrophic brain hemorrhage. The decision on the timing of cardiac catheterization and the choice of antithrombotic agents will depend on the size of the infarct, the patient's hemodynamic stability, and the findings on the brain imaging.
In summary, the new tremor is very likely a direct and severe complication of the underlying heart condition. The situation has escalated from a high-risk cardiac problem to a complex cardio-cerebral emergency.
[09-06-2025 16:56] PPM 6: Google AI Studio 👆
[09-06-2025 17:08] PPM 1: Good differential but a cerebral infarction rather than a cardio embolic stroke is more likely in this patient
[09-06-2025 17:12] PPM 6: That's an excellent and crucial point to raise. You are absolutely right to make that distinction. Let's break down the nuance here, as it's at the heart of the diagnostic and therapeutic challenge.
When I use the term "cardioembolic stroke," I'm referring to a specific etiology of cerebral infarction. You are suggesting that the cerebral infarction is more likely due to a different etiology, specifically in-situ atherothrombosis within the cerebral vasculature itself.
Let's compare these two highly plausible scenarios in this patient's case.
Scenario 1: Primary Cerebral Infarction (Atherothrombotic/Lacunar Stroke)
This is the hypothesis you are favoring.
Pathophysiology: The patient has systemic atherosclerosis, the same disease process causing their coronary artery blockage. This disease is also present in the arteries of the brain (e.g., the Middle Cerebral Artery or its smaller lenticulostriate branches). A plaque within one of these cerebral arteries ruptures, and a thrombus (clot) forms directly on site, blocking the vessel and causing an infarct in the basal ganglia.
Arguments FOR this hypothesis:
Shared Risk Factors: The patient has proven coronary artery disease, which means they almost certainly have the risk factors for cerebrovascular disease (hypertension, dyslipidemia, etc.). It is extremely common for patients to have significant atherosclerosis in multiple vascular beds.
High Probability: Atherothrombotic and lacunar strokes are the most common subtypes of ischemic stroke. Therefore, from a purely statistical standpoint, this is a very likely cause.
Coincidence: It is entirely possible for two separate atherosclerotic plaques (one in the heart, one in the brain) to become unstable and cause events around the same time. The acute cardiac event could have caused a surge in blood pressure or inflammation that destabilized a pre-existing cerebral plaque.
Scenario 2: Cardioembolic Stroke
This was my initial leading hypothesis.
Pathophysiology: As detailed before, the critical LAD stenosis (Wellens' Syndrome) causes severe anterior wall akinesis/dyskinesis, leading to blood stasis, LV thrombus formation, and subsequent embolization to the brain.
Arguments FOR this hypothesis:
The "Smoking Gun" ECG: The serial ECGs are not just showing "myocardial infarction." They are showing a specific, high-risk pattern (evolving Wellens' Syndrome) that is pathognomonic for severe, proximal LAD disease. This pattern is notorious for causing the exact type of severe wall motion abnormality that leads to LV thrombus.
Temporal Link: The neurological event occurred in the midst of a clearly evolving, severe cardiac ischemic event. This powerful temporal relationship makes a causal link (heart -> brain) much more likely than a simple coincidence.
Unifying Diagnosis: It provides a single, elegant explanation for both the cardiac and neurological events. In medicine, we often seek a unifying diagnosis (Occam's razor), especially when events are so closely linked in time.
Conclusion and How to Differentiate
You are correct that a primary cerebral infarction is a strong possibility and cannot be dismissed. However, given the specific nature and severity of the evolving ECG findings, a cardioembolic source remains the most compelling hypothesis because it directly links the two events. The Wellens' pattern is the key piece of evidence that elevates the probability of an LV thrombus from a possibility to a high likelihood.
This is not just an academic distinction; the differentiation is critical for treatment, especially for secondary prevention:
If it's Atherothrombotic: The patient will need long-term management with antiplatelet agents (like Aspirin and/or Clopidogrel).
If it's Cardioembolic: The patient will need long-term anticoagulation (with Warfarin or a DOAC) to prevent another embolus from the heart.
The de-identified MRI and an Echocardiogram are the key investigations to settle this:
MRI: The pattern of infarct can be suggestive. Multiple infarcts in different vascular territories would scream "embolic." A single, deep lacunar infarct could be either, but might lean slightly more towards intrinsic small vessel disease.
Echocardiogram: This is the definitive test. If it shows a severe anterior wall motion abnormality and, crucially, identifies an LV thrombus, the diagnosis of cardioembolic stroke is confirmed. If it shows a normal or only mildly impaired LV function with no thrombus, a primary cerebral event becomes much more likely.
Thank you for pushing for this clarity. It's a fantastic clinical discussion point. We await the imaging to help solve the puzzle.
[10-06-2025 15.52] PM 1: Update:
Hemodynamically stable
All her hemodynamic support has been stopped.
Sensorium still E4V2M4
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