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 VARIOUS INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[29-09-2025 15.21] PPM 4: https://youtube.com/shorts/uC8w5OsKiJk?si=PoxuBfv9xkaVY6wW
[29-09-2025 15.52] PPM 5: Is it wellens type B sir? Inverted T waves
[29-09-2025 16.16] PPM 1: @PPM6 please test your LLM's computer vision by sharing the ECGs and this question with it
@PPM3 please test your human pattern recognition skills and share your answer.
[29-09-2025 16.52] PPM 3: Wellens majorly involves lad,lcx also seems to be involved here.
[29-09-2025 16.53] PPM 1: That may not be the text book answer but I would prefer a epidemiology data driven answer. Now check out the ECG pattern again in your occlusive MI uncertainty patient.
[29-09-2025 17.10] PPM 1: Again from a popular text book 👇
[30-09-2025 18.04] PPM 1: V3 V4 missing?
09/08/25
12/08/25
22/05/25
[30-09-2025 19.41] PPM 1: The main PA is dilating in days!
"Diagnostic criteria:
Rhinehart et al (2002) describe the following diagnostic criteria for Wellens syndrome:
Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)"
Again because it's not from a data driven study it's difficult to rely on the above but I guess data driven studies could be available to support the above text book conclusion? @PPM6
[29-09-2025 18.43] PPM 6: Excellent question. You are right to scrutinize the source. While textbooks are essential for synthesizing knowledge, it's crucial to know if their conclusions are based on robust, data-driven studies or on smaller, foundational papers.
Let's address your specific question: **Are there data-driven studies to support the diagnostic criteria for Wellens syndrome?**
The answer is **yes, but with important context.** The criteria listed by Rhinehart et al. (2002) in the LITFL article are a **systematization of findings from earlier, seminal studies.** They are not from a single, large-scale, prospective clinical trial, but they are absolutely grounded in observational data.
Here is the evidence trail, moving from the original data to the modern criteria.
### The Data-Driven Foundation of Wellens Syndrome
The diagnostic criteria are built upon a series of key studies that established the connection between this specific ECG pattern and critical LAD stenosis.
#### 1. The Original, Landmark Study (1982) - **de Zwaan, Bär, & Wellens**
* **Study:** "Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction." (*Am Heart J.* 1982)
* **Data & Methods:** This was a prospective observational study of 145 patients admitted with unstable angina. Out of these, 26 patients were identified who developed the characteristic T-wave changes (biphasic or deeply inverted in V2-V3) when they were pain-free.
* **Key Data-Driven Findings:**
* **Angiographic Correlation:** 24 of these 26 patients (92%) had a **>90% stenosis of the proximal LAD.**
* **Outcome Data:** Of the 18 patients who were treated medically (without urgent angiography/intervention), 14 (78%) developed an extensive anterior myocardial infarction within a mean of 8.5 days.
* **Specificity:** The study quantified that this pattern was a **highly specific marker** for a critical proximal LAD lesion.
**This is the core data.** It directly links the ECG pattern (T-wave changes) with the anatomy (critical LAD stenosis) and the clinical outcome (high risk of anterior MI).
#### 2. The Precursor Studies (Gerson et al., 1979-1980)
The LITFL article mentions these, and they provide important supporting data.
* **Gerson et al. (1979):** Showed that *exercise-induced* U-wave inversion (now understood as part of the T-wave/U-wave complex) was associated with a 92% prevalence of significant proximal LAD stenosis.
* **Gerson et al. (1980):** Showed that *resting* U-wave inversion had an 89% association with LAD or left main ischemia.
#### 3. The "Criteria" Paper (Rhinehart et al., 2002)
* **Study:** "Electrocardiographic manifestations of Wellens syndrome" (*Am J Emerg Med.* 2002)
* **What it is:** This paper is **not a new primary research study** but a **comprehensive review and synthesis** of the existing literature up to that point. Its purpose was to educate emergency physicians about this under-recognized but critical syndrome.
* **Its Role:** The authors distilled the findings from de Zwaan, Gerson, and others into a clear, actionable list of diagnostic criteria to make the syndrome easier to identify in clinical practice. The "data" for this paper was the body of evidence from the earlier studies.
### So, Can We Rely on the Textbook Conclusion?
**Yes, but we must understand what the data actually supports and what its limitations are.**
The textbook narrative is a **faithful and accurate summary of the available evidence.** The sequence of events (Occlusion -> Pain/STEMI -> Reperfusion -> Pain-free with T-wave changes) is the pathophysiological model that best explains the clinical and angiographic observations made in these studies.
**Strengths of the Evidence:**
* **High Specificity:** The association between the classic Wellens T-waves and a critical LAD stenosis is one of the most specific findings in all of ECG interpretation. When you see the pattern in the correct clinical context, the probability of a "widow-maker" lesion is extremely high.
* **Strong Angiographic Correlation:** The link was proven with coronary angiography, the gold standard for defining coronary anatomy.
* **Clear Clinical Implications:** The outcome data (high rate of subsequent MI) is compelling and has driven the clinical mandate for urgent angiography.
**Limitations of the Evidence (The "But..."):**
* **Era:** The foundational studies are from the 1980s. Treatment protocols (e.g., widespread use of potent P2Y12 inhibitors) and diagnostic sensitivity (e.g., high-sensitivity troponin) have evolved.
* **Sample Size:** The number of patients in the original studies was relatively small (e.g., 26 in the de Zwaan paper). This is common for initial descriptions of a novel syndrome.
* **Lack of Large Prospective Validation:** There is no massive, multi-center, prospective trial that has re-validated the criteria in the modern era. The syndrome is now considered so well-established that withholding angiography to conduct such a trial would be unethical.
### Conclusion: Data-Driven vs. Textbook Narrative
Your distinction is insightful. The story is a **"textbook narrative,"** but it is a narrative **built directly upon a "data-driven" foundation.**
1. **The Data Says:** "A specific ECG pattern (biphasic/deeply inverted T-waves in V2-3 in a pain-free patient) is strongly correlated with critical proximal LAD stenosis and a high short-term risk of anterior MI."
2. **The Textbook Narrative Explains:** "This pattern occurs due to a cycle of transient occlusion and reperfusion of the LAD."
The narrative provides the *"why,"* while the data provides the *"what."* In this case, they are perfectly aligned. Therefore, you can rely on the textbook conclusion with a high degree of confidence because it is rooted in solid, albeit older, observational data that has been consistently confirmed in clinical practice for over 40 years.
[29-09-2025 19.24] PPP 3 Alright @PPM7 @CR this is another patient for this ProJR 👇
While not all our patients may have viral fever precipitating their heart failure, heart failure due to any cause is equally likely to produce this diagnostic uncertainty in most health professionals!
[29-09-2025 19.34] PPM 1: Please delete the identifiers and share it again. Please delete the above ASAP
[29-09-2025 19.35] PPM 3 
The EMR summary of this patient when she was admitted with UTI and acute pyelonephritis in May 2025👇
Admission Date: 22/05/2025 06:13 PM
Diagnosis
AKI SECONDARY TO LEFT ACUTE PYELONEPHRITIS ON CKD
SEVERE ANEMIA NORMOCYTIC NORMOCHROMIC
S/P 4 SESSIONS OF HD WITH 1 PRBC TRANSFUSION
Case History and Clinical Findings
PATIENT CAME WITH C/O PAIN ABDOMEN SINCE 3 DAYS
HOPI- PATIENT WAS APPARENTLY ASYMPTOMATIC 3 DAYS AGO THEN DEVELOPED PAIN
ABDOMEN WHICH IS INSIDIOUS, PROGRESSIVE, NO AGGREVATING AND RELIEVING FCTORS.
H/O FEVER HIGH GRADE ON AND OFF ASSOCIATED WITH CHILLS SINCE 3 DAYS
H/O BURING MICTURITION PRESENT
H/O COLA COLORED URINE 3 DAYS BACK 1 EPISODE
H/O SOB, COUGH +, NON PRODUCTIVE
NO H/O NAUSEA, VOMITIN, LOOSE STOOLS
NO H/O CHESTPAIN, PALPITATIONS, PEDAL EDEMA, REDUCED URINE
OUTPUT, ORTHOPNEA, PND
PAST H/O - N/K/C/O - HTN, DM, TB, ASTHMA, EPILEPSY
PERSONAL HISTORY MARRIED, MIXED DIET, NORMAL APPETITE. ADEQUATE
SLEEP, NORMAL BOWEL AND BLADDER MOVEMENTS, NO ALLERGIES OR ADDICTION.
FAMILYHISTORY - NIL
O/E-NO PALLOR, NO ICTERUS, CYNOSIS, CLUBBNG, LYMPHADENOPATHY, PEDAL EDEMA
PRESENTATION VITALSTEMPERATURE- 98.6F
BP-160/100 MMHG
Page-2
KIMS HOSPITALS
PR-92 BPM
RR-24CPM
SPO2-98%ON RA
SYSTEMIC EXAMINATONCVS-
S1,S2- HEARD, NO MURMURS
RS-B/L AE+, NVBS
CNS- NFNDTONE - NORMAL B/L IN BOTH UPPER AND LOWER LIMBSPOWER-NORMAL B/L IN BOTH UPPER AND LOWER LIMBS
REFLEXES -BICEPS - +2, +2TRICEPS- +1, +1SUPINATOR +1 +1KNEE+1, +1
ANKLE +1 +1PLANTAR - FLEXION, FLEXION
COURSE IN THE HOSPITAL: PATIENT WAS PRESENTED WITH THE ABOVE MENTIONED
COMPLAINTS, ALL THE NECESSARY INVESTIGATIONS HAVE BEEN DONE AND
PROVISIONALLY DIAGNOSED AS AKI SECONDARY TO LEFT ACUTE PYELONEPHRITIS ON
CKD, SEVERE ANEMIA NORMOCHROMIC NORMOCYTIC.THE NEED FOR DIALYSIS AND THE CONSENT FOR CENTRAL LINE INSERTION HAS BEEN TAKEN.THE RISKS AND
COMPLICATIONS OF THE PATIENT CONDITION IS EXPLAINED.THE RIGHT INTRNAL JUGULAR VEIN CENTRAL LINE HAS BEEN INSERTED AND 4 SESSIONS OF HEMODIALYSIS DONE WITH 1 PRBC TRANSFUSION.PATIENT IS STABLE AND HEMODYNAMICALLY IMPROVED, HENCE BEING DISCHARGED.
Investigation
CBP HB TC N L E M B PLT SMEAR RFT UR CR UA CA+2 P NA+ K+ CL- HIV HBSAG HCV
Name Value COMPLETE URINE EXAMINATION (CUE) 22-05-2025 06:47:PM COLOUR Pale
yellow APPEARANCE Clear REACTION Acidic SP. GRAVITY 1.010 ALBUMIN ++SUGAR Nil BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 4-5 EPITHELIAL CELLS 2-4 RED BLOOD CELLS 2-4 CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
RFT 22-05-2025 06:47:PM UREA 193 mg/dl CREATININE 6.2 mg/dl URIC ACID 11.0
mmol/LCALCIUM 9.0 mg/dl PHOSPHOROUS 19.9 mg/dl SODIUM 139 mmol/LPOTASSIUM 4.8
mmol/L.CHLORIDE 104 mmol/L LIVER FUNCTION TEST (LFT)
22-05-2025 06:47:PM Total Bilurubin1.43 mg/dl Direct Bilurubin 0.78 mg/dl SGOT(AST) 26 IU/L SGPT(ALT) 10 IU/L ALKALINE PHOSPHATASE 223 IU/LTOTAL PROTEINS 8.4 gm/dl ALBUMIN 2.24 gm/dl A/G RATIO 0.36
ABG 22-05-2025 06:47:PM PH 7.18PCO2 14.5PO2 104HCO3 5. 2 St. HCO3 8.2BEB -21.9BEecf -
22.0TCO2 11.7O2 Sat 97.2O2 Count 9.8HBsAg-RAPID 22-05-2025 06:48:PM Negative
Anti HCV Antibodies - RAPID 22-05-2025 06:48:PM Non Reactive RFT 22-05-2025 09:01:PM UREA
191 mg/dl CREATININE 6.2 mg/dl URIC ACID 12.0 mmol/L CALCIUM 9.1 mg/dl PHOSPHOROUS 20.1mg/dl SODIUM 137 mmol/L POTASSIUM 4.7 mmol/L.CHLORIDE 105 mmol/L
Page-3
KIMS HOSPITALS
LIVER FUNCTION TEST (LFT) 22-05-2025 09:01: PM Total Bilurubin 1.39 mg/dl Direct Bilurubin 0.62 mg/dl SGOT(AST) 24 IU/LSGPT(ALT) 10 IU/LALKALINE PHOSPHATASE 230 IU/L TOTAL
PROTEINS 9.0 gm/dl ALBUMIN 2.17 gm/dl A/G RATIO 0.32ABG 23-05-2025 12:12:AM PH 7.35 PCO2 26.0 PO2 87.7 HCO3 14.1 St. HCO3 16.2BEB -10.2BEecf -10.4TCO2 30.7O2 Sat 96.9O2 Count 9.5
RFT 23-05-2025 12:12:AM UREA 144 mg/dl CREATININE 4.2 mg/dl URIC ACID 9.0 mmol/L CALCIUM 9.2 mg/dl PHOSPHOROUS 19.8 mg/dl SODIUM 138 mmol/L POTASSIUM 3.7 mmol/L.CHLORIDE 102 mmol/L
RFT 24-05-2025 12:09:AM UREA 176 mg/dl CREATININE 4.2 mg/dl URIC ACID 9.7 mmol/L CALCIUM 8.9 mg/dl PHOSPHOROUS 18.9 mg/dl SODIUM 135 mmol/L POTASSIUM 3.6
mmol/L.CHLORIDE 102 mmol/L
HEMOGRAM-23/5/25
HB-6.8GM/DLTLC-12,200CELLS/CUMMNEUTROPHILS-90%LYMPHOCYTES-5%EOSINOPHILS-
01% MONOCYTES-04% BASOPHILS00% PCV-21.1 MCV-95.2 MCH-30.9 MCHC-32.4 RDW-CV-
14.5 RDW-SD-50.1 RBCCOUNT-2.22 PLATETELET-1.23LAKHS/CUMMSMEARRBCNORMOCYTICNORMOCHROMICWBC-
INCREASED U COUNTS NIL IMPRESSION- NORMOCYTIC NORMOCHROMIC ANEMIA WITH NEUTROPHILIC LEUCOCYTOSIS AND THROMBOCYTOPENIA ON SMEAR WITH NEUTOPHILIA PLATELETS-DECREASED COUNTS ON SMEAR HEMOPARASITESHEMOGRAM-
25/05/25
HB-88GM/DL TLC-13600 CELLS/CUMM
NEUTROPHILS-86% LYMPHOCYTES-08% EOSINOPHILS-02% MONOCYTES-04% BASOPHILS 00% PCV-25.8 MCV 93.1 MCH-31.6 MCHC-33.9 RDW-CV-14.7 RDW-SD 50.7
RBC COUNT-2.77 PLATETELET-1.30LAKHS/CUMMSMEARRBCNORMOCYTICNORMOCHROMICWBC-
INCREASED NORMOCHROMICWBC- INCREASEDU
CONTS NILIMPRESSION- NORMOCYTIC NORMOCHROMIC ANEMIA WITH NEUTROPHILIC
LEUCOCYTOSIS AND THROMBOCYTOPENIAON SMEAR WITH NEUTOPHILIA PLATELETSDECREASED
COUNTS ON SMEAR HEMOPARASITESUSG-
23/5/25 - IMPRESSION
GRADE1 RPD CHANGES OF B/L KIDNEYS
LEFT RENAL CORTICAL CYSTS
MILD SPLEENOMEGALY
2DECHO- 23/5/25
MILD TO MOD TR+ PAH MILD FOMODE MR+ MILD AR+/PR+
GLOBAL HYPOKINESIA NO AS/MS SCLEROTIC AV
MILD TO MOD LV DYSFNCTION+
GRADE 1 DIASTOLIC DYSFUNCTION+ NO PE NO LV CLOT
Treatment Given (Enter only Generic Name)
IV NS @ 75ML/HR
INJ PIPTAZ 2.25GM IV/BD FOR 7 DAYS
INJ. NEOMOL 1GM IV/SOS IF TEMP>101F
INJ PAN 40MG IV/OD
INJ ZOFER 4MG IV/SOS
INJ.IRON SUCROSE 200 MG IN 100 ML NS IV
INJ.EPO 4000 IU SC TWICE WEEKLY
T. PCM 650MG PO/TID
T. NODOSIS 500MG PO/OD
T. SEVELAMER CARBONATE 400MG BD
T.SHELCAL PO OD
SYP.CREMAFFIN 15 ML PO HS
Advice at Discharge
FLUID RESTRICTION <1.5 L/DAY
SALT RESTRICTION <2 GRAMS /DAY
INJ.EPO 4000 IU SC TWICE WEEKLY
T.FAROPENEM 200 MG PO BD FOR 7 DAYS 1-0-1
T.PAN 40MG PO/OD 1-0-0 FOR 5 DAYS
T. PCM 650MG PO/TID 1-1-1 FOR 3 DAYS
T. NODOSIS 500MG PO/BD 1-0-1
T.SHELCAL CT PO OD 0-1-0
T.OROFER XT PO OD 1-0-0
SYP CREMAFFIN 15 ML PO HS FOR 5 DAYS
SYP POTKLOR 15ML IN 1 GLASS OF WATER PO/TID FOR 5 DAYS
POTASSIUM RICH DIET
Follow Up
REVIEW TO NEPHROLOGY OP AFTER 1 WEEK/SOS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
Page-5
KIMS HOSPITALS
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/Attendant 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: 28/5/25
Ward: NEPHROLOGY
[29-09-2025 19.52] PPM 1: @PPM7 she was again admitted in August 2025 and the same confusion persisted as in the EMR summary from that time!👇
Age/Gender: 65 Years/Female
Address:
Discharge Type: Relieved
Admission Date: 07/08/2025 11:08 PM
Diagnosis
COMMUNITY Acquired PNEUMONIA
HEART FAILURE WITH reduced EJECTION FRACTION 42% TO Hfpef 61%
DENOVO HTN
Case History and Clinical Findings
C/O COUGH SINCE 3 DAYS
C/O OF SOB SINCE TODAY EVENING
HOPI: PATIENT WAS APPARENTLY ASYMPTOMATIC 3 DAYS BACK THEN SHE DEVELOPED
COUGH WHICH WAS NON PRODUCTIVE, PATIENT DEVELOPED SOB SINCE TODAY EVENING,
NOTA/W CHEST PAIN PALPITATIONS, PEDAL EDEMA
PAST H/O K/C/O AKI SECONDARY TO ACUTE PYELONEPHRTITIS ON CKD
NO H/O TYPE 2 DM, ASTHMA, THYROID, EPILEPSY, CAD, CVA, HTN
PERSONAL HISTORY: MARRIED, NORMAL APPETITE, MIXED DIET, REGULAR BOWEL AND BLADDER MOVEMENTS, ADEQUATE SLEEP
NO PALLOR, ICTERUS, CYANOSIS, CLUBBING, LYMPHADEONPATHY, PEDAL EDEMA
TEMP-96.4, PR- 80BPM, RR-16CPM, BP- 110/80MMHG, SPO2-98%, GRBS- 133MG%
SYSTEMIC EXAMINATION
CVS, P/A, CNS- NORMAL
RS B/L DIFFUSE CREPTS PRESENT
COURSE IN THE HOSPITAL:
Page-2
KIMS HOSPITALS
A 65 YEAR OLD FEMALE CAME TO THE CASUALITY WITH THE ABOVE COMPLAINTS, ALL THE Necessary INVESTIGATIONS WERE SENT AND DIAGNOSED AS COMMUNITY ACQUIRED PNEUMONIA, HEART FAILURE WITH RECOVERED EF FROM 42 TO 61%, DE NOVO HTN.
PATIENT WAS CONSERVATIVELY TREATED WITH IV ANTIBIOTICS, ANTI HYPERTENSIVES
AND OTHER SUPPORTIVE TREATMENTS, CULTURE REPORTS WERE SENT REPORT TO BE
AWAITED. AS PATIENT VITLS WERE STABLE PATIENT IS BEING HAEMODYNAMICALLY
DISCHRGED IN STABLE CONDITION.
Investigation
COMPLETE URINE EXAMINATION (CUE) 07-08-2025 11:22:PM COLOUR Pale
yellow APPEARANCE Clear REACTION Acidic SP. GRAVITY1.010 ALBUMIN++SUGAR Nil BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 3-4EPITHELIAL CELLS 2-4 RED BLOOD
CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
RFT 07-08-2025
11:22:PM UREA 34 mg/dl 50-17 mg/dl CREATININE1.1 mg/dl1.2-0.6 mg/dl URIC ACID5.6 mmol/L6-2.6 mmol/LCALCIUM9.2 mg/dl10.2-8.6 mg/dlPHOSPHOROUS7.5 mg/dl4.5-2.5 mg/dlSODIUM141
mmol/L145-136 mmol/LPOTASSIUM2.8 mmol/L.5.1-3.5 mmol/L. CHLORIDE102 mmol/L98-107
mmol/L Arterial Blood Gas Analysis (ABG) 07-08-2025 11:22:PM
PH7.367PCO226.7PO269.9HCO315.0 St. HCO317.2BEB-8.9BEecf-9.3TCO231.5O2 Sat94.1O2
Count12.7LIVER FUNCTION TEST (LFT) 07-08-2025 11:22:PM Total Bilurubin1.25 mg/dl1-0
mg/dl Direct Bilurubin0.29 mg/dl0.2-0.0 mg/dl SGOT(AST)23 IU/L31-0 IU/LSGPT(ALT)12 IU/L34-0
IU/L ALKALINE PHOSPHATASE 93 IU/L 128-56 IU/L TOTAL PROTEINS 8.2 gm/dl 8.3-6.4
gm/dl ALBUMIN3.3 gm/dl 4.6-3.2 gm/dl A/G RATIO 0.67 SERUM ELECTROLYTES 08-08-2025
07:09:AM SODIUM 148 mmol/L 145-136 mmol/L POTASSIUM4.1 mmol/L 5.1-3.5
mmol/L CHLORIDE106 mmol/L 98-107 mmol/L RFT 09-08-2025 12:33:AM UREA 60 mg/dl 50-17
mg/dl CREATININE1.1 mg/dl1.2-0.6 mg/dl URIC ACID7.0 mmol/L6-2.6 mmol/L CALCIUM8.9
mg/dl10.2-8.6 mg/dl PHOSPHOROUS8.4 mg/dl 4.5-2.5 mg/dlSODIUM142 mmol/L145-136
mmol/LPOTASSIUM3.5 mmol/L.5.1-3.5 mmol/L.CHLORIDE 99 mmol/L98-107 mmol/LRFT 09-08-
2025 11:42:PM UREA44 mg/dl50-17 mg/dlCREATININE1.0 mg/dl1.2-0.6 mg/dl URIC ACID6.5
mmol/L6-2.6 mmol/LCALCIUM9.1 mg/dl10.2-8.6 mg/dlPHOSPHOROUS3.8 mg/dl4.5-2.5
mg/dlSODIUM139 mmol/L145-136 mmol/L POTASSIUM3.6 mmol/L.5.1-3.5 mmol/L. CHLORIDE98
mmol/L98-107 mmol/LRFT 11-08-2025 03:41:AM UREA30 mg/dl50-17 mg/dlCREATININE1.0
mg/dl1.2-0.6 mg/dl URIC ACID5.5 mmol/L6-2.6 mmol/LCALCIUM9.4 mg/dl10.2-8.6
mg/dl PHOSPHOROUS3.30 mg/dl 4.5-2.5 mg/dl SODIUM147 mmol/L 145-136 mmol/L POTASSIUM 3.2mmol/L.5.1-3.5 mmol/L. CHLORIDE98 mmol/L98-107 mmol/L
SERUM ELECTROLYTES 11-08-2025
11:06:PM SODIUM137 mmol/L145-136 mmol/L POTASSIUM3.3 mmol/L5.1-3.5 mmol/L
CHLORIDE 98 mmol/L98-107 mmol/L
HAEMOGRAM ON 7/8/25
HB-9.4 gm/dl, TLC-10100, RBC-2.8, PLATELETS-1.9
Page-3
KIMS HOSPITALS
HAEMOGRAM ON 12/8/25
HB-9.1 gm/dl, TLC-6900, RBC-2.7, PLATELETS-2.3
2D ECHO ON 8/8/25
EF 42% MILD TR, NO PAH, MILD MR, MILD AR/PR (ECCENTRIC JET MR)
GLOBAL HYPOKINESIA, NO AS/MS, SCLEROTIC AV
MILD TO MODERATE LV DYSFUNCTION
GRADE 1 DIASTOLIC DYSFUNCTION NO LV CLOT
2D ECHO ON 12/8/25:
EF 61% MILD AR TRIVIAL TR, NO PAH, TRIVIAL MR, MILD PR
NO RWMA, NO AS/MS, SCLEROTIC AV
GOOD LV SYSTOLIC FUNCTION, NO PE
GRADE 1 DIASTOLIC DYSFUNCTION, NO LV CLOT, VEGITATION
Treatment Given (Enter only Generic Name)
INJ. AUGMENTIN 1.2gm IV/BD GIVEN FOR 6 DAYS
TAB. AZITHROMYCIN 500MG PO/OD GIVEN FOR 5 DAYS
INJ. PAN 40mg IV/OD
TAB. TELMA 40mg PO/OD
TAB. ECOSPRIN AV 75/20mg PO/HS
INJ. LASIX 20mg IV/BD
TAB. ALDACTONE 25mg PO/OD
TAB PCM 650MG PO/TID
SYP. ASCORIL D 10ml PO/TID (10ml-10ml-10ml)
MEB WITH IPRAVENT 6TH HOURLY
NEB WITH BUDECOT 12TH HOURLY
FLUID INTAKE UPTO 1.5LT/ DAY
Advice at Discharge
TAB. AUGMENTIN 625MG PO/BD FOR 3DAYS
TAB. PAN 40mg PO/OD FOR 3 DAYS
TAB. TELMA 40mg PO/ODTO BE CONTINUED
TAB. ECOSPRIN 75/20mg PO/HSTO BE CONTINUED
TAB DYTOR PLUS 10/50MG HALF PO/OD TO BE CONTINUED
TAB PCM 650MG PO/SOS
Page-4
KIMS HOSPITALS
TAB ULTRACET PO/BD FOR 3 DAYS
TAB REJUNEX CD 3 PO/OD FOR 15 DAYS
SYP. ASCORIL D 10ml PO/TID (10ml-10ml-10ml) FOR 3 DAYS
ROTAHALER FOROCORT 200MG 2 PUFFS PO TWICE DAILY
Follow Up
REVIEW TO GM OPD ON THURSDAY (14/08/25) 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/Attendant 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:12/08/2025
Ward: FMW
Unit: 4
[30-09-2025 18.00] PPM 3:
[30-09-2025 18.52] PPM 3: It was repeated again
30-09-25 7pm
07/08/25
[30-09-2025 19.33] PPM 3: Found old xrays
[30-09-2025 19.35] PPM 1: That's really very useful
[30-09-2025 19.41] PPM 1: The main PA is dilating in days!
[30-09-2025 21.42] PPM 8: Interesting case
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