THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS 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.
[27-05-2025 15.44] PPM 1: Operative scar from 30 years for perforation and 4 years back for adhesions
[27-05-2025 16.27] PPM 1: Afternoon session:
Three heart failure and one altered senso PaJRed
One of them imaged here 👇
https://youtube.com/shorts/Ek5oQEDGNLY?feature=shared
[27-05-2025 18:16] PPM 3: Skip to main content
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Okay, I will describe these medical images.
Image 1: Chest X-ray (dated 26-May-2025)
View: Anteroposterior (AP) or Posteroanterior (PA) chest X-ray. The "R" marker indicates the patient's right side.
Quality: The image is somewhat underexposed, particularly in the lower lung fields. Penetration is suboptimal.
Findings:
Cardiomediastinal Silhouette: The cardiac silhouette appears significantly enlarged (cardiomegaly). Its borders are poorly defined due to overlying opacities.
Lungs: There are extensive, bilateral, diffuse opacities predominantly in the mid and lower lung zones, appearing somewhat confluent. These obscure the underlying lung parenchyma and vascular markings.
Pleural Spaces: Costophrenic angles are obscured bilaterally, suggesting pleural effusions.
Trachea: Appears roughly midline.
Bones: Clavicles, ribs, and visible portions of the humeri do not show obvious acute fractures.
Impression: Significant cardiomegaly with features highly suggestive of pulmonary edema (due to the diffuse bilateral opacities and pleural effusions). Severe bilateral pneumonia or ARDS could also present with similar extensive opacities, but the cardiomegaly makes pulmonary edema a prime consideration. The findings appear to have worsened slightly or are at least as severe compared to the image from 24-May-2025.
Image 2: Chest X-ray (dated 24-May-2025)
View: Similar to Image 1, an AP or PA chest X-ray.
Quality: Similar suboptimal exposure and penetration as Image 1.
Findings:
Cardiomediastinal Silhouette: The cardiac silhouette is markedly enlarged.
Lungs: Widespread bilateral opacities are present, particularly in the mid and lower lung zones. These are somewhat hazy and confluent, obscuring normal lung markings. Some patchy areas of consolidation or atelectasis might be present, for example, in the right mid-lung zone.
Pleural Spaces: Bilateral costophrenic angle blunting is present, suggestive of pleural effusions.
Trachea: Appears midline.
Bones: No acute bony abnormalities seen.
Impression: Cardiomegaly with extensive bilateral pulmonary opacities and pleural effusions, likely representing pulmonary edema. Other causes like severe bilateral pneumonia are also possible. This image shows severe pathology.
Image 3: Electrocardiogram (ECG)
Rhythm: Sinus tachycardia (P waves present before each QRS, regular R-R interval, rate appears to be around 130-150 bpm, estimated from R-R interval of ~2 large squares).
Axis: Normal axis (QRS positive in Lead I and aVF).
Intervals:
PR interval: Appears normal.
QRS duration: Appears normal (narrow).
QT interval: Difficult to assess accurately without rate correction, but does not appear grossly prolonged.
Hypertrophy:
Left Ventricular Hypertrophy (LVH): Likely present. There are deep S waves in V1/V2 and tall R waves in V5/V6 (e.g., S in V2 ≈ 25mm, R in V5 ≈ 25mm; Sokolow-Lyon criteria S V1 + R V5/V6 > 35mm seems met).
ST Segment and T Wave Changes:
Significant ST depression: Present in multiple leads, most notably in V2, V3, V4, V5, V6, and also in Leads I, II, aVL, aVF. The ST depression is downsloping or horizontal.
T Wave Inversions: Present in V2, V3, V4, V5, V6, Lead I, aVL. T waves are flattened in II and aVF.
Q Waves: No obvious pathological Q waves.
Impression:
Sinus tachycardia.
Left Ventricular Hypertrophy (LVH).
Widespread ST depression and T wave inversions, most prominent in anterolateral leads (V2-V6, I, aVL). These changes are concerning for myocardial ischemia (subendocardial ischemia) or a severe LV strain pattern secondary to LVH and tachycardia.
Overall Correlation:
The ECG findings of LVH and ischemic changes (or severe strain) are consistent with the cardiomegaly seen on the chest X-rays. The combination of severe cardiac findings on ECG and X-ray (cardiomegaly, pulmonary edema) suggests significant cardiac dysfunction.
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This is a critical situation requiring urgent assessment and management. The combination of worsening pulmonary edema on X-ray, cardiomegaly, and ECG findings (sinus tachycardia, LVH, and widespread ST depression/T-wave inversions concerning for ischemia or severe strain) points towards acute decompensated heart failure (ADHF), very likely precipitated or accompanied by acute myocardial ischemia (Acute Coronary Syndrome - ACS) or severe demand ischemia.
Here's what needs to happen next, likely simultaneously and rapidly:
I. Immediate Assessment & Stabilization (ABCDE Approach):
Airway & Breathing:
Assess respiratory status: Respiratory rate, effort, use of accessory muscles, ability to speak in full sentences.
Oxygen Saturation (SpO2): Administer supplemental oxygen (e.g., nasal cannula, face mask, non-rebreather) to maintain SpO2 > 92-94%.
Auscultate lungs: Listen for crackles (pulmonary edema), wheezes.
Consider Non-Invasive Ventilation (NIV - CPAP/BiPAP): If significant respiratory distress and hypoxia persist despite oxygen, and the patient is hemodynamically stable enough. This can reduce work of breathing and improve oxygenation in ADHF.
Prepare for intubation: If respiratory failure is imminent or patient is obtunded.
Circulation:
Full Vital Signs: Heart rate (already known to be tachycardic), Blood Pressure (CRUCIAL), temperature.
IV Access: Secure at least one, preferably two, large-bore IV cannulas.
Continuous Cardiac Monitoring: For arrhythmias and further ST changes.
Assess for signs of shock/hypoperfusion: Cool peripheries, delayed capillary refill, altered mental status.
Focused Cardiac Exam: Listen for heart sounds (S3 gallop common in ADHF), murmurs (new murmur could indicate acute valvular dysfunction). Check JVP.
Disability:
Assess level of consciousness (AVPU or GCS).
Exposure:
Briefly check for peripheral edema, skin temperature.
II. Urgent Investigations:
Cardiac Biomarkers (STAT):
Troponin (high sensitivity if available): Essential to rule in/out myocardial infarction. Serial measurements will be needed.
Natriuretic Peptides (STAT):
BNP or NT-proBNP: To confirm and assess the severity of heart failure.
Arterial Blood Gas (ABG):
To assess oxygenation, ventilation, and acid-base status (e.g., respiratory acidosis, metabolic acidosis from hypoperfusion). Especially important if SpO2 is low or respiratory distress is severe.
Blood Tests (STAT):
Full Blood Count (FBC/CBC): Check for anemia (can exacerbate ischemia/HF), infection (leukocytosis).
Urea & Electrolytes (U&Es) / Renal Function Panel: Assess kidney function (can be impaired in HF, affects drug choices), check electrolytes (especially potassium, magnesium – critical for cardiac stability).
Glucose: Rule out hypoglycemia/hyperglycemia.
Liver Function Tests (LFTs): Can be deranged due to hepatic congestion in heart failure.
Coagulation screen (PT/INR, PTT): If anticoagulation or thrombolysis is being considered for ACS.
Point-of-Care Ultrasound (POCUS) - if available and operator skilled:
Cardiac POCUS: Rapid assessment of LV function (global hypokinesia? regional wall motion abnormalities suggesting ischemia?), RV function, pericardial effusion, gross valvular abnormalities.
Lung POCUS: Can confirm pulmonary edema (B-lines), pleural effusions.
III. Immediate Management (Guided by Assessment and BP):
Oxygen: As above.
Diuretics (for pulmonary edema, if BP allows):
IV Furosemide: e.g., 40-80 mg IV (or higher if patient is on chronic diuretics). Aim for diuresis.
Nitrates (if BP allows, SBP >100-110 mmHg, and no signs of RV infarction or severe aortic stenosis):
Sublingual Nitroglycerin (GTN): If chest pain or severe dyspnea.
IV Nitroglycerin infusion: For ongoing symptoms and pulmonary edema. Helps with preload and afterload reduction, and coronary vasodilation.
Antiplatelet Therapy (if ACS is suspected):
Aspirin: 300-325 mg chewed and swallowed (unless contraindicated).
Consider a P2Y12 inhibitor (e.g., clopidogrel, ticagrelor) in consultation with cardiology, especially if ST changes are clearly ischemic.
Anticoagulation (if ACS is suspected or AF is present):
e.g., Unfractionated Heparin or Low Molecular Weight Heparin (LMWH) – choice depends on renal function and local protocols.
Address Tachycardia:
The sinus tachycardia is likely compensatory or due to distress/ischemia. Treating the underlying cause (HF, ischemia) is key.
Beta-blockers are generally AVOIDED in acute decompensated heart failure with pulmonary edema unless the tachycardia is clearly supraventricular (e.g., AF with RVR) and contributing to instability, and the patient is not in cardiogenic shock.
Morphine (use with caution):
Can be considered for severe dyspnea or chest pain refractory to nitrates. It causes venodilation and can reduce anxiety. However, it can also cause respiratory depression and hypotension. Use small IV doses (e.g., 2-4 mg).
IV. Consultations:
Cardiology (URGENT): This patient needs immediate cardiology input for diagnosis, management, and consideration for further interventions (e.g., coronary angiography if ACS is confirmed/highly suspected).
Intensive Care Unit (ICU) / High Dependency Unit (HDU): Likely admission for close monitoring, potential need for advanced respiratory support, and hemodynamic management.
V. Further Diagnostic Plan (once stabilized):
Formal Transthoracic Echocardiogram (urgent): To comprehensively assess LV and RV function, valvular integrity, wall motion abnormalities, and estimate pulmonary pressures. This is a key investigation.
Consider Coronary Angiography: If troponins are elevated and/or ECG changes are convincing for ACS, and the patient is a candidate.
Key considerations:
Distinguish between different types of ADHF: "Warm and wet" (well-perfused with congestion) vs. "cold and wet" (poorly perfused with congestion). Management differs (e.g., "cold and wet" may need inotropes).
Identify and treat precipitants: Ischemia, arrhythmia, infection, non-adherence to medications, dietary indiscretion, uncontrolled hypertension.
This patient is critically ill. Prompt, coordinated action is essential to improve outcomes.
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The video shows prominent pulsations in the neck, in the region of the internal jugular vein. This is consistent with a significantly elevated Jugular Venous Pressure (JVP).
The pulsations appear venous in character (diffuse, undulating) rather than a sharp arterial pulsation. The upper level of this pulsation is very high, well above the clavicle, even with the patient in a semi-recumbent position (though the exact angle isn't clear).
Correlation with Previous Findings:
This finding of a markedly elevated JVP is highly consistent with the other clinical data you've provided:
Chest X-rays (24-May & 26-May-2025): Showed significant cardiomegaly, extensive bilateral pulmonary opacities (pulmonary edema), and pleural effusions. These are signs of fluid overload and heart failure.
ECG: Showed sinus tachycardia, Left Ventricular Hypertrophy (LVH), and widespread ST depression/T-wave inversions concerning for myocardial ischemia or severe LV strain. These indicate significant underlying cardiac pathology.
Clinical Significance of Elevated JVP in this Context:
An elevated JVP indicates increased right atrial pressure. In the context of the X-ray and ECG findings, this strongly suggests:
Volume Overload: A key feature of acute decompensated heart failure (ADHF).
Right Ventricular Dysfunction/Pressure Overload: This can be secondary to severe left ventricular dysfunction (which is strongly suggested by the ECG and pulmonary edema). High pressures in the left side of the heart back up into the pulmonary circulation, increasing the workload on the right ventricle, leading to right-sided congestion and elevated JVP. This points towards biventricular failure.
Confirmation of Congestive Heart Failure: It's a crucial physical sign supporting the diagnosis of ADHF.
What this means for "What's Next?":
The elevated JVP reinforces the urgent need for the "Next Steps" outlined previously, particularly:
Aggressive Diuresis: IV diuretics (e.g., furosemide) are critical to reduce volume overload, which will help alleviate pulmonary edema and reduce the JVP.
Vasodilators (if blood pressure allows): Nitrates can help reduce preload (venous return to the heart) and afterload, which can also help lower JVP and improve cardiac function.
Addressing the Underlying Cause: Investigating and treating potential myocardial ischemia (ACS) is paramount, as this is likely driving or significantly contributing to the acute decompensation.
Monitoring: The JVP, along with urine output, respiratory status, and hemodynamics, will be an important parameter to monitor the patient's response to treatment.
In summary, the video provides strong physical exam evidence of severe fluid overload and elevated central venous pressures, further corroborating the diagnosis of acute decompensated heart failure, likely with a significant ischemic component.
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[27-05-2025 18:42] PPM 3: The relationship between viral infections, pneumonia, pulmonary edema, and heart failure is complex and bidirectional, with each condition often exacerbating or triggering the others. Here’s a detailed breakdown of their interplay:
---### *1. Viral Infections and Pneumonia*
Viral infections (e.g., influenza, COVID-19) are common causes of pneumonia, an infection that inflames the air sacs in the lungs and fills them with fluid or pus. This inflammation can lead to:
- *Increased systemic inflammation*: Viral pneumonia triggers a widespread inflammatory response, releasing cytokines that strain the cardiovascular system and destabilize atherosclerotic plaques, raising the risk of heart attacks or arrhythmias.
- *Hypoxemia*: Reduced oxygen levels from pneumonia force the heart to work harder, worsening preexisting heart conditions.
---### *2. Pneumonia and Pulmonary Edema*
Pneumonia can lead to *non-cardiogenic pulmonary edema* through mechanisms like:
- *Direct lung injury*: Viral or bacterial pathogens damage the alveolar-capillary membrane, causing fluid leakage into the lungs (e.g., in acute respiratory distress syndrome, ARDS).
- *Inflammatory mediators*: These increase vascular permeability, allowing fluid to accumulate in the lungs even without heart failure.
However, pneumonia can also exacerbate *cardiogenic pulmonary edema* in patients with heart failure due to increased cardiac demand and fluid retention.
---### *3. Pulmonary Edema and Heart Failure*
*Cardiogenic pulmonary edema* is a hallmark of acute decompensated heart failure. When the left ventricle fails to pump effectively, blood backs up into the pulmonary circulation, increasing pressure and forcing fluid into the alveoli. Key triggers include:
- *Myocardial damage*: Viral infections like myocarditis can weaken the heart muscle, leading to systolic or diastolic dysfunction.
- *Fluid overload*: Conditions like hypertension or kidney failure exacerbate fluid retention, worsening edema.
---### *4. Heart Failure and Vulnerability to Pneumonia*
Heart failure increases the risk of pneumonia through:
- *Pulmonary congestion*: Fluid buildup in the lungs impairs immune defenses, making infections more likely.
- *Reduced mobility and weakened immunity*: Chronic heart failure patients often have comorbid conditions (e.g., diabetes) and sedentary lifestyles, further elevating infection risk.
Studies show heart failure patients have nearly double the risk of hospitalization for pneumonia compared to the general population.
---### *5. Bidirectional Cycles and Complications*
- *Viral myocarditis → Heart failure → Pulmonary edema*: Viral infections like Coxsackievirus can directly damage the heart, leading to cardiomyopathy and subsequent fluid overload.
- *Pneumonia → Systemic inflammation → Worsened heart function*: Inflammatory cytokines from pneumonia can impair cardiac contractility and destabilize existing heart disease.
- *Heart failure → Pulmonary edema → Impaired gas exchange → Hypoxia*: This creates a vicious cycle, further stressing the heart and kidneys.
---### *Key Takeaways*
- *Prevention*: Vaccinations (e.g., pneumococcal, influenza) are critical for heart failure patients to reduce pneumonia risk.
- *Diagnosis*: Differentiating cardiogenic vs. non-cardiogenic pulmonary edema is vital (e.g., using BNP levels, echocardiography).
- *Management*: Treatment includes diuretics, oxygen therapy, and addressing the underlying cause (e.g., antivirals for infections, inotropes for heart failure).
For further details, explore the sources on pneumonia-heart interactions, pulmonary edema mechanisms, and heart failure complications.
[27-05-2025 19:48] PPM 1: Where did it see the JVP video in this patient?
[28-05-2025 00:17] PPM 3: I just shared the link!
[28-05-2025 07:10] PPM 1 But that was an echocardiography video and I don't think it showed JVP!
[28-05-2025 08:41] PPM 3: May be concluded from the echocadiogrgher comments ! I would share the text of youtube video and see its response.
EMR SUMMARY
Age/Gender: 68 Years/Male
Discharge Type: Relieved
Admission Date: 24/05/2025 02:31 PM
Diagnosis
?LOBAR PNEUMONIA
?LOCULATED
PLEURAL EFFUSION
SECONDARY
TO HEART FAILURE DENOVO HYPERTENSION
Case History and Clinical Findings
PATIENT CAME TO OPD WITH C/O COUGH SINCE 3 DAYS, C/O RIGHT SIDEDCHEST PAIN SINCE LAST NIGHT (23/05/2025) HOPI:PATIENT APPARENTLY ASYMPTOMATIC 3DAYS BACK THEN HE DEVELOPED COUGH, WHICH WAS INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE IN NATURE, NOT ASSOCIATED WITH SPUTUM, NO C/O POST TUSSIVE VOMITING.
C/O SOB SINCE YERSTERDAY NIGHT, ON EXERTION FROM GRADE 2 TO 3.
C/O CHESTPAIN, RIGHTSIDED, AGGRAVATED ON WALKING, COUGHING, RADIATING TO BACK ON RIGHT SIDE NOT ASSOCIATED WITH PALPITATIONS, PND , ORTHOPNEA.
H/OFEVER8DAYS AGO, ASSOCIATED WITH CHILLS AND RIGORS, RELIEVED WITH MEDICATION
SURGICAL HISTORY: ULCER 4 YEARS AGO
PAST ILLNESS: N/K/C/ODMTYPE2,HTN, CAD, CVD, ASTHMA, THYROID, TB, EPILEPSY PERSONAL HISTORY: MIXED DIET, APPETITE NORMAL, REGULAR BOWEL MOVEMENTS, MICTURITION NORMAL, NO KNOWN ALERGIES AND ADDICTIONS: REGULAR ALCOHOL
CONSUMER SINCE 3OYEARS, DAILY 180ML, LAST BOUT 1 DAY AGO, H/O TODDY INTAKE 10 DAYSAGO.AND CHRONIC SMOKER SINCE 20YEARS, 1_-2PACKS/DAY, STOPPED 5 YEARS AGO
FAMILY HISTORY: NOT SIGNIFICANT
GENREAL EXAMINATION: NOPALLOR, CLUBBING, ICTERUS, CYANOSIS, LYMPHADENOPATHY, MALNUTRITION
VITALS: -TEMP:98.6 DEGREES F, BP:80/60MMHG, RR:22CPM, PR:96BPM, SPO2:98%AT RA, GRBS 169MG%
SYSTEMIC EXAMINATION:- CVS, CNS: NORMAL
RS: DECREASED AIR ENTRY ON RIGHT SIDE, BRONCHIAL BREATHING SOUNDS +,CREPTS
+ON RIGHT INFRA SCAPULAR, RIGHTINTERSCAPULAR, RIGHTAXILLARY AREA. P/A: SOFT, NON TENDER, NO ORGANOMEGALY
PATIENT WAS REFERRED TO PULMONOLOGY: ADVISED: TO INDUCE SPUTUM WITH 3 % NEBULISATION, PLANNED FOR BRONCHOSCOPY BUT PATIENT'S ATTENDERS WERE NOT WILLING FOR BRONCHOSCOPY.
Investigation
LIVER FUNCTIONTEST 24/5/25: TOTL BILURUBIN 1.62mg/dl, Direct Bilurubin 1.16mg/dl, SGOT (AST) 18IU/L, SGPT (ALT) 29IU/L, ALKALINE PHOSPHATASE 202 IU/L, TOTAL PROTEINS 6.0 gm/dl, ALBUMIN 3.23 gm/dl, A/G RATIO 1.17
COMPLETE URINE EXAMINATION 24/5/25 :COLOUR Pale yellow, APPEARANCE Clear, REACTION Acidic, ALBUMIN+, SUGAR Nil, BILE SALTS Nil, BILE PIGMENTS Nil, PUS CELLS 3- 6, EPITHELIAL CELLS 2-3, RED BLOOD CELLS Nil, CRYSTALS Nil, CASTS Nil, AMORPHOUS DEPOSITS Absent, OTHERS Nil
RFT 24/5/25: UREA 51 mg/dl, CREATININE 1.7 mg/dl, URIC ACID 4.9 mmol/L, CALCIUM 10.0 mg/dl, PHOSPHOROUS 3.87mg/dl, SODIUM 137mmol/L, POTASSIUM4.6mmol/L., CHLORIDE
104 mmol/L
RFT 25/5/25: UREA 50 mg/dl, CREATININE 1.4 mg/dl, URIC ACID 4.3 mmol/L, CALCIUM 10.1 mg/dl, PHOSPHOROUS 4.4mg/dl, SODIUM 135mmol/L, POTASSIUM 4.5mmol/L., CHLORIDE 104
mmol/L
RFT 26/5/25: UREA 42 mg/dl, CREATININE 1.2 mg/dl, URIC ACID 3.9 mmol/L, CALCIUM 10.0 mg/dl,PHOSPHOROUS3.7mg/dl,SODIUM139mmol/L, POTASSIUM 4.1mmol/L, CHLORIDE104
mmol/L
TROPONIN-I ON 24/5/25: 3.4 pg/ml
URINEPROTEIN/CREATININERATIOON25/05/25: SPOT URINE PROTEIN 20mg/dl.,SPOT URINE CREATININE 72 mg/dl, RATIO 0.27
HEMOGRAM ON 24/05/25:- HAEMOGLOBIN 15.9 gm/dl, TOTAL COUNT 11,600 cells/cumm, NEUTROPHILS 88 %, LYMPHOCYTES 06 %, EOSINOPHILS 00 %, MONOCYTES 06%, BASOPHILS 00 %, PCV 43.8 vol %, M C V 90.3 fl ,M C H 32.8 pg ,M C H C 36.3 %, RDW-CV 13.3%, RDW-SD 44.7 fl, RBC COUNT 4.85 millions/cumm, PLATELET COUNT 1.81 lakhs/cu.mm
SMEAR: RBC Normocytic normochromic, WBC increased in count, PLATELETS Adequate in number and distribution, NO HEMOPARASITES, IMPRESSION neutrophilic leukocytosis.
HEMOGRAM ON 25/05/25:- HAEMOGLOBIN 15.4 gm/dl ,TOTAL COUNT 17,900 cells/cumm , LYMPHOCYTES 05 %, EOSINOPHILS 01 %, MONOCYTES 07 %, BASOPHILS 00 %. PCV 44.8 vol%, M C V 95.7 fl, M C H 32.8 pg, M C H C 34.3 %, RDW-CV 13.4 %, RDW-SD 47.2 fl, RBC COUNT 4.6 millions/cumm, PLATELET COUNT 1.5 lakhs/cu.mm, SMEAR, RBC Normocytic normochromic WBC neutrophilic leukocytosis, PLATELETS Adeqaute, NO HEMOPARASITES, IMPRESSION Normocytic normochromic with neutrophilic leukocytosis
HEMOGRAM ON 26/05/25:- HAEMOGLOBIN 14.5 gm/dl, TOTAL COUNT 12,100 cells/cumm NEUTROPHILS 82 %, LYMPHOCYTES 09 %, EOSINOPHILS 02 %, MONOCYTES 07%, BASOPHILS 00 %, PCV 41.5 vol % M C V 94.6 fl , M C H 33.0 pg , M C H C 34.9 % , RDW-CV 13.8%, RDW-SD48.3fl, RBC COUNT 4.39millions/cumm, PLATELETCOUNT 1.57lakhs/cu.mm. SMEAR RBC Normocytic normochromic. WBC increased counts on smear with neutrophilia, PLATELETS Adequate, NO HEMOPARASITES, IMPRESSION Neutrophilic leucocytosis
HEMOGRAM ON 27/05/25:- HAEMOGLOBIN 14.7 gm/dl, TOTAL COUNT 10,800 cells/cumm
NEUTROPHILS 80 %, LYMPHOCYTES 10 %, EOSINOPHILS 02 %, MONOCYTES 08%, BASOPHILS 00 %, PCV 44.1 vol %, M C V 95.5 fl, M C H 31.8 pg, M C H C 33.3 %, RDW-CV 13.5%, RDW-SD46.1 fl, RBC COUNT 4.62millions/cumm, PLATELET COUNT 1.78lakhs/cu.mm. SMEAR RBC Normocytic normochromic. WBC NORMAL, PLATELETS Adequate, NO HEMOPARASITES, IMPRESSION Neutrophilic leucocytosis
HEMOGRAM ON 28/05/25:- HAEMOGLOBIN 14.7 gm/dl, TOTAL COUNT 10,800 cells/cumm
NEUTROPHILS 80 %, LYMPHOCYTES 10 %, EOSINOPHILS 02 %, MONOCYTES 08%, BASOPHILS 00 %, PCV 44.1 vol %, M C V 95.5 fl, M C H 31.8 pg, M C H C 33.3 %, RDW-CV 13.5% RDW-SD 46.1fl, RBC COUNT 4.62millions/cumm, PLATELET COUNT 1.78lakhs/cu.mm. SMEAR RBC Normocytic normochromic. WBC NORMAL, PLATELETS Adequate, NO HEMOPARASITES, IMPRESSION NORMOCYTIC NORMOCHROMIC
HRCT OF CHEST DONE ON 24/5/25: IMPRESSION: LOBAR CONSOLIDATION IN RIGHTLUNG UPPERLOBE(D/D: INFECTIONMOSTLIKELY, ADENOCARCINOMA, LYMPHOMA), SUGGEST SHORT TERM FOLLOW UP CT AFTER 3MONTH TO ASSESS FOR RESOLUTION AND TO EXCLUDE NEOPLASTIC CONSOLIDATION.
2DECHODONEON28/5/25: IMPRESSION: MILDAR, NO PR, TRIVIAL TR, NO PAH, TRIVIAL MR, NO RWMA, NO AS/MS, SCLEROTIC AV, GOOD LV SYSTOLIC FUNCTION, GARADE 1 DIASTOLIC DYSFUNCTION, NO PE/LV CLOT. EF = 64%
Treatment Given (Enter only Generic Name)
INJ.CEFTRIAXONE 1GM IV/BD 12TH HOURLY
INJ.PAN 40 MG IV/OD
INJ.PCM 1GM IV/SOS
INJ.THIAMINE 200MG IV/TID
TAB.PCM 650 MG PO/TID
NEB. WITH DUOLIN AND BUDECORT 8TH HOURLY
Advice at Discharge
TAB.LASIX 20 MG PO/OD FOR 1 WEEK
TAB.NEUROBION FORTE PO/OD FOR 1 WEEK
TAB.MONOCEF CV 200MG PO/BD FOR 3 DAYS
TAB.TELMA 40MG PO/OD 8AM-X-X TO BE CONTINUED
TAB.PAN 40 MG PO/OD BEFORE BREAKFAST FOR 3 DAYS
TAB.PCM 650MG PO/SOS
Follow Up
REVIEW TO GENERAL MEDICINE OPD ON 2/6/25 OR SOS
DischargeDate: 28/05/25 Ward: MMW Unit:1
[06-06-2025 22:58] PPM 3: Based on the provided EMR summary, here is the formatted case report for the 68-year-old male patient:
*CASE REPORT: 68-Year-Old Male with Lobar Pneumonia and Heart Failure*
*1. Patient Demographics*
* *Age/Gender:* 68 Years / Male
* *Admission Date:* 24 May 2025, 14:31
* *Discharge Date:* 28 May 2025
* *Discharge Type:* Relieved
* *Ward/Unit:* MMW / Unit 1
*2. Admission Diagnosis*
* ?Lobar Pneumonia
* ?Loculated Pleural Effusion secondary to Heart Failure
* De novo Hypertension
*3. Presenting Complaints (HOPI)*
* Cough (insidious onset, gradually progressive, non-productive) for 3 days.
* Right-sided chest pain (aggravated by walking/coughing, radiating to back) since night of 23 May 2025.
* Shortness of Breath (Grade 2-3 exertion) since night of 23 May 2025.
* History of fever with chills/rigors 8 days prior (resolved with medication).
*4. Past Medical, Surgical & Personal History*
* *Medical:* Type 2 Diabetes Mellitus, Hypertension, Coronary Artery Disease (CAD), Cerebrovascular Disease (CVD), Asthma, Thyroid disorder. No history of TB or Epilepsy.
* *Surgical:* Ulcer (4 years ago).
* *Personal:*
* Diet: Mixed. Appetite/Bowel/Micturition: Normal.
* *Addictions:*
* Chronic Alcohol: 180ml/day regularly for 30 years. Last intake 1 day prior. Toddy intake 10 days prior.
* Chronic Smoking: 1-2 packs/day for 20 years. Stopped 5 years ago.
* *Family History:* Non-significant.
*5. General Examination (Admission)*
* Vitals: Temp 98.6°F, BP 80/60 mmHg, RR 22/min, PR 96/min, SpO₂ 98% (RA), GRBS 169 mg%.
* General: No pallor, clubbing, icterus, cyanosis, lymphadenopathy, or malnutrition.
*6. Systemic Examination (Admission)*
* *Respiratory System (RS):* Decreased air entry right side. Bronchial breath sounds +. Crepitations + in right infrascapular, interscapular, and axillary areas.
* *Cardiovascular System (CVS):* Normal.
* *Central Nervous System (CNS):* Normal.
* *Abdomen (P/A):* Soft, non-tender, no organomegaly.
*7. Key Investigations*
* *HRCT Chest (24/05):* Right upper lobe consolidation (D/D: Infection most likely, Adenocarcinoma, Lymphoma). Advice: Follow-up CT in 3 months.
* *2D Echo (28/05):* Mild AR, Trivial TR/MR, Sclerotic AV, Good LV systolic function (EF 64%), Grade 1 Diastolic Dysfunction. No RWMA/PAH/Clot.
* *Hemogram (Trend):* Persistent neutrophilic leukocytosis (Peak WBC 17,900 on 25/05), improving by discharge (WBC 10,800 on 28/05). Hb stable ~15 gm/dL.
* *Liver Function (24/05):* Elevated Bilirubin (Total 1.62 mg/dL, Direct 1.16 mg/dL). Normal AST/ALT.
* *Renal Function (Trend):*
* 24/05: Urea 51 mg/dL, Creatinine 1.7 mg/dL
* 26/05: Urea 42 mg/dL, Creatinine 1.2 mg/dL (Improving)
* *Troponin-I (24/05):* 3.4 pg/mL (Mild elevation).
* *Urine Analysis (24/05):* Albumin +, Pus cells 3-6/HPF.
* *Urine Protein/Creatinine Ratio (25/05):* 0.27 (Mild proteinuria).
*8. Pulmonology Referral*
* Advised induced sputum (3% nebulization) & bronchoscopy. Procedure declined by patient's attenders.
*9. Hospital Treatment (Generic Names)*
* *Antibiotic:* Ceftriaxone 1g IV BD.
* *PPI:* Pantoprazole 40mg IV/PO OD.
* *Analgesic/Antipyretic:* Paracetamol 1g IV / 650mg PO SOS/TID.
* *Vitamin:* Thiamine 200mg IV TID.
* *Nebulization:* Duolin + Budesonide 8th hourly.
*10. Discharge Advice (Medications)*
1. Tab. Furosemide 20mg PO OD (1 week).
2. Tab. Neurobion Forte PO OD (1 week).
3. Tab. Cefixime 200mg PO BD (3 days).
4. Tab. Telmisartan 40mg PO OD (8 AM - Continue).
5. Tab. Pantoprazole 40mg PO OD before breakfast (3 days).
6. Tab. Paracetamol 650mg PO SOS.
*11. Follow-Up*
* Review in General Medicine OPD on 02 June 2025 or SOS.
---*Key Clinical Summary:* Elderly male with significant smoking/alcohol history presented with acute respiratory symptoms. Diagnosed with right upper lobe pneumonia (infection likely, neoplasm not excluded) and pleural effusion secondary to newly identified heart failure (preserved EF) and hypertension. Treated with IV antibiotics and supportive care, showing improvement in leukocytosis and renal function. Discharged on oral antibiotics, diuretic, antihypertensive (Telmisartan), and vitamins. Close follow-up and repeat CT in 3 months advised.
[07-06-2025 07:03] PPM 1: 👏👏 excellent. @CR @PPM2 let's reformat all our EMR summaries using this LLM tool
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