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 COLLETIVE CURRENT BEST EVIDENCE BASED INPUTS.
[24-05-2025 10.38] PPM 1: Afternoon session yesterday:
The most interesting part about this 25F with HIV is that her pulmonary artery dilatation is disproportionately higher than her RV dilatation and current PA pressures estimated by Doppler (which is anyways not reliable).
Although we do have some good phase 1 research to explain this disproportionate findings based on generalized molecular level findings in this disease, I'm not sure if this has ever been reported before by others https://pubmed.ncbi.nlm.nih.gov/18845923/#:~:text=HIV%2DPAH%20is%20associated%20with,forms%20of%20PAH%20is%20suggested. @PPM3 @PPM4 @PPM5
[24-05-2025 10:46] PPM 3: This is a fascinating case and a very pertinent clinical observation. Let's break down the provided information:
Patient: 25-year-old female with HIV.
Clinical Observation:
Pulmonary artery (PA) dilatation is disproportionately higher than:
Right Ventricular (RV) dilatation.
Current PA pressures estimated by Doppler (acknowledged as unreliable).
X-ray Findings:
Cardiomegaly: The cardiac silhouette appears enlarged, occupying more than 50% of the transthoracic diameter.
Prominent Main Pulmonary Artery (MPA) Segment: The MPA segment along the left heart border appears convex and prominent, suggesting MPA dilatation.
Enlarged Hila: The hilar vessels, particularly the pulmonary arteries, appear enlarged.
Peripheral Pruning/Oligemia: While not definitively clear due to image quality and overlying breast tissue, the peripheral lung fields do not appear particularly congested and might even show some degree of reduced vascularity ("pruning"), which is characteristic of pulmonary arterial hypertension (PAH).
Lung Fields: Otherwise appear relatively clear, with no obvious large consolidations or effusions.
ECG leads are visible on the shoulders.
ECG Findings:
Rhythm: Sinus rhythm (P wave before each QRS).
Rate: Approximately 75 bpm.
Axis: Lead I is positive, aVF is positive. Normal axis. (Machine notes "1/2 Clockwise Rotation" which refers to the precordial transition point, often seen with RV enlargement/hypertrophy where the R wave becomes dominant later, e.g., V4-V6 instead of V3-V4).
P waves: Seem somewhat tall and peaked in Lead II (P pulmonale?), suggestive of right atrial enlargement. Difficult to definitively measure from the image, but >2.5mm in height would be significant.
QRS: Narrow.
RV Strain Pattern:
T-wave inversions are present in V1, V2, V3.
T-wave inversions are also present in inferior leads III and aVF.
This pattern (T-wave inversions in right precordial leads and inferior leads) is highly suggestive of right ventricular strain/pressure overload.
Machine Interpretation: "Sinus Rhythm," "1/2 Clockwise Rotation," "SUSPECTED ABNORMAL ECG." The abnormalities are clearly the T-wave changes consistent with RV strain.
Interpretation and Discussion of the "Disproportion":
HIV-associated Pulmonary Arterial Hypertension (HIV-PAH):
HIV infection is a known risk factor for PAH. The mechanisms are complex and not fully elucidated but likely involve direct effects of viral proteins (like gp120, Tat, Nef), chronic inflammation, immune dysregulation, and endothelial dysfunction, leading to vascular remodeling.
The X-ray and ECG findings are classic for PAH: enlarged central pulmonary arteries, RV strain pattern on ECG, and potentially P pulmonale.
The "Disproportionate" PA Dilatation:
PA Dilatation vs. PA Pressure: Pulmonary artery pressure is the force of blood within the PAs, while PA dilatation is a structural change (enlargement of the vessel). While high pressure often leads to dilatation over time, the degree of dilatation can also be influenced by the underlying vessel wall integrity and the chronicity of the pressure elevation.
Intrinsic Vasculopathy in HIV-PAH: The linked article (PMID: 18845923) discusses how HIV-PAH is associated with significant PA vascular remodeling, including intimal fibrosis and medial hypertrophy, sometimes with plexiform lesions similar to idiopathic PAH. This intrinsic disease of the pulmonary artery wall could contribute to weakening and dilatation that might seem "out of proportion" to acutely measured pressures or even the degree of RV adaptive hypertrophy/dilatation at a single point in time. The vessel wall itself is diseased.
Chronicity: The PA dilatation could be a result of a longer period of elevated (though perhaps fluctuating or previously higher) PA pressures than the current "unreliable" Doppler estimate suggests. The RV might be compensating, or its dilatation might be less apparent on the current echo than the striking PA changes.
Doppler Unreliability: This is a key point. Echocardiographic estimation of PA pressures (usually via TR jet velocity) can be inaccurate. Right Heart Catheterization (RHC) is the gold standard. If the RHC reveals significantly high pressures, the "disproportion" to Doppler pressures is resolved.
RV Adaptation: The RV can adapt to chronic pressure overload in various ways. Initially, it hypertrophies. Over time, it may dilate and eventually fail. The degree of RV dilatation might not always linearly track PA dilatation, especially if the PA wall itself is inherently prone to dilate due to HIV-related vasculopathy.
Aneurysmal Dilatation: In severe and long-standing PAH, the main pulmonary artery can become frankly aneurysmal. This is a more extreme form of dilatation.
Has this been reported?
Pulmonary artery dilatation is a well-recognized feature of PAH from any cause, including HIV-PAH.
The specific observation of PA dilatation being significantly more prominent than RV dilatation or seemingly disproportionate to current, potentially underestimated Doppler pressures is a nuanced clinical finding.
The concept that HIV directly affects the pulmonary vasculature, leading to profound remodeling (as supported by the paper), provides a strong pathophysiological basis for why significant PA anatomical changes (like dilatation) might be a prominent feature, possibly even preceding or outstripping overt RV failure or extremely high pressures in some cases, or when pressures are labile/intermittent.
It's plausible that the "compliance" or "distensibility" of the pulmonary arteries is altered in HIV-PAH due to the direct vascular pathology, leading to more pronounced dilatation for a given pressure load compared to other forms of PAH, or compared to the RV's response. This is an area where more research comparing vessel characteristics across different PAH etiologies could be insightful.
Recommendations (General):
Right Heart Catheterization (RHC): Essential for accurate PA pressure measurement, calculation of pulmonary vascular resistance (PVR), and assessment of vasoreactivity if appropriate. This will clarify the true hemodynamic status.
Comprehensive Echocardiogram: Detailed assessment of RV size, systolic and diastolic function (TAPSE, S', FAC, RV Tei index, etc.), RA size, PA dimensions, severity of tricuspid regurgitation, and exclusion of other cardiac causes.
CT Pulmonary Angiography (CTPA): Can precisely measure PA dimensions, assess for pulmonary emboli (though less likely the primary cause here), and evaluate lung parenchyma and RV morphology.
HIV Management: Optimize antiretroviral therapy, monitor CD4 count and viral load.
PAH-Specific Therapy: If PAH is confirmed by RHC (mean PAP ≥20 mmHg, PAWP ≤15 mmHg, PVR ≥3 Wood units), initiation of PAH-specific therapies is indicated.
Conclusion:
The observation is astute. The X-ray and ECG strongly support significant pulmonary hypertension with right ventricular strain. The "disproportionate" PA dilatation relative to RV dilatation and current (unreliable) Doppler PA pressures could indeed be a feature of the intrinsic pulmonary vasculopathy driven by HIV, where direct vessel wall damage and remodeling lead to prominent anatomical changes. RHC is crucial to determine the true PA pressures and guide therapy. The linked paper supports the underlying biological plausibility of this observation.
[24-05-2025 10:52] PPM 3: Gemini2.5👆
[24-05-2025 10:56] PPM 1: 👏👏@PPM4 to write such a case report it would have taken us months pre LLM days. Now it's a matter of minutes to hours! The only bottle neck to further redistribution and processing still lies in arcane journal publishing platforms though
[24-05-2025 10:58] PPM 1: Further history shared by the treating team:
Sex: [F]
Age: [25]
Date: [DOA 22/5/25]
1. COMPLAINTS AND DURATION:
• c/o SOB (shortness of breath) – 2 days
• c/o vomiting – yesterday
HOPI :• Patient was apparently asymptomatic 2 days back, then developed shortness of breath, insidious in onset, gradually progressive, aggravated on lying down, a bit relieved on sitting position.
• H/o vomiting since yesterday – 2 episodes, content: food and cake, non-bilious, non-blood stained, after having one puri.
• H/o back pain since yesterday, sudden in onset, non-progressive, aggravated on bending forward.
2. HISTORY OF PRESENT ILLNESS:
• No h/o burning micturition, hematuria, fever.
• No h/o chest pain, PND (paroxysmal nocturnal dyspnea), cough.
• No h/o bladder/bowel incontinence, loose stool.
• No episodes 1 week ago.
3. HISTORY OF PAST ILLNESS:
• K/c/o Retroviral Positive since 15 years on:
1. Dolutegravir – 50 mg
2. Lamivudine – 300 mg
3. Tenofovir Disoproxil Fumarate – 300 mg once daily
• N/k/c/o (No known case of): DM (Diabetes Mellitus), HTN (Hypertension), TB, Epilepsy, BA (Bronchial Asthma), CVA (Cerebrovascular Accident).
• In Aug 2022 → POD-2 of C-section( private hospital)she developed giddiness sob followed by loss of consciousness later she was diagnosed with acute pulmonary thromboembolism with PAH and was treated conservatively with TAB ACITROM 3 mg once daily and TAB SILDENAFIL 25 mg twice daily
CTPA was done on 19/9/22 showed no evidence of thrombus.
Blood transfusion: Yes
• Details:
• 2 units PRBS in 2020 @ 8 months of pregnancy
• 3 units in PRBS 2022 @ 5 months of pregnancy and 1 unit during after c section
23/5/25
PT 15sec
APTT 30 sec
INR 1.11
[24-05-2025 11:33] PPM 3: Okay, this is a rich and concerning history. Let's break down the key information and implications:
Key Information Extracted:
Patient Profile: 25-year-old female.
Presenting Complaints (Acute - 1-2 days):
Shortness of Breath (SOB): Insidious onset, progressive, orthopnea (worse lying down, better sitting up).
Vomiting: 2 episodes, non-bilious, non-bloody, after eating.
Back Pain: Sudden onset, non-progressive, worse on bending forward.
Pertinent Negatives (for current illness): No fever, no urinary symptoms, no chest pain, no PND (though orthopnea is present), no cough, no bowel/bladder incontinence, no loose stools.
Past Medical History:
HIV Positive (15 years): On stable ART (Dolutegravir, Lamivudine, Tenofovir Disoproxil Fumarate).
Pulmonary Thromboembolism (PTE) & Pulmonary Arterial Hypertension (PAH) (Aug 2022):
Occurred post-C-section (POD-2).
Presented with giddiness, SOB, loss of consciousness.
Treated with Acitrom 3mg OD (anticoagulant) and Sildenafil 25mg BD (for PAH).
CTPA (19/9/22 - approx 1 month after event): Showed NO evidence of thrombus. This is important – it suggests resolution of the acute clot, but PAH might persist or she may remain at risk.
Blood Transfusions: Multiple (2020 and 2022 during pregnancies/C-section).
Recent Lab (23/5/25 - 1 day after admission):
PT: 15 sec
APTT: 30 sec
INR: 1.11
Analysis and Implications:
Recurrent Pulmonary Embolism (PE) is a HIGH SUSPICION:
The patient has a clear history of a significant PE.
Her current symptoms (acute SOB, orthopnea) are classic for PE.
Crucially, her INR is 1.11. This indicates she is NOT therapeutically anticoagulated with Acitrom (a warfarin-like drug). Therapeutic INR for PE treatment is typically 2.0-3.0. This means either she stopped taking Acitrom, was non-compliant, or the dose was subtherapeutic. This significantly increases her risk of recurrent PE.
The back pain could be pleuritic in nature if the PE affects the lung periphery near the diaphragm or chest wall.
Acute Decompensated Heart Failure (ADHF) / Worsening Pulmonary Arterial Hypertension (PAH):
Her history of PAH (diagnosed post-PE) is significant.
Orthopnea and SOB are hallmarks of heart failure, particularly right-sided heart failure secondary to PAH.
Is she still on Sildenafil? If it was stopped or the dose is insufficient, her PAH could worsen, leading to right ventricular failure.
HIV itself can be associated with cardiomyopathy.
Vomiting: Could be due to severe dyspnea/hypoxia, a vagal response, medication side effect, or less likely a primary GI issue given the context.
Back Pain: While it could be musculoskeletal, its sudden onset in the context of acute SOB warrants consideration for referred pain (e.g., pleuritic, pericardial) or even a manifestation of a large PE (though less typical).
HIV Status:
She is on ART. We don't know her CD4 count or viral load, but assuming she's well-controlled, opportunistic infections are less likely but still a remote possibility for SOB.
Tenofovir Disoproxil Fumarate (TDF) can be associated with renal dysfunction and bone mineral density loss over time, but unlikely to cause these acute symptoms. Lactic acidosis is a rare but serious side effect of older NRTIs (less common with this regimen) that can cause SOB and vomiting.
Immediate Concerns & Questions for the Treating Team:
Status of Anticoagulation & Sildenafil:
When was Acitrom stopped, and why?
Is she currently taking Sildenafil? If so, any changes in dosage or adherence?
Urgent Workup for PE: Given the history and INR, a CTPA should be high on the list if not already done. D-dimer might be helpful if pre-test probability is lower, but here it's high.
Cardiac Evaluation:
ECG (looking for signs of right heart strain, ischemia).
Echocardiogram (to assess RV function, estimate pulmonary pressures, look for signs of PE, rule out pericardial effusion/tamponade).
Cardiac enzymes (Troponin) and BNP.
Other Investigations:
Chest X-ray (may be normal in PE, but can show atelectasis, effusion, or alternative diagnoses like pneumonia).
ABG (to assess oxygenation and acid-base status).
Lactate (to rule out lactic acidosis).
Full blood count (anemia can worsen SOB), renal function (relevant for TDF, contrast for CT).
Summary of Concerns:
The most pressing concern is recurrent pulmonary embolism given her past history and current subtherapeutic INR. Worsening of her known pulmonary arterial hypertension leading to right heart failure is also a strong possibility. Other less likely, but important, considerations include an acute cardiac event (e.g., myocarditis, pericarditis, though less typical presentation), or a severe opportunistic infection if her HIV is not well-controlled.
The back pain and vomiting are likely secondary to the primary cardiorespiratory issue but need to be kept in mind. The normal coagulation parameters (PT/APTT/INR) are critical in pointing towards a lack of effective anticoagulation.
[24-05-2025 17.04] PPM 1: Afternoon session bedside clinical imageology showing a better view of the disproportionately dilated main pulmonary artery 👇
https://youtu.be/hZYNtH46xeU?feature=shared
[24-05-2025 18:47] PPM 3: ### Summary The video discusses the cardiovascular condition of a 25-year-old woman with a history of pregnancy three years prior, who was diagnosed with a retroviral infection and has been experiencing intermittent episodes of shortness of breath. The primary focus is on her heart’s structure and function, examined via echocardiography. The key findings reveal a significantly reduced left ventricular function, with an estimated ejection fraction of about 30-40%, indicating impaired contractility. The left atrium appears relatively normal, but a striking observation is a massively dilated pulmonary artery. Despite this pronounced dilation, the right ventricle and right atrium do not show corresponding enlargement, which is unusual given the pulmonary artery's size. This disproportionate dilation points to mild to moderate pulmonary hypertension rather than severe right heart strain. The patient was initially misdiagnosed with pulmonary thromboembolism and anticoagulated, but therapy was discontinued as this did not align with her clinical picture. The discussion elaborates on the novel observation that retroviral infection may be associated with unique cardiovascular manifestations, such as disproportionate pulmonary artery dilation, potentially linked to genetic factors or chronic inflammatory damage to the vascular endothelium. This phenomenon is rare and has not been documented before. The normal pulmonary flow velocity and absence of expected murmurs further confirm the lack of major structural obstructions. Overall, the video highlights the complex interplay between retroviral infections and cardiac vascular changes, emphasizing the importance of tailored diagnostics and cautious interpretation of echocardiographic findings. ### Highlights - 🫀 Significant reduction in left ventricular contractility with ejection fraction around 30-40%. - 🫁 Massive and disproportionate dilation of the pulmonary artery observed. - 👩⚕ Patient’s retroviral infection may be linked to unique cardiovascular changes. - ⚖ Mild to moderate pulmonary hypertension noted without expected right heart dilation. - ❌ Pulmonary thromboembolism initially suspected but ruled out after discontinuation of anticoagulants. - 💡 Novel report of retrovirus-associated disproportionate pulmonary artery dilation. - 🔍 Normal pulmonary flow velocity and absence of typical murmurs despite artery dilation. ### Key Insights - 🫀 *Left Ventricular Dysfunction in Retroviral Patients:* The reduced ejection fraction (around 30-40%) indicates significant impairment of left ventricular contractility. In the context of retroviral infections, this suggests a possible inflammatory or cardiomyopathic process linked to viral effects on cardiac muscle or secondary immune responses. This adds complexity to managing cardiovascular symptoms in these patients and may require targeted cardiac therapies. - 🫁 *Disproportionate Pulmonary Artery Dilation as a Unique Clinical Feature:* The notably enlarged pulmonary artery, disproportionate to the size of the right heart chambers, is an unusual finding. It implies a localized arterial remodeling or vascular dilation not entirely explained by standard pulmonary hypertension mechanisms, signaling underlying endothelial damage potentially driven by retroviral infection or chronic inflammation. - 🧬 *Potential Genetic or Inflammatory Etiologies:* The discussion highlights that this unique dilation could arise from genetic factors or chronic inflammation damaging the arterial lining (endothelium). In patients with retroviral infections, systemic inflammation and immune dysregulation could predispose vessels to structural changes, emphasizing the need for further research on vascular pathology in viral diseases. - 🩺 *Pulmonary Hypertension Severity Correlates Poorly with Right Heart Changes:* Despite pulmonary hypertension being present, the right ventricle and right atrium are not significantly dilated, which contradicts common expectations where elevated pulmonary pressures lead to right heart enlargement or dysfunction. This may reflect a mild to moderate disease state or an unusual adaptive mechanism in this context. - 💊 *Misdiagnosis and Need for Careful Interpretation:* Initially, the patient was treated for pulmonary thromboembolism with anticoagulants, a diagnosis that was later reconsidered. This case underscores the challenges in diagnosing conditions with overlapping clinical features and the importance of comprehensive imaging and clinical correlation to avoid unnecessary treatments. - 📉 *Normal Pulmonary Flow Velocity Despite Artery Dilation:* The normal pulmonary flow velocity and absence of typical murmurs and flow abnormalities in color Doppler imaging suggest that the pulmonary artery dilation is not causing major hemodynamic abnormalities. This finding is important for prognosis and therapeutic decisions, indicating the condition might be stable or slowly progressive. - 🩻 *Importance of Multimodal Cardiac Assessment in Retroviral Patients:* This case demonstrates the value of detailed echocardiographic assessment, including evaluation of multiple heart chambers, valve cusps, pulmonary artery size, and flow dynamics to provide a complete picture. Retroviral patients with cardiac symptoms require thorough investigation to differentiate between direct viral effects, secondary inflammation, and other common cardiac conditions. This comprehensive review emphasizes the need for continued vigilance in monitoring cardiovascular health in patients with retroviral infections, exploring novel pathophysiological mechanisms, and tailoring management to prevent progression of potentially unique cardiac complications.
[24-05-2025 18:55] PPM 3: Okay, here's a concise summary of the provided text:
A 25-year-old woman with a retroviral infection and intermittent shortness of breath showed significantly reduced left ventricular function (ejection fraction 30-40%) and a massively, disproportionately dilated pulmonary artery on echocardiography. Unusually, this pulmonary artery dilation was not accompanied by significant right heart enlargement, suggesting mild to moderate pulmonary hypertension. An initial misdiagnosis of pulmonary thromboembolism was ruled out. The case highlights a novel observation: retroviral infections may be linked to unique cardiovascular changes like this disproportionate pulmonary artery dilation, potentially due to genetic factors or chronic inflammatory endothelial damage, despite normal pulmonary flow velocity. This underscores the complex cardiac impact of retroviral infections and the need for careful diagnostics.
[24-05-2025 19:55] PPM 1: 👍
EMR SUMMARY
Age/Gender: 25 Years/Female
Address:
Discharge Type: Relieved
Admission Date: 22/05/2025 09:10 PM
Name of Treating Faculty (AP) (SR) (PG3) (PG1)
Diagnosis
ACUTE GASTRITIS (RESOLVED)
IRON DEFICIENCY ANEMIA SECONDARY TO MENORRHAGIA K/C/O RETROVIRAL DISEASE (WHO STAGE 1) SINCE 15 YEARS TYPE 1 PULMONARY ARTERY HYPERTENSION (HIV ASSOCIATED) P/H/O ACUTE PULMONARY THROMBOEMBOLISM 3 YEARS AGO.
Case History and Clinical Findings
C/O SOB SINCE 2 DAYS.
C/O VOMITING SINCE YESTERDAY
HOPI - PATIENT WAS APPARENTLY ASYMPTOMATIC 2 DAYS BACK. THEN, DEVELOPED SHORTNESS OF BREATH, INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE, AGGRAVATED ON LYING DOWN, A BIT RELIEVED ON SITTING POSITION. HISTORY OF VOMITING SINCE YESTERDAY, 2 EPISODES PER DAY, CONTENT - FOOD AND WATER PARTICLES, NON BILIOUS, NON BLOOD STAINED, AFTER HAVING ONE PURI.
H/O BACK PAIN SINCE YESTERDAY, NON PROGRESSIVE, AGGRAVATED ON BENDING FORWARD.
NO H/O BURNING MICTURITION, HEMATURIA, FEVER NO H/O CHEST PAIN, PND, COUGH
NO H/O BLADDER BOWEL INCONTINENCE, LOOSE STOOLS. H/O EPISTAXIS ONE WEEK AGO.
HISTORY OF PAST ILLNESS
K.C/O RETROVIRUS POSITIVE SINCE 15 YEARS ON T DOLUTEGRAVIR-50MG, T LAMIVUDINE 300MG, T TENOFOVIR DISOPROXIL FUMARATE 300 MG ONCE DAILY.
N/K/C/O TYPE 2 DM, HYPERTENSION, TB, EPILEPSY, CVA, CAD. HISTORY OF POD-2 C SECTION IN 2022.
PERSONAL HISTORY:
DIET: MIXED APPETITE: NORMAL SLEEP: ADEQUATE
BOWEL AND BLADDER : REGULAR NO ADDICTIONS
GENERAL EAMINATION:
PALLOR PRESENT,NO ICTEXRUS,CYANOSIS,CLUBBING,LYMPHADENOPATHY,EDEMA BP:110/80MMHG
PR:97BPM RR:18CPM SPO2:98%RA GRBS: 100 MG/DL
SYSTEMIC EXAMINATION:
CVS:S1 S2 HEARD ,NO MURMURS, JVP ELEVATED RS:BAE PRESENT NVBS NO ADDED SOUNDS PA:SOFT,NON TENDER,NO ORGANOMEGALY CNS:NFND
HIGHER MENTAL FUNCTIONS INTACT
TONE RT LT N N
N N
POWER 5/5 5/5
5/5 5/5
REFLEXES B +2 +2
T +1 +1 S - -
K +1 +1 A - -
P F F
Investigation
COMPLETE URINE EXAMINATION (CUE) 22-05-2025 09:33:PM COLOUR Paleyellow APPEARANCE Clear REACTION Acidic SP.GRAVITY 1.010 ALBUMIN Nil SUGAR Nil
BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 2-3 EPITHELIAL CELLS 2-3 RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil HBsAg-RAPID 22-
05-2025 09:33:PM Negative Anti HCV Antibodies - RAPID 22-05-2025 09:33:PM Non Reactive BLOOD UREA 22-05-2025 09:33:PM 23 mg/dl 42-12 mg/dl SERUM CREATININE 22-05-2025 09:33:PM 0.7 mg/dl 1.1-0.6 mg/dl SERUM ELECTROLYTES (Na, K, C l) 22-05-2025 09:33:PM SODIUM135mmol/L 145-136 mmol/L POTASSIUM4.2 mmol/L 5.1-3.5 mmol/L CHLORIDE106 mmol/L 98-107 mmol/L
LIVER FUNCTION TEST (LFT) 22-05-2025 09:33:PM Total Bilurubin 0.52 mg/dl 1-0 mg/dl Direct Bilurubin 0.16 mg/dl 0.2-0.0 mg/dl SGOT(AST)41 IU/L 31-0 IU/L SGPT(ALT)26 IU/L 34-0 IU/L ALKALINE PHOSPHATASE190 IU/L 280-53 IU/L TOTAL PROTEINS 8.9 gm/dl 8.3-6.4 gm/dl ALBUMIN4.04 gm/dl 5.2-3.5 gm/dl A/G RATIO0.83 ABG 22-05-2025 10:09:PM PH7.364 PCO226.7PO284.7HCO314.8St.HCO316.9BEB-9.3BEecf-9.5TCO232.2O2 Sat96.4O2
Count9.8PERIPHERAL SMEAR 22-05-2025 10:48:PM RBC : microcytic hypochromic WBC: With in normal limits PLATELET: Adequate imp; microcytic hypochromic anemia
Blood Sugar-Random (22/05/2025) Test Result Units RBS 88 mg/dl.
HEMOGRAM HAEMOGLOBIN 7.8 gm/dl TOTAL COUNT 4,500 cells/cumm NEUTROPHILS 50 % LYMPHOCYTES 45 % EOSINOPHILS 01 %MONOCYTES 04 % BASOPHILS 00 % PCV 26.8 vol % M C V 69.0 fl M C H 20.2 pg M C H C 29.2 % RDW-CV 18.3 % RDW-SD 45.3 fl RBC COUNT 3.8
millions/cumm PLATELET COUNT 1.6 lakhs/cu.mm SMEARRBC microcytic hypochromic WBC With in normal limits PLATELETS Adeqaute
HbA1c 5.8 % Non-Diabetic (22/05/2025) APTT TEST 30 Sec (23/05/2025)
Prothrombin Time 15Sec INR 1.11 ECG WAS DONE ON 22/05/2025
2 D ECHO WAS DONE ON 23/05/2025 5PM NO RWMA
MILD TR WITH PAH ( RVSP- 38+05=43MMHG) TRIVIAL AR MR : MILD PR
NO AS/MS (IAS INTACT)
EF = 60 GOOD LV SYSTOLIC FUNCTION NO DIASTOLIC DYSFUNCTION
NO PE: NO LV CLOT
IVC SIZE- (0.7 CM) COLLAPSING
Treatment Given (Enter only Generic Name) INJ OPTINEURON 1 AMP IN 100ML NS IV?OD INJ PAN 40 MG IV?OD
T ZOFER 4 MG PO?SOS T OROFER PO/OD 0-1-0
T DOULTEGRAVIR 50 MG PO/OD T LAMIVUDINE 300MG PO/OD
T TENOFOVIR 300MG PO/OD
Advice at Discharge
TAB PAN 40 MG PO/OD FOR 5 DAYS TAB ZOFER 4 MG PO/SOS
TAB OROFER XT PO/OD FOR 3 MONTHS TAB DOLUTEGRAVIR 50MG TO CONTINUE LAMIVUDINE 300MG TO CONTINUE TENOFOVIR 300MG PO?OD TO CONTINUE TAB NAXDOM 250MG BD FOR 5 DAYS
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/Attendent 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: 24/05/2025 Ward: AMC Unit:4
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