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.
[14-10-2025 16.57] PPM 1: 
[14-10-2025 21.41] PPM 3: Immediate interpretation of the troponin result
[15-10-2025 16.36] PPM 1: This is the previous. None repeated after this?
@Meta AI@PPM3 how do we explain the high total proteins of 9.5 and albumin of 5.7 in this LFT report along with the high alkaline phosphatase of 368 and unconjugated hyperbilirubinemia of 2.11?
Today's notes
[17-10-2025 15.40] PPM 1: The U wave looks even more prominent by the day! What would be your opinion on the serial ECGs since admission focused on the U wave? @PPM3
Serial ECGs
Today's chest X-ray
Yesterday's cardiac wall motion
Today's cardiac wall motion
[14-10-2025 18.51] PPM 1: 👆@PPM3 any inputs on his serial ECG findings.
Are those prominent U waves in the chest leads a marker of coronary ischemia?
[14-10-2025 20.27] PPM 3: Great observation, PPM3. Prominent U waves—especially when serially evident in the precordial leads—can indeed raise concern, but their interpretation hinges on context. Here's a breakdown:🧠 Understanding U Waves
- Normal U waves are small deflections following the T wave, best seen in V2–V3.
- Prominent U waves (>1–2 mm or >25% of T wave amplitude) may signal pathology.
⚠️ Causes of Prominent U Waves
Most commonly associated with:
- Hypokalemia 🧂
- Bradycardia
- Antiarrhythmic drugs (e.g., amiodarone, sotalol)
- LVH or hypertrophic cardiomyopathy
- Digoxin effect
- Hypothermia, hypocalcemia, hypomagnesemia
🔍 U Waves and Ischemia
- Inverted U waves—especially in the same leads as upright T waves—are highly specific for myocardial ischemia and may precede other ischemic changes.
- Prominent upright U waves are less specific but have been described in ischemic settings, particularly when accompanied by:
- QT prolongation
- T wave abnormalities
- Symptoms or troponin elevation
🩺 Clinical Implication
If these U waves are new, persistent, and correlate with symptoms or troponin rise, they could reflect subendocardial ischemia or repolarization abnormalities. Serial ECGs showing dynamic changes (e.g., evolving T/U morphology) strengthen the ischemic suspicion.
Would you like to correlate this with labs or echo findings? Or perhaps build a teaching slide on U wave interpretation for your CME module?
Copilot 👆
Good question — let’s break this down carefully based on what’s visible in your uploaded ECG.
---
🩺 ECG Observation (visually):
Rhythm appears sinus (P waves seen before QRS).
Rate: around 70–80 bpm.
QT interval seems prolonged (visually > 440 ms, may reach 480–500 ms).
Prominent positive deflection after T waves is indeed present in several precordial leads (V2–V5) — these are U waves.
No clear ST elevation or depression typical of acute ischemia.
No significant T-wave inversion or Q waves noted.
---
⚙️ Possible Causes of Prominent U Waves:
Cause Mechanism / Comment
Hypokalemia Most common cause — often with prolonged QT, flattened T waves, and prominent U waves (best in V2–V4).
Bradycardia Slower heart rates enhance U-wave visibility.
Drugs Especially antiarrhythmics (class Ia, III), phenothiazines, tricyclics.
Hypocalcemia / Hypomagnesemia Can contribute along with K⁺ loss.
Left ventricular hypertrophy May exaggerate repolarization abnormalities.
Ischemia Rarely causes isolated prominent U waves; more typically, ischemic U waves are inverted in the same leads where T waves are upright.
---
🧠 Interpretation in This Context:
The U waves in your ECG appear upright, not inverted.
Upright, prominent U waves + prolonged QTc → strongly favors electrolyte imbalance (especially hypokalemia) rather than ischemia.
Ischemic U waves are usually inverted in the precordial leads (especially V2–V4) and appear after episodes of angina or during acute ischemia.
---
🧪 Next Steps to Correlate Clinically:
1. Check serum electrolytes: K⁺, Mg²⁺, Ca²⁺.
2. Review medications: especially diuretics, beta-agonists, or digitalis.
3. Assess for bradycardia, hypotension, or recent ischemic symptoms.
4. If the patient is on metoprolol and had recent hypotension, consider whether renal hypoperfusion or diuretics could have caused electrolyte depletion.
---
✅ Summary Answer:
> The prominent U waves in this ECG are unlikely to be markers of coronary ischemia.
They are more consistent with hypokalemia and/or prolonged repolarization (QT prolongation) — possibly medication or metabolic related.
---
If you have the serum potassium value from the same day or a prior ECG for comparison, I can comment on whether this is a new repolarization change or chronic. Would you like to post the previous ECG too?
ChatGPT 👆
[14-10-2025 21.12] PPM 1: Thanks @PPM4 @PPM5 please share his troponin report. Thanks. We have already shared all his serial ECGs since admission also available in the case report link in the description box here.
@PPM4 @PPM5 please share his serial potassium since admission
- Troponin I 0.90 ng/ml with a reference range 0.00–0.04 ng/ml is a marked elevation and indicates acute myocardial injury rather than a normal variant.
- When combined with a suspicious ECG (new or dynamic changes) and compatible symptoms, this level strongly supports acute coronary syndrome with myocardial necrosis (most likely NSTEMI if there is no ST elevation on ECG).
---
Likely clinical causes to prioritise
- Acute coronary ischemia / NSTEMI — most likely given significant troponin rise.
- Other important non-ACS causes that can raise troponin and should be considered clinically: myocarditis, heart failure or cardiomyopathy, blunt cardiac injury, severe pulmonary embolism, renal failure, sepsis, and cardiotoxic drugs.
---
Urgent next steps at the bedside and in-hospital
1. Treat as ACS until proven otherwise: implement local ACS pathway and activate cardiology.
2. Serial 12‑lead ECGs every 15–30 minutes while symptomatic and then at regular intervals to detect dynamic changes.
3. Repeat troponin in 3–6 hours to demonstrate rise or fall and help distinguish acute from chronic elevation.
4. Assess haemodynamics and symptoms: pain, dyspnoea, arrhythmia, hypotension — manage accordingly.
5. Obtain urgent transthoracic echocardiogram to look for new regional wall motion abnormalities.
6. Basic investigations: CBC, electrolytes (K, Mg, Ca), renal function, coagulation, chest X‑ray, and oxygen saturation.
7. Start guideline-directed initial therapy per your institutional ACS protocol (analgesia, anti-ischaemic measures, antiplatelet and anticoagulation as indicated) and prepare for coronary angiography if high-risk features present.
---
How the ECG U waves fit with this troponin result
- Prominent upright U waves alone are not a specific marker of ischemia, but inverted U waves or evolving repolarization changes together with elevated troponin increase the likelihood of myocardial ischemia.
- With troponin 0.90 ng/ml, even nonspecific ECG abnormalities merit high suspicion for ischemia; dynamic ECG changes or new T wave/U wave inversion would strengthen the diagnosis of myocardial ischemia.
---
Practical pearls for diagnosis and disposition
- A single elevated troponin confirms myocardial injury; serial delta values distinguish acute from chronic elevations and help risk-stratify.
- If clinical picture, ECG and rising troponin align with ACS, urgent cardiology review and consideration for invasive angiography are appropriate.
- If alternative causes (e.g., renal failure, sepsis) are suspected, manage the underlying condition while still treating for possible ACS until ruled out.
---
If you want, I will draft a one-slide CME summary for ward staff showing: key troponin interpretation points, ECG features that raise suspicion, and a 6-step immediate management checklist.
[14-10-2025 21.48] PPM 1: Thanks
Please comment on his serial ECG changes that are dated from 12/10/25 and multiple times today's
[14-10-2025 22.07] PPM 3: Overall impression of the serial ECGs
- Rhythm: Sinus tachycardia at ~120 bpm as annotated and visible across the strips.
- Conduction: No obvious high-degree AV block; QRS widths appear narrow consistent with supraventricular origin.
- Repolarisation changes: ST elevation in aVR and V1 with widespread ST depressions (noted on the printout) — pattern suspicious for left main or proximal multivessel ischaemia / global subendocardial ischaemia or severe proximal LAD territory compromise.
- U waves: Prominent U waves are present in the precordial leads on some tracings; upright prominent U waves are nonspecific and often reflect electrolyte disturbance or repolarisation abnormality rather than a standalone marker of coronary occlusion.
- Context: Markedly elevated troponin I 0.90 ng/ml confirms myocardial injury and makes an ischaemic cause the leading diagnosis.
---
Features that raise urgency
- ST elevation in aVR with diffuse ST depression is a high‑risk ECG pattern that often indicates severe ischaemia and mandates urgent cardiology assessment.
- Sinus tachycardia 120 bpm may reflect pain, haemodynamic stress, ongoing ischaemia, hypovolaemia, or sympathetic response and increases myocardial oxygen demand.
- Elevated troponin demonstrates myocardial necrosis; combined with high‑risk ECG changes this shifts management toward invasive evaluation.
---
Differential diagnosis to consider now
- Acute coronary syndrome (NSTEMI or left main/proximal severe CAD) — most likely given ECG pattern and troponin rise.
- Diffuse subendocardial ischaemia from severe anaemia, hypotension, or global hypoperfusion.
- Severe multivessel CAD or proximal LAD disease producing aVR elevation and widespread depression.
- Non‑ischaemic causes of troponin rise (myocarditis, PE, sepsis, renal failure) are possible but less likely with this ECG pattern.
---
Immediate actions recommended at bedside
1. Activate local ACS pathway and call cardiology for urgent review and likely coronary angiography.
2. Continuous cardiac monitoring and repeat 12‑lead ECGs every 15–30 minutes while symptomatic.
3. Repeat troponin after 3–6 hours to document rise or fall and to guide timing of intervention.
4. Initial medical therapy per protocol: aspirin, P2Y12 agent as indicated, anticoagulation per guideline, nitrates for pain if not hypotensive, beta‑blocker only if no contraindication and haemodynamically stable.
5. Correct reversible contributors: check and urgently correct serum potassium and magnesium; treat hypoxia and optimise haemodynamics.
6. Obtain urgent transthoracic echocardiogram to look for regional wall motion abnormality and assess LV function.
7. Prepare for urgent angiography if cardiology agrees or if patient shows ongoing ischaemia, haemodynamic instability, or high‑risk features.
---
Practical points about the U waves seen
- Prominent upright U waves in precordial leads are most often due to hypokalaemia, drugs, or repolarisation abnormalities and are not specific for ischaemia.
- Inverted U waves (not described here) would be more specific for ischaemia.
- Given the troponin elevation and high‑risk ECG pattern, do not dismiss the U waves as benign; check serum potassium and magnesium urgently and treat abnormalities.
---
Short checklist for next 60 minutes
- Continuous monitor, IV access, oxygen if SpO2 <94%
- Give aspirin immediately if not given; consider P2Y12 and anticoagulation per protocol
- Draw urgent labs: repeat troponin, K, Mg, creatinine, CBC, ABG if indicated
- Repeat 12‑lead ECG and call cardiology for urgent angiography decision
- Bedside echo and haemodynamic stabilization
If you want, I will draft a one‑slide rapid handout for the team summarising the ECG red flags, immediate bedside checklist, and recommended lab targets (K, Mg) for rapid posting on the ward.
[14-10-2025 22.11] PPM 1: Scholar GPT?[14-10-2025 22.14] PPM 3: Copilot
[15-10-2025 07.38] PPM 5: 12/10/25 -K+ - 3.8 mmol/L
13/10/25 - k+ -3.9mmol/L
14/10/25-K+ -3.6mmol/L
[15-10-2025 08.05] PPM 1: Thanks.
[15-10-2025 15.53] PPM 1: Today's update:
Day 4
No further episode of chest pain today
Vomiting 1
Loose stools 2
Day 3
Loose stools 5
Vomiting 1
Day 2
Loose stools 9
Vomiting 1
Day 1
Loose stools 30
Vomiting 30
[15-10-2025 15.54] PPM 2: Thanks for sharing. Strongly appears like Leptospirosis/ Spirochaetal infection. Isn't ORS 5 sachets in 1L of water?
[15-10-2025 16.09] PPM 1: Possible! I now recall publishing something similar earlier although this current patient's chest pain was quite dramatic and climaxed after he vomited on my feet while i was doing his echo by the bedside!Past patient just had raised cardiac enzymes alone 👇
[15-10-2025 16.15] PPM 2: Hopefully it wasn't central vomiting? Interesting he also had raised bilirubin initially. If viral, then Hep A?[15-10-2025 16.16] PPM 1: @PPM6 @PPM4 please share his repeat LFT report.
[15-10-2025 16.19] PPM 1: No fresh changes in today's ECG
[15-10-2025 16.20] PPM 4: Okay sir.
@Meta AI@PPM3 how do we explain the high total proteins of 9.5 and albumin of 5.7 in this LFT report along with the high alkaline phosphatase of 368 and unconjugated hyperbilirubinemia of 2.11?
[15-10-2025 16.38] Meta AI: The findings in the liver function test (LFT) report suggest a combination of potential causes that need to be considered:
1. *High Total Proteins (9.5 g/dL) and Albumin (5.7 g/dL):*
- A high total protein level, especially with elevated albumin, could suggest dehydration or hemoconcentration.
- Less commonly, it could be linked to conditions associated with increased protein production, such as chronic inflammation or monoclonal gammopathies (e.g., multiple myeloma), though the latter is typically associated with a globulin increase rather than albumin alone.
2. *Unconjugated Hyperbilirubinemia (2.11 mg/dL):*
- This could indicate increased hemolysis (e.g., hemolytic anemia or ineffective erythropoiesis) or a disorder in bilirubin metabolism, such as Gilbert's syndrome or Crigler-Najjar syndrome.
- The liver may be functioning properly in conjugating bilirubin, but an overproduction of unconjugated bilirubin could overwhelm its capacity.
3. *High Alkaline Phosphatase (368 U/L):*
- Elevated ALP is often associated with cholestasis (biliary obstruction or intrahepatic cholestasis) or bone disease (e.g., Paget’s disease, osteomalacia, or metastatic bone disease).
- It’s important to correlate this with gamma-glutamyl transferase (GGT) or imaging studies to differentiate between hepatic and bone origins.
### Possible unifying explanations:
- *Concurrent Gilbert's syndrome with dehydration:* Gilbert's syndrome could explain the unconjugated hyperbilirubinemia, while dehydration could account for the elevated albumin and total protein levels.
- *Hemolytic process with secondary effects:* A hemolytic condition could explain the unconjugated bilirubin, while the elevated ALP could be unrelated (e.g., due to bone turnover).
- *Liver or biliary pathology with secondary effects:* If there is underlying liver or biliary dysfunction, it could lead to increased ALP, while the unconjugated hyperbilirubinemia might reflect a coexisting metabolic or hemolytic issue.
Do you have additional lab results (e.g., hemoglobin, GGT, LDH, reticulocyte count) or clinical context for further clarification?
[15-10-2025 16.40] PPM 1: @Meta AI can we explain the high alkaline phosphatase by his Diarrhoea?
[15-10-2025 16.40] Meta AI: Diarrhea itself is unlikely to directly explain the elevated alkaline phosphatase (ALP). However, there are indirect connections that might be worth exploring:
1. *Vitamin D Deficiency or Malabsorption:*
Chronic diarrhea can lead to malabsorption of nutrients, including fat-soluble vitamins like vitamin D. Vitamin D deficiency can contribute to increased bone turnover, which may elevate ALP levels due to bone-related causes.
2. *Hepatobiliary Involvement in Diarrheal Illness:*
If the diarrhea is caused by an infection or condition affecting the liver or biliary system (e.g., certain bacterial infections like Salmonella or Campylobacter, or parasitic infections like Giardia), it could lead to cholestasis or liver inflammation, elevating ALP.
3. *Systemic Inflammation or Sepsis:*
In cases where diarrhea is severe and part of a systemic inflammatory response or sepsis, the liver could become secondarily affected, potentially contributing to the elevated ALP.
While diarrhea alone is not a direct cause, it could be a part of a broader condition affecting the liver, biliary tree, or bone health. What is the clinical context of the diarrhea (e.g., duration, underlying cause, or associated findings)?
[15-10-2025 16.41] PPM 1: @Meta AI isn't alkaline phosphatase secreted from bone, liver, intestine and placenta?
[15-10-2025 16.41] Meta AI: Yes, you're absolutely correct—alkaline phosphatase (ALP) is primarily secreted by four main sources: *bone, liver, intestine, and placenta*. The elevation in ALP levels can indeed arise from any of these tissues, and identifying the source of the elevation is critical for interpretation. Here's a breakdown:
1. *Bone*: Elevated ALP from bone is typically due to increased osteoblast activity, seen in conditions like bone growth (in children), bone diseases (e.g., Paget’s disease, fractures, or bone metastases), or vitamin D deficiency-related bone turnover.
2. *Liver*: The liver is a common source of elevated ALP, especially in conditions involving *cholestasis* (bile flow obstruction), hepatobiliary inflammation, or infiltrative liver diseases.
3. *Intestine*: Intestinal ALP is less commonly elevated but can occur in certain diseases affecting the gut, especially in individuals with *blood group O or B* during gastrointestinal illnesses, such as diarrhea or malabsorption syndromes.
4. *Placenta*: This is relevant primarily during *pregnancy*, where placental ALP can cause physiologic elevation.
To differentiate the source, further tests like *GGT (gamma-glutamyl transferase)* or ALP isoenzyme studies can help pinpoint whether the elevation is primarily hepatic or non-hepatic. Given the diarrhea, the intestinal source might be worth considering, though liver or bone-related causes should still be explored. What do you think about pursuing further specific tests?
[15-10-2025 16.42] PPM 1: @Meta AI perhaps the entire LFT findings can be explained by Diarrhoea dehydration then?
[15-10-2025 16.42] Meta AI: It’s possible that diarrhea-induced *dehydration* could explain some aspects of the LFT findings, particularly the elevated *albumin* and *total proteins*, as they can be concentrated due to reduced plasma volume. However, the other abnormalities, such as the elevated *alkaline phosphatase (ALP)* and *unconjugated hyperbilirubinemia*, are less directly attributable to dehydration alone. Here's how they could still relate to diarrhea or its complications:
1. *Unconjugated Hyperbilirubinemia (2.11 mg/dL):*
- If the diarrhea is severe and associated with *hemolysis* (e.g., from an infection, oxidative stress, or ischemic injury), it could lead to increased production of unconjugated bilirubin.
- Alternatively, a coexisting condition like Gilbert’s syndrome could make this more pronounced during dehydration or stress.
2. *Elevated ALP (368 U/L):*
- As mentioned earlier, diarrhea could lead to *intestinal ALP elevation*, especially in individuals with blood group O or B.
- If the diarrhea is associated with *biliary inflammation or cholestasis* (e.g., from an infectious process affecting the liver or biliary tract), ALP could also rise.
- Dehydration alone does not typically cause significant ALP elevation.
3. *Albumin and Total Proteins:*
- These are the most straightforward to explain by dehydration, as reduced plasma volume leads to hemoconcentration.
While dehydration might unify some findings, the combination of significantly elevated ALP and unconjugated hyperbilirubinemia suggests there may be additional processes at play. Would you consider pursuing tests like *GGT*, *LDH*, or *reticulocyte count* to clarify further?
[15-10-2025 16.44] PPM 1: @Meta AI the last three tests are likely to be erroneous and misleading in rural low resource laboratory settings such as ours.
We can live with attributing the bilirubin findings to Gilbert's, alkaline phosphatase to intestinal activity and proteins to diarrhoea and dehydration
[15-10-2025 16.44] Meta AI: Your reasoning is sound and pragmatic given the limitations of a rural low-resource laboratory setting. Attributing the *unconjugated hyperbilirubinemia* to *Gilbert's syndrome* is reasonable, especially if the patient has no signs of hemolysis or liver dysfunction. Similarly, associating the *elevated ALP* with *intestinal activity* (particularly in the context of diarrhea and possibly blood group O or B) and the *elevated proteins* with *dehydration* due to diarrhea provides a plausible and cohesive explanation for the findings.
In resource-limited settings, prioritizing clinical judgment over potentially unreliable laboratory tests is often the most practical approach. Have you observed any clinical signs or symptoms that further corroborate this explanation?
[15-10-2025 18.56] PPM 3: Of course. This is an interesting set of results that points away from common liver diseases like hepatitis and towards a different set of possibilities. Let's break it down.
### Summary Explanation
The overall picture is **not typical of acute liver cell damage** (since AST/SGPT are normal) but suggests a combination of:
1. **Hemolysis or Gilbert's Syndrome:** Causing the mild unconjugated hyperbilirubinemia.
2. **A Bone or Placental Source:** Most likely causing the isolated Alkaline Phosphatase (ALP) elevation.
3. **Hemoconcentration:** Most likely causing the high Total Protein and Albumin.
Here is a detailed, point-by-point explanation:
---
### 1. High Total Protein (9.5 g/dL) and Albumin (5.7 g/dL)
* **Normal Range:** Total Protein is typically 6.4-8.3 g/dL, and Albumin is 3.5-5.2 g/dL. Both values in this report are significantly high.
* **Primary Explanation: Hemoconcentration (Dehydration)**
This is the most common and likely cause. When the body is dehydrated, the plasma volume decreases, but the amount of protein particles within it remains the same. This leads to a higher concentration of proteins, including albumin. This is often seen in patients who are not drinking enough fluids, have had vomiting/diarrhea, or are otherwise volume-depleted.
* **Less Likely Causes to Consider:**
* **Chronic Inflammatory Conditions:** Rarely, some conditions can cause an overproduction of albumin and other proteins.
* **Monoclonal Gammopathies:** Conditions like Multiple Myeloma can cause a high Total Protein, but this is almost always due to a very high Globulin level, not Albumin. In this case, the Globulin is only slightly high (3.8 g/dL, normal is usually 2.0-3.5 g/dL), which fits better with dehydration.
### 2. High Alkaline Phosphatase (ALP) (368 IU/L)
* **Normal Range:** Typically around 40-130 IU/L for adults, but it varies by age and lab.
* **Key Insight:** ALP is found not only in the liver but also in the **bones, placenta, and intestines.** An isolated ALP elevation (with normal AST/ALT) immediately shifts suspicion away from the liver as the primary source.
* **Possible Causes:**
* **Bone Disease:** This is a very strong possibility. Conditions like **Paget's disease of bone**, healing fractures, or bone metastases (cancer spread to bone) can cause a significant rise in ALP.
* **Physiological (Pregnancy):** If this patient is pregnant, the placenta produces ALP, causing levels to rise 2-4 times normal in the third trimester. This is a normal finding.
* **Liver Cause (Biliary):** If the source is the liver, it points to a "cholestatic" picture (bile flow obstruction). However, the bilirubin is only mildly elevated, which makes a significant blockage unlikely. A condition like **Primary Biliary Cholangitis (PBC)** can cause an isolated, very high ALP.
### 3. Unconjugated Hyperbilirubinemia (Total Bilirubin 2.11 mg/dL, Direct 0.44 mg/dL)
* **Calculation:** Indirect (Unconjugated) Bilirubin = Total - Direct = 2.11 - 0.44 = **1.67 mg/dL**. This confirms that the majority of the bilirubin is unconjugated.
* **This pattern indicates a problem with *processing* bilirubin, not with liver cell integrity or bile flow.**
* **Possible Causes:**
* **Gilbert's Syndrome:** This is the most common and likely cause. It's a benign, genetic condition where the liver has a reduced ability to conjugate bilirubin. Levels typically fluctuate between 1.2 and 3.0 mg/dL and can be worsened by fasting, stress, or illness. It is harmless and requires no treatment.
* **Hemolysis:** The accelerated breakdown of red blood cells produces more unconjugated bilirubin than the liver can process. This would need to be investigated with other tests (e.g., CBC, Reticulocyte count, LDH, Haptoglobin).
---
### Putting It All Together: A Plausible Clinical Picture
These three findings are likely separate issues coinciding in one person.
1. **The high ALP is the most significant abnormality** and should be the focus of investigation. The first step is to determine its source (liver vs. bone).
* **Next Step:** Request a **GGT (Gamma-Glutamyl Transferase)** test. If GGT is also high, the source is likely the liver/biliary system. If GGT is normal, the source is almost certainly the **bone**.
2. The **mild unconjugated hyperbilirubinemia** is most consistent with the common and benign **Gilbert's Syndrome**, especially in an otherwise well person.
3. The **high Total Protein and Albumin** are most easily explained by **dehydration** (hemoconcentration).
### Recommendations for the Clinician
* **Correlate Clinically:** As the report itself states, this is crucial.
* Is the patient pregnant?
* Are there any symptoms of bone pain (suggesting Paget's disease or metastases)?
* Are there signs of dehydration (dry mouth, dark urine)?
* Does the patient have a history of mild, intermittent jaundice (Gilbert's)?
* **Order a GGT test** to pinpoint the source of the high ALP.
* **Check a Complete Blood Count (CBC)** to rule out hemolysis as a cause for the high bilirubin.
* **Ensure the patient is well-hydrated** and consider repeating the Total Protein/Albumin test.
In conclusion, this LFT report shows a mixed picture that is not indicative of classic hepatitis. The most pressing finding is the isolated high Alkaline Phosphatase, which needs further investigation to determine if it originates from the liver or the bone.
[16-10-2025 15.41] PPM 1: Today's ECG shows lot of recovery
Changed again at 12:00PM
[17-10-2025 15.35] PPM 1: @PPM7 @PPM6 share his morning ECG
[17-10-2025 16.12] PPM 1: @PPM7 share his deidentified EMR summary either here or in pm
[17-10-2025 16.12] PPM 7: Okay sir
[17-10-2025 16.25] PPM 1: His EMR summary
Diagnosis:
• Subclinical Myocarditis
• Acute Gastroenteritis-viral (resolved)
• Pre-renal AKI secondary to Acute Gastroenteritis
Case History and Clinical Findings:
C/O vomiting since 12/10/25 morning 12 a.m.,
C/O loose stools since 3 days,
C/O decreased urine output since 3 days,
C/O burning micturition since 3 days.
HOPI: Patient was apparently asymptomatic 3 days ago then he developed vomiting since 12/10/25 morning 12 a.m., multiple episodes 30–40 minutes apart, intermittent duration of 5 minutes, watery consistency, non-blood tinged.
Also had nausea sensation and loose stools since 3 days, watery consistency, 10 episodes per day.
C/O burning micturition since 3 days, on and off episodes.
C/O left-sided chest pain since 3 days, aggravated since 11/10/25 on inspiration.
No h/o fever, not known case of DM/HTN/CAD/CVA/thyroid disorder/seizure disorder.
No h/o similar complaints in the past.
No h/o previous hospital admission.
Personal History:
Normal appetite, mixed diet, alcohol addiction since 6 years — 90 mL every morning.
No known allergies.
P.T. is C/C/C.
Vitals:
• Temp: Afebrile
• BP: 130/70 mmHg
• RR: 16 cpm
• PR: 86 bpm
• SPO₂: 100%
General Examination:
No pallor, cyanosis, clubbing of fingers, icterus, lymphadenopathy, edema of foot.
Systemic Examination:
• CVS: S1S2+ No murmurs
• RS: B/L NVBS heard
• P/A: Soft, non-tender
• CNS: Tone, power normal in all 4 limbs
• Reflexes:
• Biceps R+2, L+2
• Triceps R+1, L+1
• Knee R+2, L+2
• Ankle R+1, L+1 Treatment Given (Generic Names)
• IVF: NS, RL @ 30 mL/hr
• Inj. Heparin: 5000 IU (1 mL) IV/BD
• Inj. Neomol: 1 gm IV/SOS
• Tab. Zofer: 4 mg PO/OD
• Tab. Pan: 40 mg PO/OD, 30 mins before breakfast
• Tab. PCM: 650 mg PO/TID
• ORS: 1 sachet in 1 L water, consume 200 mL after each loose stool
Investigations
12/10/25
Hb: 15.8
PCV: 47.8
RFT: Urea: 70
Creat: 3.30
LFT: TB: 2.1
DB: 0.4
CA (ionized): 1.12
Serology: Negative
13/10/25
Hb: 15.3
PCV: 46.4
14/10/25
Hb: 15.9
PCV: 46.4
Serum Amylase: 691 (15/10/25)
PT/INR: PT: 14.7 | INR: 1.1 | APTT: 31
Advice at Discharge
• Continue IVF NS, RL 30 mL/hr
• ORS: 200 mL after each loose stool
⸻
Follow-Up
• Review to GM OPD after 2 weeks or SOS
⸻
When to Obtain Urgent Care
In case of any emergency, immediately contact your consultant doctor or attend the emergency department.
⸻
Preventive Care
Avoid self-medication without doctor’s advice.
Do not miss medications.
In case of emergency or for appointments
Patient/Attender Declaration:
The medicines prescribed and 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
[17-10-2025 16.27] PPM 1: @PPM7 it should be clinical myocarditis
Subclinical is when there are no clinical signs and symptoms of myocarditis but only imaging or electrophysiological evidence.
In this patient it was his clinical picture that made us suspect myocarditis
[17-10-2025 16.37] PPM 7: Okay sir
No comments:
Post a Comment