Monday, June 9, 2025

27F SLE Vomitings since 1 month pain abdomen since 10 days Telangana PaJR

 

09-06-2025

THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HER SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.

DESCRIPTION:

27 year old female k/c/o SLE since 3 yrs came to the casualty with c/o vomitings since 1 month
C/O Pain Abdomen since 10 days.
Vomitings for 1 month, immediately after intake of food (for both solids and liquids) associated with nausea, pain abdomen, diffuse, sudden onset, spasmodic type, non radiating, aggravated on food intake.
H/O Fever on and off 1 month back with discoid type of skin lesions.
H/O skin lesions over ear and face 2 yrs ago with alopecia, and diagnosed as SLE based on positive anti ds DNA antibodies and ANA and patient was treated with steroids and methotrexate, HCQ since then.

[09-06-2025 17.24] PPM 1: Update afternoon session:
@PPM3 please send her amazing ascitic fluid images
Mind boggling how the first 10 ml of the outflow pulled out with a syringe looks like pus and the subsequent free flow ascites fluid is clear!
The first part tested separately was low SAAG and second was high SAAG!
1st fluid
2nd fluid
X-ray erect abdomen on admission

Yesterday X-ray erect abdomen
[09-06-2025 19:26] PPM 1: Thanks! The possibility of a localised peritonitis is high
[11-06-2025 09:59] PPM 1: Update @PPM3?


[11-06-2025 10:02] PPM 3: 
S-    1 episode of loose stool at 4am 
      no vomiting
      no fever spikes
      no abdominal pain. 
O-
    Bp- 100/60 mmhg
    Pr- 98bpm
    Rr- 17cpm
    Spo2 - 99%at RA
    Cvs - s1s2 heard 
     Rs- Bae+, NVBS
     P/A - soft, no tenderness 
               Bowel sounds -  
               heard 
     I/O -2100/1000 ml 
     GRBS -100mg/dl 
 A- 
      Subacute intestinal obstruction (resolved)secondary to 
     lupus mesenteric vasculitis
      k/c/o SLE since 3 yrs
sr.k+ - 3.2
P- 
allowed soft food - ate idli 
 D5 inj.Taxim 1gm iv/bd
tab.methylprednisolone 4mg at 8:30am 
Inj.kcl 2amp in 500ml NS infusion started
[11-06-2025 10:36] PPM 1: What are the current evidences in favour of making this diagnosis of mesenteric vasculitis of her intestine? What are the next steps to confirm?
Is her current hypokalemia because she's NPO?
[11-06-2025 10:39] PPM 1: Also how did we explain her ascitic tap findings of initial pus followed by clear fluid (with the pus showing an inflammatory SAAG but no cells and the clear fluid showing high portal hypertensive SAAG?

[11-06-2025 10:41] PPM 1: All we can see is bowel edema. Please ask the radiology if they are seeing anything in particular to suggest vasculitis
[11-06-2025 10:41] PPM 3: She is on diuretic sir, furosemide 20mg
[11-06-2025 10:42] PPM 1: This is a qualitative cytology report and they haven't mentioned which fluid has how many cells!
Please ask them to do the TLC and DLC of the fluid!
[11-06-2025 10:42] PPM 1: Alright but is that a lead?
[11-06-2025 10:44] PPM 3: That is the cytology of both samples it seems sir
[11-06-2025 12:57] PPM 1: One can't mix a pus sample with clear sample in one report!
[11-06-2025 12:57] PPM 1: This is from the clear sample?
[11-06-2025 16.22] PPM 1: Revised report

[11/06, 16:10]cm: Thanks. How do we explain two different fluids pulled out from the same place with the same needle?
[11/06, 16:13] Assoc Prof Pathology: Yes sir
It might be due to loculated adhesions due to fungal infection in the peritoneal cavity as cytology of fluid is showing fungal elements.. because of needle shift during aspiration
[11/06, 16:21]cm: Is such a loculated peritoneal collection, one with pus and another with clear fluid known? Also the needle was not removed from the locule. Just the syringe was removed once it was filled, followed by plain drop by drop collection directly
[11/06, 16:23] Assoc Prof Pathology: Yes sir
Even if the needle stays in the same locule, gravity, pressure changes, or small shifts in the internal structure of the cavity can cause:
Initial fast aspiration of purulent/dependent material.
Later slow draining, clearer fluid from a different plane or channel.
[11-06-2025 16.32] PPM 1: @Meta AI @PPM4 @PPM5 @PPM6 how do we explain her ascites etiology in the background of her SLE and how do we explain two different samples, one cloudy with pus and one clear coming out one after the other in the same puncture showing different microscopic findings too?
[09/06, 17:24]cm: Update afternoon session:
@PPM3 please send her amazing ascitic fluid images
Mind boggling how the first 10 ml of the outflow pulled out with a syringe looks like pus and the subsequent free flow ascites fluid is clear!
The first part tested separately was low SAAG and second was high SAAG!
[11/06, 10:02] Medical Student CBBLE: S
-    1 episode of loose stool at 4am 
      no vomiting
      no fever spikes
      no abdominal pain. 
 O-
    Bp- 100/60 mmhg
    Pr- 98bpm
    Rr- 17cpm
    Spo2 - 99%at RA
    Cvs - s1s2 heard 
     Rs- Bae+, NVBS
     P/A - soft , no tenderness 
               Bowel sounds -  
               heard 
     I/O -2100/1000 ml 
     Grbs -100mg/dl 
A- 
      Subacute intestinal      obstruction (resolved)secondary to 
     lupus mesenteric vasculitis
      k/c/o SLE since 3 yrs
sr.k+ - 3.2
P- 
allowed soft food - ate idli 
 D5 inj.Taxim 1gm iv/bd
tab.methylprednisolone 4mg at 8:30am 
Inj.kcl 2amp in 500ml NS infusion started
[11/06, 10:36]cm: What are the current evidences in favour of making this diagnosis of mesenteric vasculitis of her intestine? What are the next steps to confirm?
Is her current hypokalemia because she's NPO?
[11/06, 10:39]cm: Also how did we explain her ascitic tap findings of initial pus followed by clear fluid (with the pus showing an inflammatory SAAG but no cells and the clear fluid showing high portal hypertensive SAAG?
 [11/06, 16:10]cm: Thanks. How do we explain two different fluids pulled out from the same place with the same needle?
[11/06, 16:13] Assoc Prof Pathology: Yes sir
It might be due to loculated adhesions due to fungal infection in the peritoneal cavity as cytology of fluid is showing fungal elements.. because of needle shift during aspiration
[11/06, 16:21]cm: Is such a loculated peritoneal collection, one with pus and another with clear fluid known? Also the needle was not removed from the locule. Just the syringe was removed once it was filled, followed by plain drop by drop collection directly
 [11/06, 16:23] Assoc Prof Pathology: Yes sir
Even if the needle stays in the same locule, gravity, pressure changes, or small shifts in the internal structure of the cavity can cause:
Initial fast aspiration of purulent/dependent material.
Later slow draining, clearer fluid from a different plane or channel.
[11-06-2025 16:32] Meta AI: Let's break down the case:
1. Ascites etiology in SLE: Ascites in Systemic Lupus Erythematosus (SLE) patients can be attributed to various factors, including lupus mesenteric vasculitis, portal hypertension secondary to autoimmune hepatitis or nodular regenerative hyperplasia, or even infections. Given the patient's background, lupus mesenteric vasculitis seems plausible.
2. Two different ascitic fluid samples: The initial cloudy fluid with pus followed by clear fluid could be due to:
    - Loculated adhesions: As suggested by the Assoc Prof Pathology, loculated adhesions due to fungal infection in the peritoneal cavity could explain the difference. The needle might have initially aspirated from a locule with purulent material and then from another with clear fluid.
    - Gravity and pressure changes: Even within the same locule, gravity and pressure changes during aspiration could cause initial purulent material to be drained first, followed by clearer fluid.
3. Different SAAG values:
    - Low SAAG in purulent fluid: Suggests an inflammatory or infectious process.
    - High SAAG in clear fluid: Indicates portal hypertension.
4. Current evidence for mesenteric vasculitis:
    - Clinical presentation (subacute intestinal obstruction)
    - History of SLE
    - Response to steroids
5. Next steps to confirm:
    - Imaging studies (CT abdomen) to evaluate for signs of mesenteric vasculitis or portal hypertension
    - Further analysis of ascitic fluid (culture, cytology) to rule out infections or other causes
6. Hypokalemia: Could be due to various factors, including NPO status, steroid use, or renal losses.
The case seems complex, and further investigation and multidisciplinary discussion would be beneficial to determine the exact cause of ascites and confirm the diagnosis of mesenteric vasculitis.
[11-06-2025 16:34] PPM 1: @Meta AI simply repeated the entire conversation in a diplomatic manner without adding much value! @PPM7
[11-06-2025 16:34] Meta AI: Let's dive deeper.
The key points to ponder are:
1. Fungal infection: Could the patient have developed a fungal peritonitis secondary to immunosuppression? This might explain the loculated collections and differing fluid characteristics.
2. Mesenteric vasculitis: How likely is it that lupus mesenteric vasculitis directly caused the ascites, and could it also contribute to the differing fluid samples?
3. Portal hypertension: Is there evidence of chronic liver disease or nodular regenerative hyperplasia that could explain the high SAAG in the clear fluid?
To further elucidate:
- Imaging: A CT abdomen would be crucial to identify any loculations, signs of mesenteric vasculitis, or portal hypertension.
- Fluid analysis: Further cytology, culture, and fungal studies on both fluid samples could provide more insights.
Given the complexity, a multidisciplinary approach involving rheumatology, gastroenterology, and pathology would indeed be beneficial to piece together the findings and manage the patient effectively.
[11-06-2025 16.44] PPM 1: Thanks!
@PPM3 This is the cloudy ascites fluid report shared by @PPM Ma'am.  Isn't it strange that inspite of the cloudiness the number of cells are just 10 more than that in the clear fluid! Also no neutrophils in the cloudy fluid!
[11-06-2025 16:48] PPM 3: yes sir
[11-06-2025 17:04] PPM 1: More from another CBBLE:
[11/06, 16:59]an: Localised peritonitis?
[11/06, 16:59]cm: Well why would it be different in the same needle in the same location?
[11/06, 17:01] an: Another thing which comes to my mind is during ascitic tap we keep the patient in lateral position with the site of tap and needle pointed downwards. So pus being heavier than the ascitic fluid gravitated down and came out first. 🥲😅
[11/06, 17:02]an: Thinking on my feet.
[11-06-2025 22:12] PPM 6: Please do an IgG, ASMA, SLA and LKM. Ideally transjugular liver biopsy should be attempted but we can look at the autoimmune markers first.
How is her LFT, platelets and INR?
[11-06-2025 22:13] PPM 6: Also, was SBP ruled out in culture?
[11-06-2025 22:52] PPM 4: Based on the clinical details and ascitic tap findings, here's a breakdown of the ascites etiology and the dual-fluid phenomenon:
### *Ascites Etiology in SLE*
1. *Lupus Peritonitis*  
   - Common cause of ascites in SLE (15-40% of cases).  
   - Typically presents with *low SAAG (<1.1 g/dL)* and elevated protein (>2.5 g/dL).  
   - Steroid-responsive, but this patient's high SAAG in the clear sample complicates this.
2. *Nephrotic Syndrome*  
   - SLE nephritis can cause hypoalbuminemia → *high SAAG transudative ascites*.  
   - Fits the clear fluid findings (high SAAG).
3. *Mesenteric Vasculitis*  
   - Supported by resolved intestinal obstruction, abdominal pain, and steroid use.  
   - Can cause exudative ascites due to inflammation/ischemia.  
   - Evidence needed: CT angiography (vessel "beading"), laparoscopy, or biopsy.
4. *Spontaneous Bacterial Peritonitis (SBP)*  
   - "Pus-like" initial sample suggests infection.  
   - But low SAAG in pus sample is atypical (SBP usually high SAAG).
5. *Fungal Peritonitis*  
   - Cytology showing fungal elements + loculated fluid supports this.  
   - Rare but reported in immunosuppressed SLE patients.
6. *Mixed Etiology*  
   Likely *two coexisting causes*:  
   - *Portal hypertension* (high SAAG clear fluid) from lupus nephritis.  
   - *Localized exudative process* (low SAAG pus) from infection/vasculitis.
---
### *Explaining the Dual-Fluid Tap*
The same needle yielded:  
- *Initial 10 mL*: Cloudy "pus," low SAAG, no cells.  
- *Subsequent fluid*: Clear, high SAAG.  
#### *Possible Mechanisms*
1. *Dependent Material Aspiration*  
   - The initial syringe pull aspirated thick, viscous material settled at the bottom (pus/debris).  
   - Later gravity drainage collected supernatant clear fluid from above.
2. *Compartmentalized Peritoneal Cavity*  
   - *Loculated abscess* communicating with free ascites:  
     - Needle tip first entered a localized pus-filled pocket (exudative, low SAAG).  
     - After aspirating this, the needle breached into free-flowing transudative ascites (high SAAG).  
   - Supported by: Fungal cytology, adhesions in SLE, and abrupt fluid change.
3. *Pressure/Flow Dynamics*  
   - High-pressure suction via syringe extracts denser material.  
   - Low-pressure gravity flow drains lighter fluid.
4. *Sampling Artifact*  
   - "Pus" could represent *fibrin/amorphous debris* (not true pus) if cell count was low.  
   - Fungal elements may form clumps that settled, explaining initial turbidity.
---
### *Key Diagnostic Steps*
1. *Imaging*  
   - *Ultrasound/CT abdomen*: Assess for loculations, bowel wall thickening (vasculitis), or portal hypertension signs.  
2. *Ascitic Fluid*  
   - Repeat tap with simultaneous SAAG, cell count, culture (bacterial/fungal), and albumin in both samples.  
3. *Infection Workup*  
   - Blood/urine cultures, fungal serology (β-D-glucan).  
4. *Renal/Liver Assessment*  
   - 24-hr urine protein, serum albumin, LFTs to confirm portal hypertension.  
5. *Vasculitis Confirmation*  
   - Mesenteric angiography or MR enterography for "comb sign."  
---
### *Hypokalemia Explanation*
- *Steroids* (methylprednisolone): Cause kaliuresis.  
- *NPO status*: Reduced oral K⁺ intake.  
- *Diarrhea/NG suction*: Extra GI losses.  
- Management: IV KCl replacement + monitor.
### *Conclusion*
This case suggests *two concurrent pathologies*:  
1. *Portal hypertension* (clear fluid, high SAAG) from lupus nephritis.  
2. *Localized exudative process* (pus-like, low SAAG) likely due to *fungal peritonitis* or *mesenteric vasculitis* with adhesions.  
*Next step*: Aggressive fungal workup + imaging to rule out loculations before escalating immunosuppression.
[11-06-2025 22:52] PPM 4: DeepSeek 👆
[12-06-2025 08:01] PPM 1: @PPM3 when are we going to get the culture report of the ascitic fluid pus? It's already 48 hours I guess?
[12-06-2025 08:03] PPM 1: @PPM3 please share her LFT, platelets, inr here as currently it's not available in her case report link in the description box.



[12-06-2025 15:07] PPM 6: Polymicrobial infection might suggest a likelihood of secondary bacterial peritonitis. Any perforation? Even if concealed or healed?
[12-06-2025 16:10] PPM 1: Not on clinical examination as well as CT abdomen and ultrasound
[12-06-2025 16:15] PPM 1: PT INR?

[12-06-2025 16.31] PPM 1: ðŸ‘†Above are the fungal elements visible in the peritoneal fluid
[12-06-2025 16.58] PPM 1: Microbiology Inputs:
[12/06, 16:42] Prof Microbology:
Is it high power or oil immersion? Not looking like Fungal hyphae
But may be Nocardia(filamentous bacteria)
Acid fast staining with 1% H2so4 as decolouriser 
Please send the sample to microbiology department tomorrow sir. I will get it done and see
@PPM3 please coordinate this with pathology department.
[12/06, 16:55]cm: 👆 Ma'am some sample is available with the Microbiology department as well which has shown polymicrobial growth although nocardia I guess would either take longer or different media?

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