08-01-2026
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.
[10.43 am, 09/01/2026] PPM 3: Patient was brought to the casualty in the state of altered sensorium to the casualty on 7/1/26 around 7 pm
Patient was in her home with her daughter (who is in 2 grade) she was apparently snapping chilly stems and had giddiness and fell down, the daughter called people around her, and she was taken to the hospital, in the hospital she had 2 seizures episodes, tonic movements, up rolling of eyes(+), drooling of saliva(+), protrusion of tongue (+),it lasted for around 3-5 min ,then she had another episode after sometime and was bought to our hospital In our casualty patient was in altered sensorium
Gcs: E4V1M5, pupils-normal size reactive to light, exaggerated reflexes with vitals
Pr:82 b/min
Bp:110/70 mmhg
Rr:18 cpm
Spo2:96 % on RA
Temp 101F
[4:38 pm, 09/01/2026] PPM 1: Her metabolic acidosis worsened yesterday? No repeat Abgs because her current condition is completely normal?
Why does she still have mild but progressive metabolic acidosis till yesterday is perhaps a question that may remain unanswered due to her lack of symptoms.
[4:39 pm, 09/01/2026] PPM 1: Well presented 👏
[7:00 pm, 09/01/2026] PPM 3: Possibly acidosis is related to cause of seizures which leads to the starting differentials of toxin induced with a high osmolar gap
After improving of her sensorium she is not giving history of consuming anything though
[8:32 pm, 09/01/2026] PPM 1: @Meta AI @PPM4 what are the possible toxins that could be responsible for Seizures and metabolic acidosis in this patient?
[8:32 pm, 09/01/2026] Meta AI: Given the clinical presentation, some possible toxins that could be responsible for seizures and metabolic acidosis with a high osmolar gap include:
- Methanol
- Ethylene glycol
- Ethanol
- Salicylates
- Propylene glycol
- Isopropyl alcohol
To narrow down the differential, can you tell me more about the patient's lab results, like the anion gap and any specific electrolyte imbalances? 🧐
[8:33 pm, 09/01/2026] PPM 1: @PPM3 what was her anion gap?
[8:40 pm, 09/01/2026] PPM 3: 15.8 sir
[8:43 pm, 09/01/2026] PPM 1: Calculated or measured?
[8:44 pm, 09/01/2026] PPM 3: Calculated
[9:11 pm, 09/01/2026] PPM 4: Excellent question. You've correctly identified the major toxins that cause seizures and metabolic acidosis with an elevated osmolar gap. Narrowing the list is precisely what we need to do.
The *anion gap* is the single most critical piece of information to start differentiating these.
Here’s how we can systematically approach it based on the *Anion Gap Metabolic Acidosis (AGMA)* and other key lab findings:
### Step 1: Is there an Elevated Anion Gap (AGMA)?
The classic mnemonic for AGMA is *MUDPILES CAT, with the most relevant toxins in **bold*:
* *M*ethanol
* *U*remia
* *DKA, **A*KA (Alcoholic Ketoacidosis)
* *P*ropylene Glycol
* *Iron, **I*soniazid
* *L*actic Acidosis (e.g., from cyanide, carbon monoxide, metformin, seizures themselves)
* *E*thylene Glycol
* *S*alicylates
*If the patient has a HIGH ANION GAP metabolic acidosis*, the top suspects from your list become:
1. *Methanol*
2. *Ethylene Glycol*
3. *Salicylates* (though these often cause a mixed respiratory alkalosis + AGMA)
4. *Propylene Glycol* (a solvent in IV lorazepam, phenobarbital, etc.)
*If the patient has a NORMAL ANION GAP (hyperchloremic) metabolic acidosis*, it makes some toxins less likely, but doesn't rule them out entirely if mixed disorders exist.
---
### Step 2: Analyze the Osmolar Gap
You've already noted it's high. This measures the difference between the measured serum osmolality and the calculated osmolality. A high gap (>10) suggests the presence of unmeasured, low-molecular-weight solutes (like toxins).
* *Very High Osmolar Gap:* *Methanol, Ethylene Glycol, Isopropyl Alcohol, Ethanol.*
* *Moderate Osmolar Gap:* Propylene glycol.
* *Minimal/Low Osmolar Gap:* Salicylates (molecular weight is high, so it doesn't contribute much to osmolar gap).
*Crucial Caveat:* The osmolar gap is time-sensitive. As alcohols/toxins are metabolized into acids, the osmolar gap falls while the anion gap rises. A patient presenting late may have a normal osmolar gap but a huge AGMA.
---
### Step 3: Look for Other Specific Clues & Patterns
Here’s a breakdown of your list with key differentiating features:
| Toxin | Seizures? | Metabolic Acidosis? | Key Clues & Labs |
| :--- | :--- | :--- | :--- |
| *Methanol* | Yes (late) | *Severe AGMA* | *Visual disturbances* (blurry vision, photophobia, "snowfield" vision). *High osmolar gap*. |
| *Ethylene Glycol* | Yes (late, CNS stage) | *Severe AGMA* | *Calcium oxalate crystals* in urine. *Hypocalcemia*. Oxalate can look like hippurate crystals. |
| *Salicylates* | Yes (severe toxicity) | *AGMA* (often mixed with respiratory alkalosis) | *Tinnitus, hyperventilation, hyperthermia. **Respiratory alkalosis* on ABG. Direct salicylate level. |
| *Propylene Glycol* | Yes (CNS depression, seizures) | *Lactic Acidosis (AGMA)* | Iatrogenic exposure from *high-dose IV drips* (lorazepam, phenobarbital, etomidate). Elevated lactate. |
| *Isopropyl Alcohol* | Yes (in severe cases) | *NO metabolic acidosis* (metabolized to acetone) | *Ketosis without acidosis, "fruity acetone breath," hemorrhagic gastritis. **High osmolar gap*. |
| *Ethanol* | Yes (withdrawal) | Can cause AGMA via *Alcoholic Ketoacidosis (AKA)* | History of chronic use. Beta-hydroxybutyrate elevated. May have normal or low ethanol level on presentation. |
---
### Step 4: Direct Questions to Narrow Further
To pinpoint the culprit, I would ask for these specific results:
1. *Arterial Blood Gas (ABG):* Confirms the metabolic acidosis and checks for a *mixed respiratory alkalosis* (suggestive of salicylates).
2. *Serum Ketones/Beta-hydroxybutyrate:* To rule out DKA/AKA. *Isopropyl alcohol* causes ketonuria without acidosis.
3. *Serum Lactate:* Marked elevation is classic for *propylene glycol* and can occur with seizures themselves or cyanide/CO.
4. *Urinalysis:* Looking for *calcium oxalate crystals* (*ethylene glycol*) or evidence of rhabdomyolysis.
5. *Serum Calcium:* *Hypocalcemia* is common in *ethylene glycol* toxicity.
6. *Specific Levels:* If available/indicated: *Salicylate level, **acetaminophen level* (co-ingestion common).
7. *Patient Context:* Any history of accidental ingestion (antifreeze, windshield fluid), occupational exposure, suicidal intent, or chronic IV medication use (e.g., ICU sedation)?
*In summary, without the anion gap:* The combination of *seizures + AGMA + high osmolar gap* makes *methanol, ethylene glycol, and propylene glycol* the most likely primary suspects from your list, with salicylates as a key contender if the osmolar gap is not markedly elevated.
Could you provide the *anion gap, serum lactate, and calcium level*? That would allow for a much more targeted differential.
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