06-12-2025
THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S 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 EXPERT WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[2.57 pm, 07/12/2025] PPM 1: Here's the handwritten history. Unfortunately this is something that AI may not be able to convert to legible text and human volunteers like @PPM3@PPM4 may be able to help by typing the gist of it here, if when they are free?
[3.02 pm, 07/12/2025] PPM 1: He was admitted with altered sensorium suggestive of delirium tremens and on further labs was found to have azotemia, renal failure with severe metabolic acidosis and hyponatremia.
He was taken up for dialysis, and they may have also adjusted his sodium during dialysis when it jumped up 10 Meq from 115 to 125!
@PPM5 @Meta AI what are the precautions one needs to take during dialysis of hyponatremia patients as in how would they set the dialysate sodium to adjust for the patient's Hyponatremia to ensure that there is no rapid correction precipitating osmotic demyelination syndrome?
@PPM5
[3:02 pm, 07/12/2025] Meta AI: Dialyzing a patient with severe hyponatremia requires careful attention to avoid rapid correction, which can lead to osmotic demyelination syndrome (ODS). Here are some precautions:
1. Set dialysate sodium: The dialysate sodium concentration should be set to gradually increase the patient's sodium levels. A common approach is to set the dialysate sodium around 10-15 Meq/L above the patient's current sodium level.
2. Gradual correction: Aim for a sodium correction rate of 4-6 Meq/L in the first 24 hours, not exceeding 8 Meq/L.
3. Monitor sodium levels: Frequently check sodium levels during dialysis (e.g., every 2-4 hours) to adjust the dialysate sodium as needed.
4. Adjust dialysate sodium: If the sodium level is rising too quickly, reduce or stop the sodium increase in the dialysate.
5. Consider sodium modeling: Some dialysis machines allow sodium modeling, which can help achieve a more gradual correction.
In this case, the patient's sodium jumped 10 Meq (from 115 to 125), which might be too rapid. The dialysis team should closely monitor the patient for signs of ODS and adjust the dialysate sodium accordingly.
Would you like more details on managing hyponatremia during dialysis or ODS prevention strategies?
[3.05 pm, 07/12/2025] PPM 1: Serial sodiums and creatinine and platelets
MRI video of the patient: https://youtube.com/shorts/n2CRkRSjhXc?si=jUUPp2Ygj59G_lK7
[3:08 pm, 07/12/2025] PPM 1: Going by his history of Alcoholism since 20 years, what are the likely differentials for his acute delirium, Hyponatremia, acute renal failure and pulmonary edema, metabolic acidosis? What would be the best way to confirm methanol poisoning in this patient?
@PPM5 @Meta AI
[3:08 pm, 07/12/2025] Meta AI: Given the patient's history of alcoholism, here are some likely differentials:
- Delirium: Delirium tremens, Worsening hepatic encephalopathy, CNS infection, traumatic brain injury, or toxic ingestion (e.g., methanol, ethylene glycol)
- Hyponatremia: SIADH, volume overload, or hypovolemia
- Acute renal failure: Acute tubular necrosis (ATN) secondary to hypovolemia, sepsis, or toxins (e.g., alcohol, medications)
- Pulmonary edema: Cardiogenic (e.g., alcoholic cardiomyopathy) or non-cardiogenic (e.g., sepsis, ARDS)
- Metabolic acidosis: Lactic acidosis, ketoacidosis, or toxic ingestion (e.g., methanol, ethylene glycol)
For methanol poisoning:
- Clinical suspicion: High anion gap metabolic acidosis, visual disturbances, and altered sensorium
- Lab tests:
- Serum methanol levels (gold standard)
- Arterial blood gas (ABG) showing high anion gap metabolic acidosis
- Serum osmolality and osmolar gap
- Urine methanol levels
- Confirmation: Gas chromatography can measure methanol levels, but treatment often starts based on clinical suspicion and lab findings.
Best way to confirm: Send serum for methanol levels and consider empiric treatment with fomepizole or ethanol if clinical suspicion is high.
Would you like more on management or investigation strategies?
[3:26 pm, 07/12/2025] PPM 2: Industrial antifreeze contamination comes to mind.
[3:27 pm, 07/12/2025] PPM 2: Aka Polyethylene glycol, which, unfortunately through cough syrups and subsequent catastrophic events, has taught me, is a common contaminant.
### **Key Likely Differentials (in order of suspicion):**
1. **Methanol or Ethylene Glycol Poisoning (Toxic Alcohols)**
* **Why it fits:** This is a **top contender**. Patients with chronic alcoholism may ingest methanol or ethylene glycol as substitutes. Both cause:
* **Severe high anion gap metabolic acidosis** (due to formic acid from methanol or glycolic/oxalic acid from ethylene glycol).
* **Acute delirium/encephalopathy.**
* **Acute renal failure** (especially prominent with ethylene glycol due to calcium oxalate crystal deposition).
* **Pulmonary edema** can occur from direct toxicity, acidosis, or complicating acute renal failure.
* Hyponatremia may be pre-existing or exacerbated by vomiting/volume depletion.
2. **Acute Alcoholic Hepatitis with Multi-Organ Failure**
* **Why it fits:** Severe inflammation from alcohol can precipitate:
* **Acute renal failure** (hepatorenal syndrome).
* **Metabolic acidosis** (lactic acidosis from liver failure, hypoperfusion, or alcohol metabolism).
* **Delirium** (hepatic encephalopathy).
* **Pulmonary edema** (due to volume overload from renal failure or less commonly hepatopulmonary syndrome).
* Hyponatremia is a classic feature of advanced cirrhosis due to reduced free water clearance.
3. **Sepsis/Infection (e.g., Spontaneous Bacterial Peritonitis, Pneumonia) Complicating Cirrhosis**
* **Why it fits:** Patients with alcoholic cirrhosis are immunocompromised and prone to infections, which can trigger:
* **Delirium** (septic encephalopathy).
* **Acute renal failure** (acute kidney injury due to sepsis).
* **Metabolic acidosis** (lactic acidosis from sepsis).
* **Pulmonary edema** (could be due to ARDS from sepsis or fluid resuscitation).
* Hyponatremia is often worsened by sepsis.
4. **Wernicke's Encephalopathy with Decompensation**
* **Why it fits:** Thiamine deficiency is common. While classic Wernicke's presents with ophthalmoplegia, ataxia, and confusion, it can be atypical. Severe metabolic stress (infection, withdrawal) in a thiamine-deficient state can lead to global decompensation, including lactic acidosis and organ failure, though it's less directly causative of the full picture.
5. **Combined Alcohol Withdrawal Delirium (DTs) and Other Complications**
* **Why it fits:** Delirium tremens itself is a hyperadrenergic state that can cause fever, tachycardia, and agitation. However, the associated **hyponatremia, renal failure, pulmonary edema, and severe metabolic acidosis** are not typical features of pure DTs and point to a separate, severe underlying metabolic or toxic insult.
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### **Best Way to Confirm Methanol Poisoning in This Patient:**
Given the high suspicion from the clinical picture, confirmation requires a **multi-step laboratory approach**:
1. **Immediate Critical Tests (Should be ordered STAT):**
* **Serum Methanol Level:** **The definitive diagnostic test.** Any detectable level is abnormal, but toxicity typically correlates with levels >20 mg/dL. However, treatment should not be delayed while awaiting this result if clinical suspicion is high.
* **Arterial or Venous Blood Gas (ABG/VBG):** Confirms the **severe metabolic acidosis** (low pH, low bicarbonate).
* **Serum Electrolytes:** To calculate two crucial gaps:
* **Anion Gap (AG):** AG = Na - (Cl + HCO3). Will be **elevated** (>12-15 mEq/L) due to the unmeasured anions (formate).
* **Osmolal Gap (OG):** OG = Measured osmolality - Calculated osmolality. Calculated Osm = (2*Na) + (Glucose/18) + (BUN/2.8). An **elevated osmolal gap** (>10 mOsm/kg) suggests the presence of an unmeasured, low-molecular-weight solute like methanol or ethylene glycol.
* **Key Pattern:** **High Anion Gap Metabolic Acidosis + Elevated Osmolal Gap** is **highly suggestive of toxic alcohol poisoning.**
2. **Supportive Tests to Strengthen the Diagnosis:**
* **Serum Ethanol Level:** Important because ethanol competitively inhibits alcohol dehydrogenase, slowing the metabolism of methanol to its toxic byproducts. A high ethanol level may "mask" methanol poisoning by preventing acidosis initially, but the osmolar gap will be high.
* **Urinalysis:** While methanol itself doesn't cause crystals, its presence may be sought. More importantly, urinalysis helps rule out other causes (e.g., oxalate crystals in ethylene glycol poisoning).
* **Serum Formate Level:** A more specific marker of methanol toxicity, as formic acid is the primary toxic metabolite. It may be elevated even when methanol levels are declining. However, this test is often less readily available.
* **Fundoscopic Examination:** The finding of **optic disc hyperemia or retinal edema** is a highly specific (though not always present) sign of methanol poisoning.
3. **Rule-Out Other Key Differentials:**
* **Ethylene Glycol Level:** Must be checked simultaneously, as the presentation overlaps significantly.
* **Lactate, Ketones (β-hydroxybutyrate), Creatinine Kinase:** To evaluate for other causes of high anion gap metabolic acidosis (lactic acidosis, alcoholic ketoacidosis, rhabdomyolysis).
* **Liver Function Tests, Ammonia, Coagulation Panel:** To assess for acute alcoholic hepatitis/hepatic failure.
* **Blood and Urine Cultures, Chest X-ray:** To evaluate for sepsis as a cause or complication.
### **Clinical Takeaway:**
In this patient, **the combination of a high anion gap metabolic acidosis with an elevated osmolal gap is the most immediate and strong laboratory evidence pointing to methanol (or ethylene glycol) poisoning.** The definitive confirmation is a **serum methanol level**. Management with **fomepizole** (or ethanol infusion) and **hemodialysis** must be initiated immediately based on strong clinical and initial laboratory suspicion, without waiting for the methanol level result, as delays can lead to permanent blindness, neurological damage, or death.
