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.
---
### **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.
[6.19 pm, 07/12/2025] PPM 1: https://youtube.com/shorts/n2CRkRSjhXc?si=jUUPp2Ygj59G_lK7
👆Thankfully no signs of osmotic demyelination on his MRI although given the events timeline of intradialyitic sodium correction it won't be surprising if he develops clinical features later. @PPM6 @PPM7 can you share his dialysis notes particularly how his dialysate sodium was set? Else I'll have to look for it tomorrow afternoon.
Serial chest x-rays since admission
This one is during admission 5/12/25
06/12/2025 3.30 am
07/12/2025
[9:20 pm, 07/12/2025] PPM 7: Sir, why will correction of acute hyponatremia lead to demyelination where the osmotic gradient has not changed as compared to chronic
[9:22 pm, 07/12/2025] PPM 7: Why is the t waves here like this?
As assumed hyperkalemia,but the simultaneously lab value of k+ is normal
Ischemia related changes,it doesn't show anything on 2d echo
Is the ischemia not being picked up by echo?
Or is it false stemi kind of?
[10:08 pm, 07/12/2025] PPM 1: @Meta AI @PPM5 what is the data driven evidence around the differences in incidence of osmotic demyelination precipitated by acute Hyponatremia correction vs chronic hyponatremia correction? Doesn't acute Hyponatremia correction need a slower approach to prevent osmotic demyelination?
[10:08 pm, 07/12/2025] Meta AI: Osmotic Demyelination Syndrome (ODS) and Hyponatremia Correction
The risk of ODS is generally associated with the correction of chronic hyponatremia, not acute hyponatremia. Here's why:
1. Brain adaptation: In chronic hyponatremia, the brain adapts by losing organic osmolytes, making it susceptible to shrinkage during rapid correction.
2. Osmotic gradient: In acute hyponatremia, the brain hasn't had time to adapt, so the risk of ODS is lower.
Evidence:
- Studies suggest that rapid correction of chronic hyponatremia (>10-12 Meq/L in 24 hours) increases the risk of ODS.
- Acute hyponatremia correction is generally considered safer, but guidelines recommend cautious correction (<10 Meq/L in 24 hours) to avoid potential risks.
Data-driven evidence:
- A review of cases showed ODS incidence was significantly higher with correction rates >10 Meq/L/24 hours in chronic hyponatremia (Sterns et al., 1986).
- Guidelines recommend slower correction for chronic hyponatremia (<8-10 Meq/L in 24 hours).
Acute vs Chronic Hyponatremia Correction:
| | Acute Hyponatremia | Chronic Hyponatremia |
| --- | --- | --- |
| Risk of ODS | Lower | Higher |
| Recommended Correction Rate | <10-12 Meq/L in 24 hours | <8-10 Meq/L in 24 hours |
In summary, while acute hyponatremia correction is generally safer, cautious correction is still recommended to avoid potential risks.
References:
- Sterns RH, et al. (1986). Neurologic aspects of therapeutic serum sodium lowering. Am J Kidney Dis, 8(5), 304-313.
- Verbalis JG, et al. (2013). Diagnosis and management of hyponatremia. J Clin Endocrinol Metab, 98(3), 1021-1030.
Would you like more details on hyponatremia management or ODS prevention?
[4.27 pm, 08/12/2025] PPM 1: @PPM7 please share today's update soap notes
Attaching an image from our dialysis user interface which shows how the planned sodium is entered and the machine pumps draw the sodium from the can in the left containing sodium bicarbonate while the right can contains electrolytes and potassium acetate.
Unfortunately in our dialysis notes there's no provision for the tech to enter what sodium he had set on the first day.
[7.50 pm, 08/12/2025] PPM 7: Subjective: Patient is under sedation
Objective:
Pupils: Mild dilated and reactive to light
Urea:58
Creat:3.3
Sodium:134
Potassium:4.2
Chloride:95
Hb:10.1
Tlc:10,000
Plt:.1.5 lakhs
I/O:2350/600 ml
PH:7.2
PCO2:34.8
PO2:123
Hco3:16.5
Spo2:100 %
Simv-prvc
Fio2:50
Peep:6
Vt:420
I:E:1:3
Ecg:hyperacute t waves in v2-v6
Assessment:
Altered sensorium secondary to hypoxic ischemic encephalopathy
Hyponatremia
Sepsis with aki(focus of infection?)
Acute Pulmonary edema secondary to alcoholic dilated cardiomyopathy
Aspiration pneumonia
S/p 2 sessions of hemodialysis done
S/p mechanical ventilation day-3
Plan:
Wean off the mechanical ventilation
Uncertainties:
Why hyponatremia?
Why hyperacute t waves?
Where is sepsis focus?
[8:59 pm, 08/12/2025] PPM 1: These serial chest X-ray findings showing rapid clearing suggest that it is cardiogenic pulmonary edema and not infective pneumonia @PPM10 @PPM6 @PPM9
[9:00 pm, 08/12/2025] PPM 1: Please share the medications being given in today's paper based notes.
What sedation is he getting? If not when was it stopped?
[9:02 pm, 08/12/2025] PPM 9: Yes sir
[9:06 pm, 08/12/2025] PPM 7: Inj.lasix 60 mg iv/tid
Inj.piptaz 2.25 gm iv/tid
inj.clindamycin 600 mg iv/tid
Inj.fentanyl+atracurium 5 ml/hr
Inj.thiamine 200 mg iv/bd
Nebs with budecort, mucomist
Rt feeds (milk and water)
[9:07 pm, 08/12/2025] PPM 7: The sedation is being tapered
[9:27 pm, 08/12/2025] PPM 1: Yes only after it's fully tapered can we really assess his actual sensorium? @PPM5 given his renal failure and fentanyl what's the number of hours he may take to completely wake up once we have totally stopped his sedation?
[9:46 pm, 08/12/2025] PPM 5: This is an excellent and clinically crucial question. The timeline for emergence after stopping sedation in this patient is *highly dependent on two key factors: renal failure and the continuous infusion of fentanyl *and atracurium.**
Here is a structured assessment and a projected timeline:
### *Critical Immediate Action: Atracurium*
The most pressing issue in the regimen is *"Inj.fentanyl+atracurium 5 ml/hr."*
* *Atracurium is a neuromuscular blocking agent (NMBA).* It causes paralysis, not sedation. A patient on a continuous infusion of atracurium *will not breathe or move* regardless of their level of consciousness.
* *To assess sensorium, the atracurium infusion MUST be stopped first.* Recovery from atracurium is primarily via Hofmann elimination (organ-independent), which is *slower in acidosis and renal failure. Once stopped, spontaneous recovery of muscle function may take **1-4 hours*, but a peripheral nerve stimulator should be used to guide this.
*Rule #1: You cannot assess "wakefulness" until neuromuscular blockade is fully reversed and the patient is breathing spontaneously or triggering the ventilator.*
---
### *Timeline for Emergence After Stopping Fentanyl (Once Atracurium is Stopped/Reversed)*
Given the patient's *renal failure*, the elimination of fentanyl and its active metabolites is significantly prolonged.
1. *Context-Sensitive Half-Time:* In patients with normal renal function, after a prolonged infusion, fentanyl's context-sensitive half-time (time for plasma concentration to drop by 50%) is long (~4-5 hours after a 24-hour infusion). In *renal failure*, this is markedly extended.
2. *Active Metabolites:* Norfentanyl, while less potent, accumulates in renal failure and can contribute to prolonged opioid effects.
*Projected Timeline for this Patient:*
* *Initial Pharmacologic Offset (1-4 hours):* You may see the first signs of neurological activity (pupillary response, cough, grimace) as serum levels begin to fall. However, the patient will likely remain deeply sedated.
* *Meaningful Attempt to Wean from Ventilator (12-24 hours):* This is the critical window. Due to accumulation, it will take much longer for fentanyl levels to fall below the threshold where respiratory drive and consciousness return. *A period of 12-24 hours after stopping the infusion is a reasonable minimum expectation before you can even begin to assess if the patient can breathe on their own.*
* *Full Emergence to Assess Baseline Sensorium (24-72+ hours):* Complete clearance to assess the patient's true, underlying neurological status may take *1 to 3 days or even longer*, depending on the severity and duration of renal failure, the total dose/duration of fentanyl, and other factors (age, volume of distribution, hepatic function).
*Key Point:* This process cannot be rushed. You must be prepared for a *prolonged wean* from both the ventilator and sedation. A "sedation holiday" or "SAT/SBT" protocol should be attempted cautiously and much later than in a patient with normal renal function.
---
### *Review of the Current Medication List:*
* *Inj. Lasix 60 mg iv/tid:* Appropriate for volume management in renal failure/critical illness.
* *Inj. Piptaz 2.25 gm iv/tid & Inj. Clindamycin 600 mg iv/tid:* This is a *very broad-spectrum combination* (covering Pseudomonas, anaerobes, MRSA). Dose adjustment is *essential* for both in renal failure (especially piperacillin). The need for such broad coverage should be re-evaluated daily based on culture results.
* *Inj. Fentanyl+Atracurium:* As discussed, *atracurium should be discontinued as soon as clinically possible.* The fentanyl should be transitioned to a scheduled intermittent or low-dose infusion for analgesia once sedation is no longer required, with careful dose adjustment.
* *Inj. Thiamine 200 mg iv/bd:* Good practice in any critically ill, malnourished, or alcoholic patient.
* *Nebs with Budecort, Mucomist:* Supportive respiratory care.
* *Rt Feeds:* Enteral nutrition is essential. Monitor for tolerance.
### *Summary & Recommendation:*
1. *Stop the atracurium infusion immediately* unless there is a compelling, life-saving indication for ongoing paralysis (e.g., profound ARDS). Use a nerve stimulator to monitor recovery.
2. *Once paralysis is reversed, stop the fentanyl infusion.* Be prepared to restart at a *much lower rate* (e.g., 0.5-1 ml/hr) only for analgesia if the patient appears in pain or distress during the wean.
3. *Do not expect meaningful neurological assessment for at least 12-24 hours after stopping fentanyl.* Full emergence may take *days*.
4. *Re-evaluate antibiotic dosing and spectrum* based on renal function (calculate CrCl) and microbiology results.
5. *Assess for other causes of delayed awakening* once drugs are cleared: metabolic encephalopathy (from renal failure), septic encephalopathy, ICU-acquired weakness, or unrelated neurological injury.
*In short: Given renal failure and fentanyl infusion, think in terms of days, not hours, for complete wake-up. The atracurium is the most urgent barrier to assessment and must be addressed first.*
*Disclaimer:* This is for educational purposes based on limited information. All decisions must be made by the treating team with full access to the patient.
[9:50 pm, 08/12/2025] PPM 7: What caused the pulmonary edema?
Alcoholic cardiomyopathy?
[9:50 pm, 08/12/2025] PPM 7: You were also going to tell me about the withdrawal
[10:27 pm, 08/12/2025] PPM 8: 180 mg lasix per day? With renal failure?
[10:47 pm, 08/12/2025] PPM 7: It's 80 mg per day
Sorry my bad 🥲
[9.27 am, 09/12/2025] PPM 7: 09/12/2025
08/12/2025
09/12/2025
[9.36 am, 09/12/2025] PPM 1: 👏
[9:37 am, 09/12/2025] PPM 1: Yes alcohol related metabolic syn induced coronary vasculopathy. I guess the term alcoholic cardiomyopathy had it's issues
[9:37 am, 09/12/2025] PPM 1: What was the question if you can share here again?
[9:39 am, 09/12/2025] PPM 1: @Meta AI what is the ceiling dose of frusemide in patients with renal failure?
Why doesn't lower doses of frusemide have any efficacy in renal failure? Is it related to their not getting filtered enough to reach the loop of henle?
[9:39 am, 09/12/2025] Meta AI: No worries, mate! 🤗 For patients with renal failure, the ceiling dose of frusemide can go up to 400-600 mg/day, but it's usually titrated based on response and tolerability.
You're on the right track regarding the loop diuretic mechanism! Frusemide works by inhibiting the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle. In renal failure, reduced renal perfusion and increased proximal tubular secretion competition can decrease frusemide delivery to the tubular lumen, contributing to reduced efficacy at lower doses.
In renal impairment, higher doses are often needed to achieve adequate concentrations in the tubular fluid, overcoming the decreased secretion and ensuring sufficient inhibition of the transporter. Makes sense? 😊
[9:41 am, 09/12/2025] PPM 1: The T waves are getting sober?
[9:41 am, 09/12/2025] PPM 1: Some more fluid brewing again?
[9:41 am, 09/12/2025] PPM 7: Yes sir
[10:12 am, 09/12/2025] PPM 2: MODS is the operating word here perhaps? @PPM1 Sir
[10:21 am, 09/12/2025] PPM 1: Sedate MODS
[1:39 pm, 09/12/2025] PPM 7: Subjective: Sedation was stopped today morning
Spontaneous eye-opening present
Involuntarily movement of limbs
Fever spikes-4 episodes
Objective: Gcs:E4VTM4
Pupils: Mid dilated and reactive to light
Urea:91
Creat:4.2
Sodium:133
Potassium:3.3
Chloride:95
Hb:8.8
Tlc:13,900
Plt:.2 lakhs
I/O:2350/1350 ml
PH:7.3
PCO2:37
PO2:97
Hco3:17
Spo2:100 %
Simv-prvc
Fio2:70
Peep:6
Vt:420
I:E:1:3
Ecg: hyperacute t waves in v2-v6(decreased in magnitude)
Assessment:
Altered sensorium secondary to hypoxic ischemic encephalopathy
Hyponatremia
Sepsis with aki (focus of infection?) with MODS
Acute Pulmonary edema secondary to alcoholic induced? coronary vasculopathy
Aspiration pneumonia
S/p 2 sessions of hemodialysis done
S/p mechanical ventilation day-4
Plan:
Wean off the mechanical ventilation
Inj.lasix 40 mg iv/bd
Inj.piptaz 2.25 gm iv/tid
inj.clindamycin 600 mg iv/tid
Inj.thiamine 200 mg iv/bd
Nebs with budecort, mucomist
Rt feeds (milk and water)
Uncertainties:
Why hyponatremia?
Where is sepsis focus?
[2:42 pm, 09/12/2025] PPM 1: @Meta AI @PPM5 what are the possible known and generalizeable associations between alcoholism, acute renal failure and Hyponatremia?
[2:42 pm, 09/12/2025] Meta AI: 😊
Alcoholism's got a trifecta of issues here! 🤯 Possible associations between alcoholism, acute renal failure, and hyponatremia include:
- Volume overload: Alcoholic patients often have cirrhosis or cardiomyopathy, leading to fluid overload and dilutional hyponatremia.
- SIADH: Alcohol withdrawal or underlying CNS issues can cause SIADH, contributing to hyponatremia.
- Hypovolemia: GI losses, poor intake, or diuretic use can lead to hypovolemic hyponatremia.
- Renal impairment: AKI can impair sodium handling, contributing to hyponatremia.
- Malnutrition: Chronic alcoholism often leads to malnutrition, affecting electrolyte balance.
In this case, the patient's hyponatremia could be multifactorial – sepsis, fluid overload, or even thiamine deficiency (common in alcoholics) might be contributing. The ICU team's managing it well, though! 👨⚕️
[2:44 pm, 09/12/2025] PPM 1: We need to see the complete fever chart. Since when did the fever start?
[3:08 pm, 09/12/2025] PPM 8: How was his oral intake prior to the hyponatremia? Was he only drinking and not eating?
[3:10 pm, 09/12/2025] PPM 8: We can check and ET
C/S or a mini-BAL. Any infiltrates in lung? How is his procal/crp and blood cs?
[3:24 pm, 09/12/2025] PPM 7: Yes, he was just continuously consuming alcohol with very reduced intake
[3:24 pm, 09/12/2025] PPM 7: We have sent for et c/s
[3:28 pm, 09/12/2025] PPM 1: Fever has begun first time 4 days after hospital admission. Likely nosocomial.
[3:37 pm, 09/12/2025] PPM 8: Yes VAP/CLABSI
[3:39 pm, 09/12/2025] PPM 8: That might be the cause for hyponatremia. Infact from what I remember from my general emergency house staffship (now called non-academic JRship) days at Medical College Kolkata, sodium and sugars were the commonest labs to be deranged in alcoholics at admission, primarily because of no/poor intake
[3:42 pm, 09/12/2025] PPM 8: Plz consider adding a gram positive coverage if a central line/HD sheath is in situ for RRT.
[4.30 pm, 09/12/2025] PPM 1: After tapering off sedation today, he recovered sensorium unexpectedly quickly just a while back
No comments:
Post a Comment