27-05-2025
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.
EMR SUMMARY
Age/Gender: 38 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 15/10/2024 05:05 PM
Name of Treating Faculty
(ASSOC PROFF)
(ASST PROFF)
[PGY2]
[PGY1]
Diagnosis
CHRONIC RENAL FAILURE
HYPERTENSIVE URGENCY(RESOLVED)
DENOVO HTN
Case History and Clinical Findings
CHIEF COMPLAINTS:
C/O SOB SINCE 15 DAYS
C/O DRY COUGH SINCE 15 DAYS
HOPI:
PATIENT WAS APPARENTLY ASYMPTOMATIC TILL 15 DAYS AGO THEN PATIENT DEVELOPED SHORTNESS OF BREATH (GRADE II-III) WHICH IS INSIDIOUS IN ONSET,
GRADUALLY PROGRESSIVE ASSCIATED WITH DRY COUGH AND ORTHOPNEA (NOW
DECREASED), HEADACHE, BLURRING OF VISION , PEDAL EDEMA AND DECREASED URINE OUTPUT.
NO C/O FEVER, COLD, BURNING MICTURITION, VOMITINGS, LOOSE STOOLS, PAIN
ABDOMEN
PAST HISTORY:
H/O POLIOMYELITIS OF RIGHT LOWER LIMB SINCE CHILDHOOD
N/K/C/O HTN,DM,CAD,CVA,TB,ASTHMA,EPILEPSY,THYROID DISORDERS
PERSONAL HISTORY
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KIMS HOSPITALS,
DIET: MIXED
APPETITE: NORMAL
SLEEP: ADEQUATE
BOWELS: REGULAR
ADDICTIONS: NIL
ALLERGIES: NIL
GENERAL EXAMINATION:
NO PALLOR, ICTERUS, CYANOSIS, CLUBBING, LYMPHADENOPATHY, PEDAL EDEMABP:220/150MMHG
PR:102BPM
RR:20CPM
SPO2:99@ RA
GRBS: 103 MG%
SYSTEMIC EXAMINATION:
CVS: S1 S2 HEARD, NO MURMURS
RS: BAE PRESENT
CNS: NFND
P/A: SOFT, NT
CNS- CONSCIOUS, PUPILS-NSRL
MOTOR SYSTEM : WASTING OF RIGHT LOWER LIMB
GCS-15/15 E4V5M6
REFLEXES BICEPS TRICEPS SUPINATOR KNEE ANKLE
RIGHT 2+ 2+ 2+ - -
LEFT 2+ 2+ 2+ 2+ +
FINGER NOSE AND KNEE HEEL INCOORDINATION: NO
Investigation
CBP HB TC N L E M B PLT SMEAR RFT UR CR UA CA+2 P NA+ K+ CL- HIV HBSAG HCV
BLOOD UREA 15-10-2024 12:01:PM 196 mg/dl
SERUM CREATININE 15-10-2024 12:01:PM 8.0 mg/dl
Page-3
KIMS HOSPITALS,
COMPLETE URINE EXAMINATION (CUE) 15-10-2024 12:01: PMCOLOUR Paleyellow APPEARANCE Clear REACTION Acidic SP.GRAVITY 1.010 ALBUMIN ++++SUGAR Nil BILE
SALTS Nil BILE PIGMENTS Nil PUS CELLS 4-6 EPITHELIAL CELLS 2-4 RED BLOOD CELLS
Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
Anti HCV Antibodies - RAPID 15-10-2024 12:12:PM Non ReactiveHBsAg-RAPID 15-10-2024
12:12:PM Negative
ABG 15-10-2024 12:12:PM PH 7.38PCO2 24.2PO2 97.2HCO3 14.2 St.HCO3 17.1BEB -9.1BEecf -
9.8TCO2 29.6O2 Sat 97.2O2 Count 13.9LIVER FUNCTION TEST (LFT) 15-10-2024 12:12:PM Total
Bilurubin 1.59 mg/dl Direct Bilurubin 0.43 mg/dl SGOT(AST) 21 IU/LSGPT(ALT) 10 IU/LALKALINE
PHOSPHATASE 151 IU/LTOTAL PROTEINS 6.4 gm/dl ALBUMIN 3.8 gm/dl A/G RATIO 1.46
SERUM ELECTROLYTES (Na, K, C l) 15-10-2024 12:12:PM SODIUM 137 mmol/LPOTASSIUM 3.5mmol/L CHLORIDE 104 mmol/L RFT 16-10-2024 06:21:AM UREA 137 mg/dl CREATININE 6.0
mg/dl URIC ACID 5.8 mmol/L CALCIUM 8.8 mg/dl PHOSPHOROUS 5.0 mg/dl SODIUM 140
mmol/LPOTASSIUM 3.2 mmol/L.CHLORIDE 105 mmol/L
RFT 18-10-2024 07:31:PM UREA 76 mg/dl CREATININE 5.6 mg/dl URIC ACID 4.7 mmol/L CALCIUM
10.1 mg/dl PHOSPHOROUS 4.3 mg/dl SODIUM 140 mmol/L POTASSIUM 3.6 mmol/L. CHLORIDE 99mmol/L
USG DONE ON 15-10-2024
LIVER: N S/E, NO F/L, NO IHBRD
PANCREAS AND SPLEEN: N S/E
RT.KIDNEY: 8X3.6 CM
LT KIDNEY: 8.2X 3.2CM
AORTA IVC: NORMAL
NO LYMPHADENOPATHY
U.BLADDER: DISTENDED
V-U JUNCTION: INTERNAL ECHOES +
PROSTATE: 20 CC N S/E
IMPRESSION:
GRADE I-II RPD CHANGES IN B/L KIDNEYS
2D ECHO
MILD TO MODERATE MR, MILD AR, TRIVIAL TR
NO RWMA, NO AS/MS, CONCENTRIC LVH
GOOD LV SYSTOLIC FUNCTIONS
NO DIASTOLIC DYSFUNCTION, NO LV CLOT
Treatment Given (Enter only Generic Name)
Page-4
KIMS HOSPITALS
1.FLUID RESTRICTION<1.5 L/DAY
2.SALT RESTRICTION<2 GM/DAY
3.INJ.EPO 4000 IU SC/WEEKLY ONCE
4.TAB.NICARDIA 20MG PO/TID 1-1-1
5.TAB.MET XL 50MG PO/OD 1-0-0
6.TAB.NODOSIS 500MG PO/BD 1-0-1
7.TAB.SHELCAL-CT PO/OD 0-1-0
8.TAB.OROFER XT PO/OD 1-0-0
9.TAB.DYTOR 10MG PO/BD 1-0-1
Advice at Discharge
FLUID RESTRICTION<1.5 L/DAY
SALT RESTRICTION<2 GM/DAY
TAB.NICARDIA 20MG PO/TID 1-1-1
TAB.MET XL 50MG PO/OD 1-0-0
TAB.NODOSIS 500MG PO/BD 1-0-1
TAB.SHELCAL-CT PO/OD 0-1-0
TAB.OROFER XT PO/OD 1-0-0
TAB.DYTOR 10MG PO/BD 1-0-1
INJ.EPO 4000 IU SC/WEEKLY ONCE
Follow Up
REVIEW TO NEPHROLOGY OPD AFTER 2 DAYS FOR POSSIBLE MAINTAINANCE
HEMODIALYSIS WITH AV FISTULA ACCESS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR
ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
For Treatment Enquiries Patient/Attendent Declaration: - The medicines prescribed
and the 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
Page-5
KIMS HOSPITALS,
SIGNATURE OF PG/INTERNEE
SIGNATURE OF ADMINISTRATOR
SIGNATURE OF FACULTY
Discharge Date
Date:22/10/24
Ward: NEPHROLOGY
[27-05-2025 16:59] PPM 3: *Discharge Summary Analysis and Recommendations*
*Patient Overview:*
A 38-year-old male with *chronic renal failure (CKD Stage 5)* and resolved hypertensive urgency, presenting with symptoms of volume overload (SOB, orthopnea, pedal edema) and severe hypertension (220/150 mmHg). Past history of poliomyelitis (right lower limb).
---
*Key Findings:*
1. *Renal Function:*
- *Admission creatinine*: 8.0 mg/dL (improved to 5.6 mg/dL post-treatment).
- *Ultrasound*: Bilateral small kidneys (8–8.2 cm) with Grade I-II RPD changes, indicative of chronic kidney disease.
- *Proteinuria*: ++++ albumin on urinalysis.
2. *Hypertensive Emergency:*
- BP 220/150 mmHg with end-organ damage (LVH on echo, blurred vision).
- Managed with *nicardipine* (calcium channel blocker) and *metoprolol XL* (beta-blocker).
3. *Metabolic Abnormalities:*
- *Metabolic acidosis* (HCO₃⁻ 14.2, corrected with sodium bicarbonate).
- *Hypokalemia* (K⁺ 3.2 mmol/L; addressed with monitoring and supplements).
- *Hyperphosphatemia* (5.0 mg/dL; managed with calcium carbonate).
4. *Anemia of CKD:*
- Treated with *EPO injections* and *iron supplementation* (Orofer XT).
---
*Management:*
1. *Blood Pressure Control:*
- *Nicardipine* (20 mg TID) and *metoprolol XL* (50 mg OD) for hypertension.
- *Salt restriction* (<2 g/day) to reduce volume overload.
2. *CKD Complications Addressed:*
- *Fluid restriction* (<1.5 L/day) for volume management.
- *Torasemide* (10 mg BD) for diuresis.
- *Sodium bicarbonate* (Nodosis) for acidosis.
- *Calcium/vitamin D* (Shelcal-CT) and *phosphate binders* for mineral metabolism.
3. *Anemia Management:*
- *Erythropoietin (EPO)* weekly injections and oral iron.
---
*Follow-Up Plan:*
1. *Nephrology Review in 2 Days:*
- Prepare for *maintenance hemodialysis* (AV fistula creation advised).
2. *Monitoring:*
- *Electrolytes* (K⁺, PO₄³⁻), *BP, and **volume status*.
- *Symptoms of uremia/fluid overload* (SOB, edema, urine output).
3. *Lifestyle Modifications:*
- Strict adherence to *fluid/salt restrictions* and medications.
- Avoid NSAIDs/nephrotoxins.
---
*Critical Considerations:*
- *Etiology of CKD*: Unclear; evaluate for glomerulonephritis or hypertensive nephrosclerosis (despite "denovo HTN" label).
- *Dialysis Planning*: Timely AV fistula creation to ensure vascular access.
- *Hypokalemia Risk*: Monitor with diuretic use; consider dietary potassium or supplements.
*Conclusion:*
This patient has advanced CKD with hypertensive urgency, managed acutely with BP control and metabolic stabilization. Long-term focus includes dialysis preparation, anemia/electrolyte management, and strict BP control to delay progression.
[27-05-2025 17:01] PPM 3: *Comprehensive Analysis of the Case:*
*1. Clinical Presentation and Diagnosis:*
- *Patient Profile:* 38-year-old male with *chronic kidney disease (CKD Stage 5)* and resolved *hypertensive urgency/emergency* (given end-organ symptoms: blurred vision, headache).
- *Key Symptoms:* Volume overload (SOB, orthopnea, pedal edema), severe hypertension (220/150 mmHg), and uremia (decreased urine output).
- *Diagnostic Findings:*
- *Renal Function:* Elevated creatinine (8.0 mg/dL at admission, improving to 5.6 mg/dL post-treatment), bilateral small kidneys on ultrasound (8–8.2 cm).
- *Metabolic Acidosis:* ABG showed HCO₃⁻ 14.2 mmol/L, managed with sodium bicarbonate (Nodosis).
- *Proteinuria:* ++++ albumin on urinalysis, indicating significant glomerular damage.
- *Anemia:* Addressed with erythropoietin (EPO) and iron supplementation (Orofer XT).
*2. Management Strategies:*
- *Hypertension Control:*
- *Nicardipine* (rapid-acting calcium channel blocker) and *metoprolol XL* (beta-blocker) for acute BP lowering.
- *Salt restriction* (<2 g/day) and *fluid restriction* (<1.5 L/day) to reduce volume overload.
- *Renal Complications:*
- *Torasemide (Dytor):* Loop diuretic for edema and fluid overload.
- *Sodium bicarbonate:* Corrects metabolic acidosis.
- *Calcium/vitamin D (Shelcal-CT):* Manages mineral bone disorder.
- *Anemia:* Weekly *EPO injections* and oral iron supplementation.
*3. Critical Considerations:*
- *Etiology of CKD:* Unclear, but possibilities include hypertensive nephrosclerosis or glomerulonephritis. Small kidneys suggest chronic, irreversible damage.
- *Hypokalemia Risk:* K⁺ dropped to 3.2 mmol/L (likely diuretic-induced); requires monitoring and possible supplementation.
- *Dialysis Planning:* Follow-up for *AV fistula creation* is urgent to prepare for hemodialysis.
*4. Follow-Up and Long-Term Care:*
- *Immediate Priorities:*
- *Nephrology review in 2 days* to initiate dialysis planning.
- *AV fistula creation* to ensure vascular access.
- *Monitoring:*
- Electrolytes (K⁺, PO₄³⁻), BP, fluid status, and symptoms of uremia.
- EPO-related risks (hypertension, thrombosis).
- *Patient Education:*
- Adherence to fluid/salt restrictions, medications, and dialysis schedule.
- Recognition of emergency symptoms (e.g., worsening SOB, confusion).
*5. Unaddressed Questions:*
- *Etiology Workup:* Despite “denovo HTN” label, consider renal biopsy if size permits (unlikely with small kidneys) or serologic tests (e.g., ANA, ANCA) to rule out autoimmune causes.
- *Peritoneal Dialysis:* Viability as an alternative to hemodialysis, given poliomyelitis-related mobility issues.
- *Social Support:* Ensure patient can manage EPO injections and follow-up appointments.
*Conclusion:*
The patient has *end-stage renal disease (ESRD)* secondary to hypertensive nephropathy or undiagnosed glomerular disease. Acute management successfully addressed hypertensive urgency and volume overload. Long-term survival hinges on *timely dialysis initiation*, strict BP control, and management of CKD complications (anemia, acidosis, mineral disorders). Multidisciplinary care involving nephrology, dietetics, and social work is essential to optimize outcomes.
[27-05-2025 20:00] PPM 1: Thanks
From our data capture pov we needed to have also shared the BP chart along with the initial interventions mentioned in it's timeline.
[28-05-2025 15.35] PPM 1: What time was he noted to have Type 1 @PPM4?
[28-05-2025 16:10] PPM 4: Sir initially at admission the patient came with ambu bag to casualty then we connected him to ventilator on simv modr as patient was conscious and obeying commands but later on the ventilator was showing airway obstruction then on examination we found to have a block in his ET tube and changed it
[28-05-2025 16:12] PPM 4: Then patient was irritable and having tachypnoea we gave sedation and converted to acmv vc mode sir.
[28-05-2025 16:14] PPM 1: So it was a transient type 2 respiratory failure due to tube block but every day the notes are showing type 2 respiratory failure?
[28-05-2025 16:14] PPM 1: Can you share the main learning points from our project on respiratory failure?
[28-05-2025 16:20] PPM 4: Sir patients coming with heart failure and CKD have respiratory failure and I found out patients with heart failure recovered better than the patients with CKD.
The outcome is good in heart failure rather than kidney disease.
[28-05-2025 16:21] PPM 4: Initial identification of the cause for respiratory failure will help in good prognosis of the patient sir.
[28-05-2025 16:50] PPM 1: That must be dependent on their underlying etiology for the heart failure as well as their comorbidities.
What were the etiologies for the respiratory (assuming type 1) failure in the CKD group and what comorbidities did they have in comparison to the pure heart failure group?
[28-05-2025 16.54] PPM 4: Yes sir the heart failure patients have also got the same comorbidities as CKD but there were additional things uncontrolled sugars and hypertension leading to CKD with associated heart failure
[28-05-2025 16:54] PPM 4: Also genetic issues and nsaid abuse
[28-05-2025 16:55] PPM 1: You mean the CKD patients in your 50 patient convenience sampling cohort had more comorbidities in the form of diabetes and hypertension which your heart failure patients didn't have? Can you give us the break up in terms of numbers?
[28-05-2025 17.04] PPM 3: Based on the WhatsApp screenshot content, here's a breakdown of the key medical and communication points:
### Patient Summary
* *38-year-old male*
* *Diagnoses:*
* CKD (Chronic Kidney Disease)
* LVF (Left Ventricular Failure - heart failure)
* HTN (Hypertension - high blood pressure)
* *Current Emergency:* Hypertensive LVF crisis.
### Clinical Presentation & Problem
* Presented with *Type 1 Respiratory Failure* (low oxygen levels without high CO2 retention).
* This respiratory failure was *not resolving* despite the patient being *mechanically ventilated*.
* The clinical team believes the unresolved respiratory failure is *directly linked to the uncontrolled LVF*.
### Proposed Management Plan
1. *Initiate NTG (Nitroglycerin):* A potent vasodilator used to treat heart failure and hypertensive crises. It reduces the heart's workload by dilating veins (reducing preload) and arteries (reducing afterload and blood pressure).
2. *Aggressively Reduce BP (Blood Pressure):* Essential to treat the underlying hypertensive crisis driving the LVF.
### Team Communication & Data Capture Focus
* *PPM3* is updating the record with events from this admission.
* The core event being highlighted is the *persistent respiratory failure despite ventilation* and the *need for NTG/BP control* to resolve the LVF.
* The message stresses that capturing this specific clinical reasoning and decision point ("his LVF won't respond till we begin NTG and reduce his BP") is crucial from a *"data capture point of view" (POV)*.
* *PPM1* sent the message, tagging *PPM5* (likely PPM3 or another key clinician) and *PPM4* (likely another team member involved in data capture/analysis).
### Key Takeaway
The patient is in a critical state where standard ventilation isn't sufficient. The team identifies uncontrolled hypertension as the root cause perpetuating the heart failure (LVF) and the consequent respiratory failure. *Immediate treatment with Nitroglycerin and aggressive blood pressure reduction is deemed essential* to break this cycle and improve the patient's condition. Documenting this specific clinical decision logic is emphasized as important data.
[28-05-2025 17.07] PPM 3: Based on the second WhatsApp screenshot, here's a structured analysis of the clinical documentation workflow being established:
### Key Documentation Requirements
1. *Timeline Focused*
Nursing notes required at strict intervals:
3 PM → 2:30 PM → 4 PM → 5 PM → 6 PM → 7 PM → 8 PM
(Note: 2:30 PM appears retroactive; others are hourly from 3 PM onward)
2. *Accountability Protocol*
‣ *Mandatory Sign-off:* Each entry requires signature
‣ *Identification:* Must include nurse's *name + ID number*
3. *Linked Clinical Context*
‣ Relates directly to *Dr. Abdulsalam's updates* (spelling varies slightly from prior "Abdusalam")
‣ Documents evolution of:
> ➔ Hypertensive LVF emergency
> ➔ Type 1 respiratory failure unresponsive to ventilation
> ➔ Critical NTG (Nitroglycerin) initiation and BP reduction efforts
---
### Actionable Implications
| *Time* | *Expected Documentation Focus* | *Clinical Goal* |
|----------|----------------------------------|------------------|
| *2:30 PM* | Baseline status before NTG initiation | Record pre-intervention vitals (BP, O2 sat, resp. effort) |
| *3-8 PM* | *Hourly response tracking* | Monitor: <br>• BP reduction efficacy <br>• LVF/respiratory failure response <br>• NTG titration needs <br>• Adverse effects |
*Why this matters:*
- Creates an *auditable trail* of the NTG intervention’s impact.
- Captures whether respiratory failure resolves as BP is controlled (validating the team’s hypothesis).
- Supports real-time clinical decision-making (e.g., escalating care if no improvement by 6 PM).
---
### Next Steps for the Team
1. *Dr. Abdulsalam/Nursing Lead:*
→ Clarify if 2:30 PM is retrospective documentation of pre-NTG status.
→ Define specific metrics for each timepoint (e.g., "BP must be <160/100 by 5 PM").
2. *Rakesh Biswas/Nithin Goutham:*
→ Ensure EHR templates reflect this structured timeline.
→ Verify all signatures include *printed name + ID* (compliance safeguard).
3. *ICU Team:*
→ Correlate nursing notes with vent settings/ABGs to track respiratory failure resolution.
> ⚠ *Critical Insight:* This structured approach transforms clinical reasoning into actionable data – essential for both immediate care and retrospective analysis of why NTG was deemed imperative.
[30-05-2025 16:44] PPM 1: Update:
Current issues: persistent coma after the iv midazolam 30 mg over 24 hours administered on the first day of admission on 24/5/25 at 3:30PM
Partial explanation: Inability of the patient's failed renal system to excrete the midazolam?
Off midazolam and on no other sedatives since 25/5/25 and yet comatose and reacting only to deep painful stimuli. @PPM6 @PPM4 please share his serum creatinine chart since admission.
On examination, oculocephalic reflexes normal indicating brain stem is functioning well.
Question: How common is it for a patient given midazolam over 24 hours to not wake up for the next 5 days due to improper renal excretion?
[30-05-2025 16.45] PPM 1: Today had a tracheostomy followed by another hypertensive episode as visible in his chart!
Was it due to the tracheostomy pain?
[30-05-2025 16:47] PPM 3: Based on the search results and your description of the case, prolonged coma following midazolam administration in a patient with renal impairment is an established phenomenon, though a 5-day duration is at the extreme end of what's typically observed. Here's a synthesis of key insights:
### ⚕ 1. *Mechanism of Prolonged Sedation in Renal Failure*
- Midazolam is metabolized to *1-hydroxymidazolam (1-OH-MDZ)* and its *glucuronidated conjugate (1-OH-MDZ-Glu). While 1-OH-MDZ is rapidly cleared, **1-OH-MDZ-Glu accumulates significantly in renal failure* due to reliance on renal excretion .
- *Pharmacological Activity*: 1-OH-MDZ-Glu has only ~10x weaker affinity for GABA receptors than midazolam itself (affinity constant 16 nmol/L vs. 1.4 nmol/L) . This metabolite contributes substantially to prolonged sedation when kidneys fail to clear it.
### 📊 2. *Clinical Evidence and Prevalence*
- *Renal Impairment Severity Matters*: Studies report coma reversal with flumazenil in renal failure patients even when parent midazolam levels are subtherapeutic, confirming metabolite-mediated effects . - *Kinetics in Critical Illness: A 2024 study found midazolam and its metabolites follow **first-order elimination kinetics, but the **AUC of midazolam strongly correlates with awakening time* (R²=0.96, p<0.001). Mean serum concentration at awakening was ~16.8 ng/mL . In your patient, levels likely remain elevated due to metabolite accumulation.
- *Frequency*: While exact prevalence is unquantified, prolonged sedation >48–72 hours is frequently linked to renal dysfunction in ICU settings, especially with doses >0.2 mg/kg/h .
### ⚠ 3. *Contributing Factors Beyond Renal Failure*
- *Age & Critical Illness: Elderly patients and those with hypoperfusion (e.g., post-cardiac arrest) have **reduced hepatic metabolism* of midazolam, compounding renal effects .
- *Drug Interactions*: Concomitant opioids/propofol or CYP3A4 inhibitors (e.g., erythromycin) can delay clearance .
- *Midazolam Infusion Syndrome*: High doses (>10 mg/h) may cause prolonged coma due to tissue accumulation, even without renal disease .
### 🧪 4. *Diagnostic and Management Considerations*
- *Flumazenil Challenge*: A transient response to flumazenil (benzodiazepine antagonist) supports metabolite-mediated sedation. However, this carries seizure risk in mixed overdoses .
- *Monitoring: Serum creatinine trends are essential. **Creatinine clearance <50 mL/min* significantly increases metabolite half-life .
- *Alternative Causes*: Normal oculocephalic reflexes suggest intact brainstem function, but exclude hypoxic brain injury, sepsis, or other toxins .
### 💎 Key Takeaway
Prolonged coma *beyond 5 days* is uncommon but biologically plausible in severe renal failure, particularly with higher midazolam doses. Metabolite accumulation is the primary mechanism, though contributions from critical illness, age, and drug interactions should be evaluated. Review the patient’s *creatinine trajectory, fluid balance, and concurrent medications* to stratify risk. Flumazenil may aid diagnosis but requires caution.
> [!NOTE]
> If serum creatinine shows acute kidney injury (e.g., doubling from baseline or eGFR <30 mL/min), metabolite accumulation is highly likely. Share creatinine data for further refinement of this assessment.
[30-05-2025 16:53] PPM 3: The role of dialysis in reversing midazolam/1-OH-midazolam-glucuronide (1-OH-MDZ-Glu)-induced coma is *limited but potentially beneficial in severe renal failure*, depending on the clinical context and modality used. Here’s a concise analysis:
---
### ⚠ Key Constraints for Dialysis Efficacy
1. *Metabolite Characteristics*:
- The primary sedative culprit in renal failure is *1-OH-MDZ-Glu* (accumulating glucuronide metabolite).
- *Properties*: Low molecular weight (~450 Da), water-soluble, minimal protein binding.
- *Dialyzability: **Yes* – but efficiency varies by dialysis modality.
2. *Dialysis Modality Matters*:
- *CRRT (Continuous Renal Replacement Therapy)*:
- Low clearance due to *low flow rates* (effluent rates typically 20-35 mL/kg/h).
- Case reports show *modest reductions* in sedation time (e.g., 24–48h faster awakening).
- *Intermittent HD (Hemodialysis)*:
- Higher clearance potential (blood flow 200–400 mL/min), but *short duration* (3–4h/session).
- Removes metabolites faster but may not eliminate deep tissue stores.
3. *Clinical Evidence*:
- *Supportive*: Cases report flumazenil-responsive coma resolving faster with CRRT/HD.
- *Limitations*: Most evidence is from case reports (e.g., ICU patients with AKI on CVVHDF).
- *No RCTs*: Insufficient data to confirm routine benefit.
---
### 🩺 Practical Recommendations
| *Scenario* | *Action* |
|----------------------------------|----------------------------------------------------------------------------|
| *Patient already on CRRT* | *Optimize CRRT settings*: Maximize effluent flow (≥35 mL/kg/h), use high-flux filters. |
| *Severe AKI (CrCl <15 mL/min) with coma* | Consider *intermittent HD* for rapid metabolite reduction if clinically stable. |
| *No dialysis access* | *Not recommended* to initiate dialysis solely for midazolam clearance. |
---
### ⚖ Risk-Benefit Considerations
- *Pros*:
- May accelerate awakening by 1–2 days in profound renal failure.
- Addresses concurrent uremia/acidosis contributing to encephalopathy.
- *Cons*:
- *Hemodynamic instability* (especially with intermittent HD).
- *Incomplete clearance*: Tissue redistribution prolongs sedation.
- *No substitute for supportive care*: Time remains the primary "antidote."
---
### 🚨 Critical Adjuncts
1. *Flumazenil challenge*:
- *Diagnostic use*: Transient arousal confirms benzodiazepine etiology.
- *Caution*: Risk of seizures in mixed overdoses/chronic users; use microdosing (e.g., 0.1–0.3 mg IV).
2. *Metabolite testing*:
- If available, measure *serum 1-OH-MDZ-Glu levels* (confirms accumulation).
3. *Rule out other causes*:
- Check ammonia, EEG (non-convulsive seizures), CT/MRI (hypoxic injury).
---
### 💎 Bottom Line
Dialysis (especially CRRT optimization) *may help but is not first-line therapy*. Prioritize:
1. *Confirm renal impairment* (share creatinine/eGFR trends).
2. *Exclude non-toxicologic causes* of coma.
3. *Supportive care + time* (metabolite half-life may exceed 7 days in ESRD).
> 📌 *If the patient is already on CRRT for renal indications: Maximizing clearance is reasonable. If not, reserve dialysis for *refractory cases with severe AKI after multidisciplinary discussion.
[30-05-2025 16:57] PPM 1: Thanks!
Assuming deepseek.
Would be nice to have some journal references for the statements it makes above. The best combo is perplexity and deep seek for this I guess?
[30-05-2025 16:58] PPM 1: He's already on dialysis even before the current admission but it doesn't seem to have helped in the presumed midazolam wash out
[30-05-2025 17:00] PPM 3: The following references from the search results support the topic of prolonged midazolam-induced coma in renal failure, focusing on metabolite accumulation, pharmacological mechanisms, and clinical management:
### ⚕ 1. *Metabolite Accumulation in Renal Failure*
- *Bauer et al. (1995)*: Demonstrated that conjugated metabolites of midazolam (particularly α-hydroxymidazolam glucuronide) accumulate in renal failure, causing prolonged sedation even when parent drug levels are subtherapeutic. Flumazenil rapidly reversed coma, confirming benzodiazepine receptor-mediated effects. Affinity of glucuronidated metabolites for CNS receptors is only ~10x weaker than midazolam .
- *Caballero et al. (2024)*: Highlighted midazolam's active metabolites (hydroxymidazolam) as key contributors to oversedation in ICU patients with kidney disease, leading to delayed awakening .
### 💧 2. *Renal Excretion Mechanisms*
- *StatPearls (2025)*: Noted that 60–80% of midazolam is excreted renally as conjugated metabolites. Impaired renal function prolongs elimination, increasing sedation duration .
- *DrugBank*: Confirmed midazolam's metabolism to α-hydroxymidazolam glucuronide, which relies on renal excretion. Accumulation occurs in renal impairment, extending half-life .
### 🧪 3. *Clinical Evidence and Case Reports*
- *Korean Journal of Nephrology (2010)*: Reported a 76-year-old peritoneal dialysis patient with 280-hour sedation after midazolam infusion cessation, illustrating extreme prolongation in end-stage renal disease (ESRD) .
- *Critical Care Medicine (1998)*: Identified altered kinetics and metabolite accumulation as causes of prolonged sedation in ICU patients, especially with renal dysfunction .
### ⚠ 4. *Pharmacokinetics in Critical Illness*
- *Medicina Intensiva (2024)*: Emphasized midazolam's cumulative effects in renal/hepatic failure due to reduced clearance and large volume of distribution. Compared unfavorably to alternatives (e.g., propofol) for faster awakening .
- *Wikipedia*: Cited prolonged elimination half-life (up to days) with continuous infusion in renal impairment, leading to "midazolam infusion syndrome" .
### 🩺 5. *Management Considerations*
- *Pfizer Medical Information*: Advised dose reduction in renal impairment and cautioned about respiratory depression risks. Flumazenil is indicated for reversal but carries seizure risks in mixed overdoses .
- *Drugs.com Monograph*: Recommended avoiding midazolam infusions for long-term ICU sedation in renal failure due to unpredictable recovery and metabolite accumulation .
### 📊 6. *Guidelines and Alternatives*
- *ICU Sedation Debates (2024)*: Advocated against midazolam in ventilated patients with renal failure, favoring propofol/ketamine for quicker awakening and reduced delirium risk .
These references collectively validate that *prolonged coma (>5 days) is uncommon but mechanistically plausible in severe renal failure*, primarily due to active metabolite accumulation. Key management strategies include flumazenil trials, renal replacement therapy optimization, and alternative sedatives .
[30-05-2025 17:04] PPM 3: Based on the search results, dialysis (particularly CRRT) plays a *limited but context-dependent role* in managing prolonged midazolam-induced coma in renal failure, primarily through clearance of the active metabolite *1-OH-midazolam-glucuronide*. Key evidence and considerations are summarized below:
---
### 🧪 *1. Metabolite-Specific Clearance*
- *1-OH-midazolam-glucuronide* (the primary sedative metabolite) is *moderately dialyzable* due to its low molecular weight (~450 Da), water solubility, and minimal protein binding .
- *CRRT clearance*:
- *CVVHD/CVVHDF* achieves ~15.7 mL/min clearance for 1-OH-midazolam-glucuronide, removing *up to 43%* of accumulated metabolite .
- *Parent midazolam and 1-OH-midazolam* are *poorly dialyzed* (clearance: 1.4 mL/min and 2.7 mL/min, respectively) due to high protein binding and lipophilicity .
---
### ⚠ *2. Clinical Evidence for Dialysis Efficacy*
- *Supportive case data*:
- Prolonged coma reversed faster with CRRT in some renal failure patients, likely due to metabolite reduction .
- A study of COVID-19 ICU patients on CRRT showed accelerated awakening after optimizing effluent flow rates .
- *Limitations*:
- *No significant midazolam clearance* was observed during continuous hemodiafiltration (CHDF) in MODS patients .
- *Rebound sedation* may occur due to redistribution from adipose tissue, limiting dialysis benefits .
---
### ⚖ *3. Dialysis Modality Matters*
| *Modality* | *1-OH-Midazolam-Glucuronide Clearance* | *Clinical Utility* |
|---------------------|------------------------------------------|--------------------------------------------------------------------------------------|
| *CRRT (CVVHDF)* | Moderate (15–28 mL/min) | Best option if already initiated; optimize effluent flow (>35 mL/kg/h) and high-flux filters. |
| *Intermittent HD* | Low to moderate | Short sessions (3–4 hr) limit extraction; risk of hemodynamic instability. |
| *Peritoneal Dialysis* | Negligible | Ineffective; prolonged sedation up to 280 hours reported . |
---
### ⚠ *4. Risks and Practical Considerations*
- *Initiation criteria*:
- Only justified if *severe AKI (eGFR <15 mL/min)* necessitates renal replacement independent of midazolam clearance .
- Avoid dialysis solely for metabolite removal—*supportive care and time* are primary .
- *Key risks*:
- Hemodynamic instability during intermittent HD .
- Filter clotting/downtime reduces delivered clearance .
---
### 💎 *5. Adjunct Management Recommendations*
1. *Flumazenil challenge*: Diagnostic/test dose (0.1–0.3 mg IV) to confirm benzodiazepine etiology .
2. *Metabolite monitoring*: Measure serum 1-OH-midazolam-glucuronide if available .
3. *Exclude alternatives*: Hypoxic brain injury, sepsis, or drug interactions (e.g., CYP3A4 inhibitors) . ---
### 📊 *Evidence Summary Table*
| *Key Study* | *Finding* | *Implication* |
|-----------------------------------|-----------------------------------------------------------------------------|--------------------------------------------------|
| Bauer et al. (1995) | Glucuronide metabolite has 10% midazolam potency; accumulates in renal failure. | Flumazenil reverses coma; dialysis may aid metabolite clearance. |
| CRRT Clearance Study (2023) | 43% glucuronide clearance with CVVHDF; parent drug not cleared. | Optimize CRRT settings if already in use. |
| Peritoneal Dialysis Case (2010) | 280-hour sedation after midazolam cessation in ESRD. | Avoid midazolam infusions in dialysis patients. |
| CHDF in MODS (2001) | Zero midazolam clearance during hemodiafiltration. | Dialysis unlikely to benefit without severe AKI. |
---
### 💎 *Conclusion*
Dialysis (especially CRRT) has a *limited role—it may reduce 1-OH-midazolam-glucuronide levels in severe renal failure but is **not first-line therapy*. Reserve for patients already requiring renal replacement. Prioritize:
1. *Confirm renal impairment* (track creatinine/eGFR trends 📉).
2. *Flumazenil trial* for diagnosis.
3. *Supportive care* while awaiting metabolite elimination (half-life >7 days in ESRD) .
> ⚠ *Key Takeaway: In non-dialysis patients, initiating CRRT/HD solely for midazolam clearance is **not recommended* due to marginal benefits vs. risks .
[30-05-2025 17:07] PPM 1: Wow! Perplexity?
[30-05-2025 17:08] PPM 3: DeepSeek
[30-05-2025 17:09] PPM 3: DeepSeek is a Joker 🃏
[30-05-2025 17:11] PPM 1: I guess it can be trained to share journal article links too like perplexity to support each statement?
[05-06-025 15.46] PPM 1: Can we get the LLM to comment on this patient's hypertension monitoring chart with reference to the interventions for the hypertension and what could have been done better?
[05-06-2025 16:26] PPM 3: Based on your query, I can provide a framework for analyzing a hypertension monitoring chart and evaluating interventions. *To give specific feedback, I would need the actual chart data* (readings, dates, medications, lifestyle interventions, etc.), but here’s how an LLM would approach this:
---
### *Key Elements the LLM Would Analyze:*
1. *Blood Pressure Trends*
- Consistency of readings (e.g., morning vs. evening, pre/post-medication).
- Patterns (e.g., uncontrolled spikes, white-coat hypertension).
- Goal achievement (e.g., sustained <130/80 mmHg per most guidelines).
2. *Interventions Implemented*
- Medications: Adherence, timing, dosages, combinations.
- Lifestyle: Salt restriction, exercise, weight management, alcohol/smoking cessation.
- Monitoring: Frequency of readings, home vs. clinic measurements.
3. *Red Flags*
- Systolic >180 mmHg or diastolic >110 mmHg (urgent action needed).
- Side effects (e.g., hypotension from overmedication).
- Inconsistent data logging.
---
### *Common Gaps & Improvements the LLM Might Suggest:*
#### ⚠ *Typical Shortcomings in Hypertension Management*
| *Area* | *What Could Be Done Better* |
|-------------------------|-----------------------------------------------------------------------------------------------|
| *Medication* | - Inadequate titration or lack of combination therapy (e.g., not using ACEI + CCB/thiazide).<br>- Poor timing (e.g., taking all meds at once instead of staggered doses). |
| *Lifestyle* | - No documented salt intake tracking or DASH diet adherence.<br>- Exercise plans missing specificity (e.g., "walk more" vs. "150 mins/week aerobic"). |
| *Monitoring* | - Irregular home readings (e.g., gaps >3 days).<br>- No ambulatory BP monitoring if "white-coat effect" suspected. |
| *Patient Engagement* | - No education on proper BP measurement technique (e.g., rest 5 mins, arm at heart level).<br>- Lack of symptom journals (e.g., dizziness, edema). |
#### ✅ *Evidence-Based Interventions to Optimize*
1. *Pharmacology*
- Add low-dose thiazide if not already used (e.g., chlorthalidone 12.5 mg/day).
- Switch to evening dosing if nocturnal hypertension is present.
2. *Lifestyle*
- *Structured program:* 30-min daily exercise + <1,500 mg sodium/day.
- *Alcohol:* Limit to ≤1 drink/day (if applicable).
3. *Technology*
- Use validated Bluetooth BP cuffs with automated data logging.
- Telehealth follow-ups every 2 weeks until controlled.
4. *Risk Factor Management*
- Screen for/comanage OSA, CKD, or diabetes if not addressed.
---
### *Example LLM Commentary (Hypothetical):*
> "The chart shows inconsistent evening systolic spikes (150–170 mmHg) despite morning lisinopril dosing. *Key gaps:*
> - No evening BP medication (consider adding amlodipine at night).
> - Only 3 home readings/week → recommend daily AM/PM logs.
> - No recorded salt intake → provide a 7-day food diary.
> *Intervention success:* Medication adherence is excellent (95%), but lifestyle modifications lack tracking. *Action:* Add a low-sodium diet plan and schedule 24-hr ABPM to rule out masked hypertension."
---
*To get a tailored analysis, please share:*
- The hypertension chart (readings with dates/times).
- Current medications/dosages.
- Lifestyle interventions attempted.
- Patient demographics (age, comorbidities like diabetes/kidney disease).
I’ll then provide specific insights! 🩺📊
[05-06-2025 16:28] PPM 3: To provide *specific insights* on a hypertension monitoring chart, I would need the actual data (e.g., BP readings, medications, lifestyle logs). Since that isn’t attached, I’ll demonstrate using a *hypothetical case* with common clinical patterns. Below is an example analysis structured for real-world use:
---
### *Patient Hypertension Chart Review*
(Hypothetical Data Based on Common Scenarios)
*Patient Profile*: 58M, Type 2 Diabetes, BMI 31
*Goal BP*: <130/80 mmHg
| *Date* | *Time* | *SBP/DBP (mmHg)* | *Medications* | *Notes* |
|----------------|----------|--------------------|--------------------------|-------------------------------|
| 2025-05-01 | 08:00 | 148/92 | Lisinopril 10mg AM | Skipped exercise |
| 2025-05-03 | 20:00 | 162/98 | ... | Ate takeout (high salt) |
| 2025-05-05 | 08:00 | 136/84 | ... | Walked 30 mins |
| 2025-05-08 | 20:00 | 158/96 | ... | Stressful work day |
---
### *Specific Insights & Recommendations*
#### 🔴 *Critical Observations*
1. *Uncontrolled Evening Hypertension*:
- Consistently elevated PM readings (avg. 160/95 mmHg vs. AM avg. 142/88 mmHg).
- *Cause*: Likely inadequate 24-hour coverage from AM-only lisinopril.
2. *Salt Sensitivity Signs*:
- Spikes correlate with high-salt meals (e.g., 162/98 after takeout).
3. *Insufficient Monitoring*:
- Gaps in data (only 4 readings over 8 days). No weekend readings.
#### 💊 *Intervention Critique*
| *Current Approach* | *Gaps* | *Evidence-Based Fix* |
|----------------------------|-------------------------------------------|-----------------------------------------|
| *Lisinopril 10mg AM* | Wears off by evening; no renal protection | ➞ *Add* amlodipine 5mg PM or switch to ARB (e.g., telmisartan for diabetes). |
| *No diuretic* | Missed first-line therapy for salt sensitivity | ➞ *Add* chlorthalidone 12.5mg AM. |
| *Lifestyle: "Walk more"* | Unstructured; no accountability | ➞ *Prescribe* 150 min/week aerobic exercise (track via app). |
#### 🚨 *Missed Opportunities*
- *No nocturnal BP assessment: Risk of masked nighttime hypertension → **Order 24hr ABPM*.
- *No DASH diet guidance: Patient unaware of sodium targets → **Provide 7-day low-salt meal plan*.
- *Inconsistent home monitoring: Readings 2–3x/week → **Require BID (AM/PM) logs daily*.
#### ✅ *Action Plan for Rapid Control*
1. *Medication Optimization*:
- *AM*: Lisinopril 20mg + Chlorthalidone 12.5mg
- *PM*: Amlodipine 5mg
2. *Lifestyle Prescription*:
- Salt: <1,500 mg/day (use urine Na+ test to verify).
- Exercise: Brisk walking 30 min/day, 5x/week (track with pedometer).
3. *Monitoring Protocol*:
- *Daily*: BP AM/PM + symptom log (dizziness, edema).
- *Weekly*: Telehealth check-ins until BP <130/80 sustained.
---
### *Why This Would Work*
- *Evening BP Control*: Adding PM amlodipine counters nocturnal spikes ([Hermida et al., 2020](https://pubmed.ncbi.nlm.nih.gov/32240511/)).
- *Salt Sensitivity*: Chlorthalidone reduces volume overload (NIH SPRINT Trial).
- *Structured Lifestyle*: Specificity improves adherence (AHA Hypertension Guidelines 2023).
> ⚠ *Red Flag*: If BP >180/110 occurs, evaluate for secondary causes (e.g., renal artery stenosis).
*To tailor this to your patient, share the actual chart!* I’ll refine every recommendation based on real data. 🩺
[05-06-2025 16:30] PPM 1: Any way to make it convert the hand written data from the image into it's own readable text format?
[06-06-2025 15.17] PPM 1: Today's ENT follow up on tracheostomy notes.
[06-06-2025 15.31] PPM 1: Other than his Hypertension crisis for which we can see the number of drugs he's getting in this attached progress notes and in yesterday's handwritten BP chart
Can we suggest how best to work him up for his coma that currently appears to be a persistent vegetative state?
[06-06-2025 16.35] PPM 1: Afternoon bedside clinical learning session:
[06-06-2025 16.46] PPM 1: History reviewed:
One and a half years back the patient experienced a sudden loss of his ability to talk and it subsided in a day after hospitalization.
After that stroke TIA he was fine till 7 months ago when he started experiencing shortness of breath keeping him awake at night for seven days and on the seventh day after he met the doctor he was told to have a renal failure with hypertension following which he was initiated on weekly hemodialysis.
Currently in this admission after his recent hypertensive emergency and LVF for which he was intubated and sedated one of the issues was persistent coma that now appears to be a locked in syndrome where the patient is able to open his eyes and perhaps understand what's going on but completely unable to move a limb to communicate.
Asked @PPM7 @PPM8to try to communicate with him using this locked in code described here 👇
[06-06-2025 20:47] PPM 3: Based on the provided progress note from *June 6, 2025*, here's a structured summary of the patient's status and care plan:
### Patient Overview
* *Demographics:* 38-year-old male
* *Major Diagnoses:*
* Status post (S/P) Axis-SIP tracheostomy (POD 7).
* Type II Respiratory Failure (residual).
* Sepsis secondary to UTI (residual).
* Chronic Renal Disease (CRD) on Maintenance Hemodialysis (MHD).
* Grade II Bed sores.
* *Relevant History:* Hypertension (HTN), Heart Failure (HF), mild impairment (?), likely history of malignancy (SIP 4 cycles of chemotherapy done + 1 session of IM? done).
### Current Status (C/6/25)
1. *Respiratory:*
* On T-piece trial (weaning trial).
* FiO₂: 0.4 (24% Venturi mask equivalent).
* SpO₂: 100% on current support.
* *Tracheostomy:* Size 7 tube in place.
* Stoma site: Healthy.
* Secretions: Minimal, thin consistency.
* Air entry: Present bilaterally.
* Breath sounds: Clear.
2. *Vitals:*
* BP: 110/70 mmHg
* PR: 90 bpm
* SpO₂: 100% (on T-piece FiO₂ 0.4)
3. *Other:*
* Pain Score: Not documented/applicable at this time ().
* Bed Sores: Grade II present.
### Nursing Care Plan / Orders
1. *Medications:* Continue all medications as prescribed by the primary doctor.
2. *Tracheostomy Care:*
* *Suctioning:* Perform tracheostomy tube suctioning *every hour* as needed (PRN).
* *Secretion Management:* Administer *2-3 doses of diluted sodium bicarbonate* along the inner walls of the tracheostomy tube to help loosen secretions (as needed).
3. *Monitoring:* Continue close monitoring of respiratory status, vital signs, tracheostomy site, and secretions.
4. *Pain Management:* Assess pain score regularly. *Intervene if pain score is 4 or above* (per protocol).
5. *Wound Care:* Manage Grade II bed sores per protocol.
### Key Notes
* The patient is undergoing a T-piece trial, indicating progress in weaning from ventilator support.
* Respiratory status is currently stable on the T-piece with good oxygenation.
* Tracheostomy site is healthy with minimal, manageable secretions.
* Residual issues from respiratory failure and sepsis are noted but improving.
* Pain assessment documentation is required if applicable.
*Documentation Reminder:* Progress notes must be signed clearly with name and designation. Pain score should only be filled if applicable to the patient.
[06-06-2025 20:51] +964 750 136 1306: Based on the June 6, 2025 progress note, here are the key clinical priorities and next steps for this patient:
### Immediate Clinical Priorities
1. *Respiratory Weaning:*
* *Continue & Monitor T-piece Trial:* Closely observe work of breathing, SpO₂, and comfort. Document tolerance hourly.
* *Plan:* If stable >24-48 hours, consider decannulation assessment or downsizing tracheostomy tube. Goal: Liberate from artificial airway.
2. *Tracheostomy Care:*
* *Strict Hourly Suctioning:* Perform PRN suction every hour as ordered (due to "Suction PRN" and "Secretions D" - likely meaning secretions present). Focus on minimizing irritation.
* *Sodium Bicarbonate Instillation:* Administer 2-3 doses diluted NaHCO₃ along tube walls PRN to manage secretions. Document effectiveness.
* *Stoma Care:* Continue daily inspection/cleaning (site noted as healthy).
3. *Infection Management:*
* *Residual Sepsis/UTI:* Review cultures/sensitivities. Ensure appropriate antibiotic course completion. Monitor WBC, CRP, fever, urinalysis. Goal: Resolve residual infection.
4. *Comorbidity Management:*
* *Renal (CRD on MHD):* Coordinate with nephrology/dialysis team. Ensure next HD session scheduled. Monitor electrolytes/fluid balance.
* *Cardiac (HTN, HF):* Continue cardiac meds. Monitor BP/volume status closely, especially during weaning/HD.
* *Malignancy (SIP):* Confirm oncology follow-up plan post-discharge.
5. *Wound Care:*
* *Grade II Pressure Ulcer:* Implement strict pressure relief protocol (turning schedule, support surface). Document wound characteristics & treatment.
### Specific Next Steps for the Next Progress Note (C/7/25)
1. *Vitals & Respiratory:*
* Document T-piece tolerance (hours tolerated, FiO₂, SpO₂, work of breathing).
* Reassess breath sounds, secretion amount/character, air entry.
* Recheck tracheostomy stoma site.
2. *Pain Assessment:*
* *Mandatory:* Assess and document Pain Score (______ is invalid). Intervene if ≥4.
3. *Secretions & Suctioning:*
* Document frequency of suctioning needed and response to NaHCO₃.
* Assess if hourly suctioning remains necessary or can be de-escalated.
4. *Infection & Sepsis Markers:*
* Review/documented latest WBC, CRP, temperature, urine output/character.
5. *Dialysis:*
* Document last/next HD session and tolerance.
6. *Wound:*
* Document pressure ulcer stage, size, exudate, and any signs of infection.
7. *Overall Assessment & Plan:*
* Update problem list (e.g., "Improving resp failure," "Resolving UTI").
* Adjust plan based on above assessments (e.g., wean O₂, reduce suction frequency, plan decannulation, schedule HD, wound consult).
* *Address Discharge Planning:* Start considering needs (home O₂? home nursing? dialysis transport? caregiver trach care training?).
### Critical Reminders
* *Sign Note Clearly:* Include full name and designation.
* *Pain Score:* MUST be documented for this patient (chronic conditions, wounds, procedures).
* *Re-evaluate Orders:* Is hourly suctioning still indicated? Is the NaHCO₃ dose effective? Communicate with the primary team if adjustments seem needed.
*The overarching goals are:* 1) Successfully wean from the tracheostomy, 2) Fully resolve the sepsis, 3) Manage chronic conditions (renal, cardiac, malignancy), 4) Heal pressure injuries, and 5) Plan for safe discharge. The next 24-48 hours are crucial for assessing respiratory weaning progress and infection resolution.
[06-06-2025 21:03] PPM 3: Based on the limited details in the provided progress note and the new concern for *persistent coma/vegetative state*, here is a structured diagnostic approach to identify potentially reversible causes and establish a diagnosis. This workup should be prioritized alongside his critical care management:
---
### *Step 1: Urgent Bedside Assessment & Stabilization*
1. *Neurological Exam:*
- *Glasgow Coma Scale (GCS):* Quantify level of consciousness (absent in the note).
- *Brainstem Reflexes:* Pupillary light reflex, corneal reflex, gag/cough reflex (tracheostomy complicates assessment).
- *Motor Response:* Purposeful vs. posturing (decorticate/decerebrate), seizures.
- *Pain Response:* Central vs. peripheral reflex (e.g., supraorbital pressure).
2. *Vital Signs:*
- Exclude hypoxia (SpO₂), hypercapnia (ABG), BP extremes (hypertensive encephalopathy/hypotension), fever (sepsis).
---
### *Step 2: Review/Discontinue Sedating Medications*
- *Screen ALL current meds:* Opioids, benzodiazepines, antipsychotics, antihistamines, or residual anesthetic agents (common in post-op/POD7).
- *Check for Polypharmacy Interactions:* Especially with renal/liver impairment (e.g., CRD on MHD reduces drug clearance).
---
### *Step 3: Core Diagnostic Workup*
#### *A. Metabolic & Toxicologic (REVERSIBLE CAUSES)*
- *Labs:*
- Electrolytes (Na⁺, Ca²⁺, Mg²⁺), glucose, ABG (pH, CO₂).
- Renal/Liver Function (BUN/Cr, LFTs - CRD/sepsis risk).
- Ammonia (hepatic encephalopathy).
- Thyroid (TSH, free T4).
- Serum osmolality (toxins/alcohol).
- *Toxicology Screen:* Urine/blood (opiates, benzos, ethanol, illicit drugs).
#### *B. Infectious (Sepsis Residual?)*
- *Cultures:* Blood, urine, tracheal aspirate (UTI/sepsis noted).
- *CNS Infection:* LP if febrile or WBC elevated (after CT rule-out of mass).
- *Empiric Antibiotics:* If infection suspected.
#### *C. Neurological Imaging*
1. *STAT Non-Contrast Head CT:*
- Rule out hemorrhage, large infarct, mass effect, hydrocephalus.
- Critical given HTN crisis history (posterior reversible encephalopathy syndrome/PRES?).
2. *MRI Brain (if CT negative):*
- Diffuse axonal injury, anoxic injury, brainstem/pontine lesions, subtle strokes.
#### *D. Neurophysiology*
- *EEG:*
- Rule out non-convulsive status epilepticus (common in sepsis/CRD).
- Assess background activity (e.g., burst-suppression vs. diffuse slowing).
#### *E. Endocrine*
- Cortisol (adrenal insufficiency in sepsis).
- Pituitary panel (if hypothalamic injury suspected).
---
### *Step 4: Etiology-Specific Considerations*
| *Possible Cause* | *Supporting Clues* | *Action* |
|---------------------------------|-----------------------------------------------|-----------------------------------------|
| *Anoxic Brain Injury* | Hx of respiratory failure, cardiac arrest? | MRI: DWI for hypoxic injury |
| *Sepsis-Associated Encephalopathy* | UTI/sepsis, "residual" Type II RF | Treat infection; EEG |
| *Hypertensive Encephalopathy* | HTN crisis, renal failure | MRI: Posterior white matter edema (PRES)|
| *Uremic Encephalopathy* | CRD on MHD; electrolyte shifts | Optimize dialysis; check ammonia |
| *Medication Toxicity* | Polypharmacy in critical care | Hold sedatives; reversal agents (e.g., naloxone trial)|
| *Paraneoplastic* | Hx of malignancy (SIP = solid tumor?) | Autoimmune encephalitis panel (anti-NMDA, etc.)|
| *Wernicke’s* | Malnutrition (common in critical illness) | IV Thiamine |
---
### *Step 5: Prognostic Tools & Monitoring*
- *Serial Exams:* Daily GCS, brainstem reflexes.
- *Prognostic Scales:*
- *FOUR Score* (Full Outline of UnResponsiveness): More detailed than GCS for ventilated patients.
- *CRS-R* (Coma Recovery Scale-Revised): If PVS suspected.
- *Evoked Potentials:*
- Somatosensory (SSEPs): Poor prognosis if bilateral N20 absence.
---
### *Critical Actions*
1. *Document Neurological Baseline:* GCS, pupils, motor response.
2. *Exclude Reversible Causes FIRST:* Toxins, metabolic, infection, seizures.
3. *Neuroimaging STAT:* Head CT → MRI if inconclusive.
4. *EEG within 24h:* Especially with fluctuating consciousness.
5. *Multidisciplinary Input:* Neurology, Nephrology, ID, Palliative Care (if PVS confirmed).
> *Note:* "Persistent Vegetative State" (PVS) is a clinical diagnosis *only after reversible causes are excluded* and >4 weeks of unchanged unresponsiveness. Early intervention may prevent irreversible injury.[handwritten text could not be extracted]
[06-06-2025 21:52] PPM 3: Based on the comprehensive clinical history, investigations, and team discussions, here's a systematic approach to evaluating and managing this complex case:
## 1. *Locked-in Syndrome (LIS) Evaluation & Communication Strategy*
- *Urgent confirmation*: Perform a structured neurological exam focusing on:
- Vertical eye movements/blinking (only preserved voluntary motor function in classic LIS)
- Visual tracking of objects
- Response to yes/no questions via eye-coded communication
- *Implement the AAC protocol* referenced ([PMC10642070](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10642070/)):
python
# Sample eye-gaze communication code
YES = 1 blink | NO = 2 blinks
PAIN = 3 blinks | NEED = prolonged gaze
- *Diagnostic studies*:
- *MRI Brain*: Diffusion-weighted imaging to detect acute/pontine infarcts
- *EEG*: Rule out non-convulsive status epilepticus
- *Evoked Potentials*: Assess brainstem auditory and somatosensory pathways
### 2. *Hypertension Crisis Management*
- *Current regimen critique*:
| *Drug* | *Dose* | *Issue* | *Optimization* |
|----------------|----------|-------------------------|-------------------------------|
| Nicardipine | 20mg TID | Short-acting | Switch to cilnidipine (dual L/N-type CCB) |
| Metoprolol XL | 50mg OD | Inadequate HR control | Titrate to 100mg OD |
| Torasemide | 10mg BD | Hypokalemia risk | Add spironolactone 12.5mg OD |
| Missing | - | No CNS-acting agent | Add clonidine 0.1mg TDS PRN |
- *Neuroprotective strategy*:
- Target MAP 85-100 mmHg (avoid cerebral hypoperfusion)
- Continuous arterial line monitoring
- Nicardipine → Labetalol transition if HR >100 bpm
### 3. *Coma Etiology Workup*
- *Metabolic*:
- Serum midazolam/1-OH-MDZ-Glu levels (confirm accumulation)
- Ammonia, lactate, osmolality
- *Toxicologic*:
- Comprehensive drug screen (especially renally excreted metabolites)
- *Structural*:
- MRI/MRA: Posterior circulation, pontine evaluation
- CT venography (rule out cortical vein thrombosis)
- *Infectious*:
- CSF analysis (cell count, culture, autoimmune encephalitis panel)
### 4. *Renal-Neurologic Cross-Adaptations*
- *Dialysis modifications*:
- CVVHDF > IHD (prevent ICP fluctuations)
- Heparin-free protocol (reduce hemorrhage risk)
- *Sedative clearance*:
- Charcoal hemoperfusion if toxic levels confirmed
- Flumazenil microdosing trial (0.1mg IV q3min; max 1mg)
### 5. *Prognostication & Rehabilitation*
- *CRS-R Scale* application twice daily:
- Auditory/visual/motor/communication subscales
- *Early interventions*:
- Vertical prism glasses for visual field expansion
- Neuromuscular electrical stimulation (prevent contractures)
- *Family training*:
- Eye-tracking tablet systems (e.g., Tobii Dynavox)
- Home ventilator management drills
### Critical Action Plan
1. *48-hr Diagnostic Pathway*:
- *Day 1*: MRI + EEG, initiate eye-coding protocol
- *Day 2*: LP + toxicology, reassess BP targets
2. *Therapeutic Trial*:
- IV edrophonium 10mg (test for myasthenic crisis)
- Methylprednisolone 1g IV (empirical autoimmune trial)
3. *Palliative Integration*:
- Advance directive clarification via eye communication
- Tracheostomy speaking valve trial
This approach balances diagnostic rigor with therapeutic pragmatism, focusing on functional communication restoration as the immediate priority. The hypertensive history suggests brainstem involvement is likely - outcomes depend on time-to-treatment during the initial crisis.
[06-06-2025 19:31] PPM 9: Was just wondering if the PAH and LV systolic dysfunction came about because of the paralytic leg, and lack of soleus muscle support for venous blood return?
[06-06-2025 19:39] PPM 9: Sorry RV dysfunction. Was thinking of something like this as a possible adjunct therapy for paraplegics? https://pmc.ncbi.nlm.nih.gov/articles/PMC5678724/
[06-06-2025 22:13] PPM 1: Great idea!
Also a space age solution for sarcopenia! 👏👏
[06-06-2025 22:17] PPM 1: It has read the handwritten notes quite well 👏👏
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