12-11-2025
THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HER SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
[7.50 pm, 12/11/2025] PPM 1: History on presentation
[7.51 pm, 12/11/2025] PPM 1: https://youtube.com/shorts/_9qo1F85bXU?si=egvbUzi3YotCWLZm
Admission Date: 19/09/2025 05:56 PM
Diagnosis
ACUTE CARDIOGENIC PULMONARY EDEMA [RESOLVED]MODERATE AR/MR; MODERATE TR WITH PAH; MODERATE LV DYSFUNCTION AKI ON CKD
S/P 1 PINT PRBC TRANSFUSION
Case History and Clinical Findings
PT WAS BROUGHT WITH C/O BREATHLESSNESS GRADE IV. HISTORY OF PRESENT
ILLNESS: PATIENT WAS APPARENTLY ASSYMPTOMATIC TILL TODAY AFTER 2 PM THEN SHE DEVELOPED BREATHLESSNESS OF GRADE IV, GRADUALLY PROGRESSIVE. THEN SHE WAS IMMEDIATELY BROUGHT TO CASUALITY IN GASPING STATE. NO C/O ALTERED SENSORIUM LOSS OF SENSORIUM, INVOLUNTARY MOVEMENTS, BLURRING OF VISION, CHEST PAIN, PALPITATIONS. NO H/O FEVER, COLD &COUGH
PAST HISTORY: K/C/O T2 DM SINCE 10 YEARS ON TAB. VOGLIBOSE 0.3 MG+ TAB.
GLIMIPERIDE 2 MG + METFORMIN 500 MG
HTN SINCE 10 YEARS. ON UNKNOWN MEDICATION.
PERSONAL HISTORY: MARRIED, MIXED DIET, REGULAR BOWEL AND BLADDER MOVEMENTS, NO KNOWN ALLERGIES; ADDICTIONS -OCCASIONAL ALCOHOL, CHEWING TOBACCO LEAF EVERYDAY
GENERAL EXAMINATION: -NO PALLOR, NO ICTERUS, CYANOSIS, CLUBBING,
LYMPHADENOPATHY, PEDAL EDEMA, MALNUTRITION
VITALS: - TEMP: 98.0 F, BP: 180/010MMHG, RR: 38 CPM, PR: 112BPM, SPO2: 70% AT RA, GRBS 365
SYSTEMIC EXAMINATION-CVS - S1 S2 +; RS - BAE +, B/L DIFFUSE CREPTS PRESENT; PER
ABDOMEN - NORMAL; CNS- GCS E4M5V6 HIGHER MENTAL FUNCTION INTACT, NFND
KIMS HOSPITALS
Investigation
CUE ALBUMIN+30MG/DL, SUGAR NIL, N PUS CELLS 3-6 0-5/HPF
SEROLOGY: HIV, HBS, HCV: NEGATIVE
ABG PH 7.410, PCO2 25.2, PO2 71.5 HCO3- 18.2
URINE FOR KETONE BODIES NEGATIVE
HAEMOGRAM: NHAEMOGLOBIN 6.9 gm/dl TOTAL COUNT 14500 cells/cum RBC COUNT 2.69
millions/cumm PLATELET COUNT 4.10lakhs/cu.mm, PCV 19.9
LFT: Total Bilurubin 0.43 mg/dl Direct Bilurubin 0.15 mg/dl SGOT(AST) 15 IU/L SGPT(ALT) 11 IU/L ALKALINE PHOSPHATASE 224 IU/L TOTAL PROTEINS 7.6 gm/dl ALBUMIN 4.3 gm/dl A/G RATIO 1,38
RFT: UREA 40. 50 mg/dl CREATININE 2.20 mg/dl URIC ACID 7.4 mmol/L CALCIUM 9.0 mg/dl
PHOSPHOROUS 4.6 mg/dl SODIUM 139 mmol/LPOTASSIUM 3.6 mmol/L. CHLORIDE 101 mmol/L
FBS: 210 mg/dl
USG ABDOMEN- B/L GRADE II RPD CHANGES WITH B/L RENAL CORTICAL CYSTS, B/L MILD PLEURAL EFFUSION
2D ECHO: MODERATE TR PAH, MODERATE MR, MILD TO MODERATE AR, MILD PR. GLOBAL HYPOKINETIC; NO AS/MS, SCLEROTIC AV. MODERATE LV DYSFUNCTIONAL; NO
VEGETATIONS. GRADE II DIASTOLIC DYSFUNCTION, NO LV CLOT.
21/9/25: HAEMOGRAM: HAEMOGLOBIN 8.6 gm/dl TOTAL COUNT 12400 cells/cum RBC COUNT 3.4 millions/cumm PLATELET COUNT 4.20 lakhs/cu.mm, PCV 24.9
21/9/25 ABG PH 7.410, PCO2 25.2, PO2 71.5 HCO3- 18.2
21/9/25 RFT: UREA 54. 50 mg/dl CREATININE 2.40 mg/dl URIC ACID 5.9 mmol/L CALCIUM 9.0
mg/dl PHOSPHOROUS 4.0 mg/dl SODIUM 135 mmol/LPOTASSIUM 3.3 mmol/L. CHLORIDE 98
mmol/L.
Treatment Given (Enter only Generic Name)
Rx
INJ. MONOCEF 1 ML/BD
INJ. NTG 1.6ML/HR/IV
INJ.NAHCO3 100 MEQ /IV/ STAT
INJ LASIX 20 MG/ TLD (IF BP IS OVER 110 MM HG)
INJ. HEPARIN 5000 IU/IV/QID
INJ. HAI SC/ ACC TO GRBS
INJ KCL (2 AMP) IN 600 ML NS+ 2 AMP MGSO4 OVER 2 HOURS
TAB. ECOSPIRIN 150 MG PO/OD
TAB. CLOPITAB 75 MG PO/BD
KIMS HOSPITALS
TAB. ATORVAS 20 MG PO/HS
TAB CINOD 10 MG PO/OD
1 PRBC TRANSFUSION
INTERNMITTENT CPAP
Advice at Discharge
INJ. HAI S/C TID 4U-4U-4U
TAB. PANTOP 40MG PO/OD 1-0-0
TAB. DYTOR 10MG PO/OD 1-0-0
TAB. ECOSPIRIN 150 MG PO/OD 0-0-1 TO CONTINUE
TAB. CLOPITAB 75 MG PO/OD 0-0-1 TO CONTINUE
TAB. ATORVAS 20 MG PO/HS 0-0-1 TO CONTINUE
TAB CINOD 10 MG PO/BD1-0-1 TO CONTINUE
Follow Up
REVIEW TO GM OPD AFTER 4 DAYS ON 26/9/25
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/Attendant 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.
SIGNATURE OF PG/INTERNEE.
SIGNATURE OFADMINISTRATOR.
SIGNATURE OF FACULTY
Discharge Date
Date:22/9/25 Ward: FMWUnit:5
Examination findings documented this admi again from the EMR summary 👇
GENERAL EXAMINATION: PALLOR PRESENT, NO ICTERUS, CYANOSIS, CLUBBING,
GENERALISED LYMPHADENOPATHY, PEDAL EDEMA.
VITALS: TEMP AFEBRILE; BP 100/60 MMHG; PR 118BPM; RR 24 CPM; SPO2 90% AT RA;
SYSETMIC EXAMINATON: CNS: LEVEL OF CONSCIOUSNESS: COMA; SPEECH: NO
RESPONSE; GLASGOW SCALE- E4V1M4
CVS S1 S1 +; RS BAE+; P/A; SOFT NON TENDER
[7.59 pm, 12/11/2025] PPM 1: MRI BRAIN DONE ON 6/11/25: GRADE II CHANGES OF PERIVENTRICULAR LEUCOENCEPHALOPATHY, GENERALISED CEREBRAL ATROPHY, VR SPACES PROMINENCE AT B/L GANGLIO CAPSULAR REGION, SUBTLE T1 HYPERINTENSITY AT RIGHT BASAL GANGLIA
[8.14 pm, 12/11/2025] PPM 1: Current EMR summary:
Age/Gender: 73 Years/Female
Admission Date: 06/11/2025 04:04 PM
Diagnosis
?STATUS EPILEPTICUS
SEPTIC SHOCK SECONDARY TO UROSEPSIS
? UREMIC SEPTIC ENCEPHALOPATHY
AKI ON CKD
GRADE II BED SORES
ON MECHANICAL VENTILATION DAY III
K/C/O TYPE 2 DM, HTN
Case History and Clinical Findings
PATIENT WAS APPARENTLY NORMAL TILL PREVIOUS NIGHT. THIS MORNING SHE DIDNT
RESPOND TO ATTENDERS ON WAKING UP AT AROUND 8.30 AM. PATIENT DEVELOPED
INVOLUNTARY MOVEMENTS OF UPPER LIMBS, LOWER LIMBS, MOUTH Which WAS
INSIDIOUS IN ONSET, PROGRESIVE, LASTED FOR 1/2 HOUR. ONE MORE EPISODE STARTED AFTER 15 MINS AND WAS CONTINOUS FROM THEN. LOCAL RMP CHECKED THE PATIENT AND THE GRBS WAS NOTED AS HIGH AND BROUGHT TO HOSPITAL.
PAST HISTORY: K/C/O DMT2 SINCE 10 YEARS, ON INJ HAI S/C 40 TID
K/C/O HTN SINCE 10 YEARS ON TAB. CINOD 10 MG PO/BD
ADMITTED IN OUR HOSPITAL 15 DAYS AGO WITH ACUTE CARDIOGENIC PULMONARY EDEMA AKI ON CKD
PERSONAL HISTORY: MARRIED, APPETITE NORMAL.DIET MIXED, BOWEL AND BLADDER
MOVEMENTS REGULAR, TOBACCO CHEWING SINCE 20 YEARS, NO OTHER ADDICTIONS
KIMS HOSPITALS
GENERAL EXAMINATION: PALLOR PRESENT, NO ICTERUS, CYANOSIS, CLUBBING,
GENERALISED LYMPHADENOPATHY, PEDAL EDEMA.
VITALS: TEMP AFEBRILE; BP 100/60 MMHG; PR 118BPM; RR 24 CPM; SPO2 90% AT RA;
Systemic Examination: CNS: LEVEL OF CONSCIOUSNESS: COMA; SPEECH: NO
RESPONSE; GLASGOW SCALE- E4V1M4
CVS S1 S1 +; RS BAE+; P/A; SOFT NON TENDER
USG ABDOMEN ON 6/11/25: RIGHT GRADE I AND LEFT GRADE II RPD, GRADE I FATTY LIVER
USG CHEST ON 7/11/25: RIGHT MILD PLEURAL EFFUSION WITH Underlying
CONSOLIDATION, LEFT MODERATE Pleural EFFUSION WITH LUNG CONSOLIDATION AND
LUNG COLLAPSE
REVIEW 2D ECHO ON 10/11/25:NO RWMA, CONCENTRIC LVH, MILD AR, TRIVIAL TR /MR NO PR, SCLEROTIC AV, NO AS/MS IAS-INTACT, EF 62%, RVSPZ 36MMHG, GOOD LV SYSTOLIC FUNCTION, GRADE I DIASTOLIC DYSFUBCTION, NO PE NO LV CLOT, IVC SIZE (0.9 CMS) COLLAPSING
MRI BRAIN DONE ON 6/11/25: GRADE II CHANGES OF PERIVENTRICULAR
LEUCOENCEPHALOPATHY, GENERALISED CEREBRAL ATROPHY, VR SPACES PROMINENCE AT B/L GANGLIO CAPSULAR REGION, SUBTLE T1 HYPERINTENSITY AT RIGHT BASAL GANGLIA -P/O METABOLIC CAUSE RULE OUT NONKETOTIC HYPER GLYCEMIC HEMICHOREA
NEPHROLOGY REFFERAL DONE ON 8/11/25: IVF NS AT THE RATE 30 ML/HR, PLAN FOR
DIALYSIS AFTER PATIENT GETS HEMODYNAMICALLY STABLE, MONITOR VITALS
NEPHROLOGY REFFERAL DONE ON 11/11/25: ADVISED FOR CRRT
Investigation
06/11/2025.
HEMOGRAM HB 8.3; PCV 22.4; TLC 22080; RBC 3.23; PLT 3.65.
RFT: BU 136; S.CR 2.6; S.NA 131; S.K 3.2; S.CL 95.
LFT; T.BIL 1.51; D.BIL 0.58; SGPT 21; SGOT 71; ALP 267; TP 6.2; ALB 2.7; GLOB 3.50; A/G 0.77.
CUE; KETONES NEGATIVE PUS CELLS 3-4, ALB TRACE; SUGARS ++++
LIPID PROFILE: TC 61; TG 67; HDL 8.4; LDL 23; VLDL 13.4; LDH 549;
BLOOD GROUP O+; BT 2:30; CT 4:30; PT 16; INR 1.11; APTT 33.
T3 0.5, T4 5.7; TSH 2.86.
SEROLOGY NEGATIVE
FERRITIN 211.5; RETIC COUNT 0.8%
PERIPHERAL SMAER: MICROCYTIC HYPOCHROMIC ANEMIC WITH NEUTROPHILIC
2 LYMPHONIA
KIMS HOSPITALS
MALARIAL PARASITE NEGATIVE, DENGUE NEGATIVE, WIDAL O-1;20, H-1;20, AH, BH NO
AGGLUTINITION
CUE; ALBUMIN TRACE
07/11/2025;
HEMOGRAM HB 9.9; PCV 28.2; TLC 28100; RBC 3.84; PLT 3.95.
RFT: BU 102; S.CR 3.6; S.NA 135; S.K 3.3; S.CL 98.
ABG:PH 7.313 PCO2 18.7 PO2 63.6 HCO3 9.2
08/11/2025.
HEMOGRAM HB 10.2; PCV 29; TLC 26700; RBC 3.8; PLT 1.8.
RFT: BU 119; S.CR 3.50; S.NA 135; S.K 3.7; S.CL 98.
ABG:PH 7.153 PCO2 48.2 PO2 212 HCO3 16.2
09/11/2025.
HEMOGRAM: HB 7.2 TLC 17720 RBC 2.8 PCV 25.4 MCV 75.9 PLT 1.1 LACTATE 21.6
RFT: BU 148; S.CR 3.8; S.NA 134; S.K 4.2; S.CL 98;
ABG:PH 7.061 PCO2 53 PO2 66.3 HCO3 14.4
10/11/25:
HEMOGRAM: HB 7.1 TLC 14200 RBC 2.75 PCV 21.1 MCV 76.7 PLT 35000
RFT: BU 163; S.CR 4; S.NA 137; S.K 4.5; S.CL 99;
ABG:PH 7.261 PCO2 25.30 PO2 176HCO3 11
11/11/25:
HEMOGRAM: HB 7.7 TLC 32000 RBC 2.8 PCV 22.5 MCV 80.6 PLT 14000
RFT: BU 170; S.CR 4.2; S.NA 142; S.K 2.0; S.CL106.
ABG:PH 6.826 PCO2 55.2 PO2 108 HCO3 8.6
URINE CULTURE: ESCHERICHIA COLI ISOLATED
BLOOD CULTURE: ESCHERICHIA COLI ISOLATED
Treatment Given (Enter only Generic Name)
RT FEEDS 4TH HOURLY MILK 400 ML 2ND HOURLY WATER 100 ML
IVF NS @100ML/HR
INJ. HAI 40 UNITS IN 39 MLNS AT THE RATE 60 ML/HR
INJ. KCL 2 AMP IN 500 ML NS AT THE RATE 100 ML/HR
INJ. PIPTAZ 2.25GM IV/TID X 5DAYS
INJ NORAD 8MG IN 36 ML NS @32ML/HR INCREASE OR DECREASE TO MAINTAIN MAP >65 MMHG
KIMS HOSPITALS,
INJ DOBUTAMINE 250MG IN 45ML NS @6.5ML/HR INCREASE OR DECREASE TO MAINTAIN
MAP >65 MMHG
INJ. DOPAMINE 200 MG(5ML) IN 45 ML NS @ 200 MG /HR, 5 ML /HR INCREASE OR DECREASE
TO MAINTAIN MAP>65 MMHG
INJ. VASOPRESSIN 2ML (40U) IN 38 ML /NS @ 2.2 ML/HR TO INCREASE OR DECREASE TO
MAINTAIN MAP
INJ. MIDAZ 5MG(5ML) @5 ML/HR
INJ. SODIUM VALPROATE 500 MG IV/BD
INJ. FENTANYL 80 MCG /HR INF. (16ML/HR)
INJ. PAN 40 MG IV/OD
INJ. HAI SC TID ACCORDING TO GRBS
INJ LEVIPILL 1 G IV/BD
INJ. MEROPANEM 1G IV/STAT-(HB) 500MG IV/OD X1 DAY
NEOSPORIN POWDER FOR L/A
NEB WITH BUDECORT 8TH HOURLY
TRIPLE LUMEN CENTRAL LINE WAS PLACED IN RIGHT FEMORAL VEIN USING SELDINGER
TECHNIQUE, INDICATION-INOTROPES
POSITION CHANGE FREQUENTLY 2ND HOURLY
ETA AND ORAL SUCTIONING 2ND HOURLY
Advice at Discharge
PATIENT ATTENDERS HAVE BEEN EXPLAINED ABOUT THE PATIENT CONDITION THAT IS
REFRACTORY METABOLIC ACIDOSIS AND ANURIA SINCE 3 DAYS AND REQUIREMENT OF
CRRT THERAPHY SO THE PATIENT IS BEING REFFERED TO HIGHER CENTRE IN VIEW OF
CRRT. DOCTORS, HOSPTIAL STAFF AND MANAGEMENT ARE NOT RESPONSIBLE FOR ANY UNTOWARDS EVENTS THAT HAPPEN TO PATIENT OUTSIDE THE HOSPITAL
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/Attendant 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
KIMS HOSPITALS
SIGNATURE OF PG/INTERNEE
SIGNATURE OF ADMINISTRATOR
SIGNATURE OF FACULTY
Discharge Date
Date:11/11/2025
Ward: ICU
Unit: IV
[1:40 pm, 13/11/2025] PPM 3: Of course. Here is a detailed summary and analysis of the provided EMR, structured for clarity and clinical understanding.
### *Case Summary & Analysis*
This is a complex case of a *73-year-old female with multiple comorbidities* who was admitted in a critical state with status epilepticus and septic shock, and is now being transferred to a higher center due to worsening, refractory organ failure.
*Key Problem List:*
1. *Refractory Septic Shock* secondary to E. coli Urosepsis.
2. *Severe Metabolic Acidosis & Anuria* due to Acute Kidney Injury on Chronic Kidney Disease (AKI on CKD), now requiring Continuous Renal Replacement Therapy (CRRT).
3. *Status Epilepticus / Encephalopathy* (Etiology likely multifactorial: septic, uremic, and/or hyperglycemic hemichorea).
4. *Multiple Organ Dysfunction Syndrome (MODS):* Neurological, Renal, Hematological (thrombocytopenia), and Respiratory (on mechanical ventilation).
5. *Comorbidities:* Type 2 Diabetes Mellitus, Hypertension, Chronic Kidney Disease.
---
### *Clinical Course Timeline*
* *Admission (06/11):* Patient found unresponsive, with continuous seizure-like movements. Admitted with suspected status epilepticus, septic shock, and severe metabolic derangement (high Blood Urea, elevated blood sugar, hyponatremia).
* *Hospital Stay (06/11 - 11/11):* Despite aggressive treatment in the ICU (broad-spectrum antibiotics, multiple vasopressors/inotropes, anti-epileptics, mechanical ventilation), the patient's condition deteriorated.
* *Key Deterioration:* The patient developed *anuria and progressive, refractory metabolic acidosis*, indicating renal failure that was not responding to conventional management.
* *Outcome (11/11):* Due to the need for CRRT, which is unavailable at the current facility, the patient is being transferred to a higher center. The discharge note clearly states the critical nature of the condition and the reason for transfer.
---
### *Detailed Analysis of Key Issues*
#### *1. Source of Infection & Shock*
* *Diagnosis:* Septic Shock secondary to *Urosepsis*.
* *Evidence:* Both *Urine Culture* and *Blood Culture* grew Escherichia coli, confirming a bloodstream infection originating from the urinary tract. This is the primary inciting event.
#### *2. Neurological Condition*
* The initial presentation was coma and continuous involuntary movements, diagnosed as *Status Epilepticus*.
* *MRI Brain Finding:* "Subtle T1 hyperintensity at right basal ganglia - P/O Metabolic cause rule out Nonketotic Hyperglycemic Hemichorea." This suggests the movements could be a rare presentation of severe hyperglycemia rather than a true epileptic seizure, known as *Hyperglycemia-Induced Hemichorea*. The treatment with Midazolam and Sodium Valproate was appropriate for either condition in the acute setting.
* The encephalopathy is multifactorial, with contributions from *Sepsis, Uremia (from AKI/CKD), and possible hyperglycemia*.
#### *3. Renal Failure & Metabolic Crisis*
* *Diagnosis:* *AKI on CKD*. The patient had a prior admission for AKI, and the current baseline is significantly worse.
* *Progression:* Despite fluid management, renal function worsened dramatically:
* *S. Creatinine* rose from 2.6 (06/11) to *4.2 mg/dL* (11/11).
* *Blood Urea* rose from 136 to *170 mg/dL*.
* *The Critical Issue: Refractory Metabolic Acidosis & Anuria*
* The serial ABGs show a progressively severe, life-threatening metabolic acidosis that is not correcting:
* 07/11: pH 7.313, HCO3 9.2
* 09/11: pH 7.061, HCO3 14.4
* 11/11: *pH 6.826, HCO3 8.6* (Extremely critical)
* The anuria for 3 days confirms the kidneys are no longer functioning. This is the primary reason for initiating *CRRT*.
#### *4. Hematological Issues*
* *Thrombocytopenia:* Platelets dropped significantly to a dangerous low of *14,000* (11/11), increasing the risk of spontaneous bleeding. This is a common complication of severe sepsis.
* *Leukocytosis:* Persistently high WBC count (peaking at 32,000), indicative of the ongoing severe infection.
* *Anemia:* Consistent microcytic hypochromic anemia, likely due to chronic disease and renal failure.
#### *5. Treatment Summary*
The management was comprehensive and appropriate for an ICU setting:
* *Antibiotics:* Piperacillin-Tazobactam (Piptaz) and a dose of Meropenem for broad-spectrum coverage of the identified E. coli.
* *Vasopressor/Inotrope Support:* *Noradrenaline (Norad), Dopamine, Dobutamine, and Vasopressin* were all required to maintain blood pressure, indicating profound and refractory shock.
* *Sedation & Seizure Control:* Midazolam infusion and IV Sodium Valproate.
* *Supportive Care:* Mechanical Ventilation, Insulin for hyperglycemia, Pantoprazole for stress ulcer prophylaxis, etc.
---
### *Conclusion and Reason for Transfer*
The patient is being transferred in an *extremely critical and unstable condition. Despite maximal medical management, she has developed **refractory metabolic acidosis and anuria* due to end-stage acute kidney injury superimposed on chronic kidney disease. Her survival is dependent on *Continuous Renal Replacement Therapy (CRRT)* to correct the acid-base and electrolyte imbalances and manage fluid overload, which the current hospital cannot provide. The transfer is a necessary, high-risk step for a potentially life-saving intervention.
[1:43 pm, 13/11/2025] PPM 3: Impression of MRI findings
- Grade II periventricular leukoencephalopathy — moderate signal changes in the white matter around the ventricles consistent with chronic small vessel ischemic change or demyelination.
- Generalized cerebral atrophy — diffuse loss of brain parenchyma greater than expected for age.
- Prominent Virchow‑Robin (VR) spaces at bilateral gangliocapsular regions — enlarged perivascular spaces in the basal ganglia area.
- Subtle T1 hyperintensity at the right basal ganglia — focal T1 shortening in the right basal ganglia suggesting one of: early chronic blood product (methemoglobin or mineralization), calcification, fat-containing lesion (less likely), or proteinaceous material; in the appropriate clinical context could also reflect subacute blood or paramagnetic deposition.
---
Differential considerations (ranked by likelihood given these MRI terms)
1. Chronic microvascular ischemic disease / small vessel disease causing periventricular leukoencephalopathy and atrophy.
2. Neurodegenerative/age‑related atrophy contributing to global volume loss.
3. Prior small deep hemorrhage, mineral deposition, or resolved petechial bleed for the T1 hyperintensity in the right basal ganglia.
4. Demyelinating or inflammatory white‑matter disease (less likely with predominately periventricular chronic changes and generalized atrophy but consider if clinical history supports).
5. Metabolic/toxic leukoencephalopathy (consider if history of exposure or rapidly progressive course).
---
Clinical correlations that matter
- Age and vascular risk factors (hypertension, diabetes, hyperlipidemia, smoking) favor chronic small vessel disease.
- Acute or subacute focal neurological signs, recent head trauma, anticoagulation use, or coagulopathy increase likelihood that the right basal ganglia T1 hyperintensity represents hemorrhage.
- Cognitive decline, gait disturbance, urinary symptoms, or stepwise deterioration suggest vascular cognitive impairment related to small vessel disease.
- Fever, systemic inflammation, rapid onset focal deficits, or prior demyelinating events would shift consideration toward inflammatory/demyelinating causes.
---
Recommended next steps (practical, ordered)
1. Review prior imaging (if available) to determine chronicity and evolution of white‑matter changes and the basal ganglia T1 signal.
2. Correlate with clinical exam and history: vascular risk profile, recent events, anticoagulant use, infective or inflammatory signs.
3. If uncertainty about the nature of the basal ganglia signal: obtain susceptibility‑weighted imaging (SWI) or gradient echo to look for blood products and consider CT (better for calcification) if suspicion for mineralization.
4. Basic labs: CBC, coagulation profile, metabolic panel, and inflammatory markers as clinically indicated.
5. If cognitive impairment or gait disturbance present, consider neurocognitive testing and vascular risk optimization (BP, glucose, lipids) and secondary prevention measures.
6. If demyelinating or inflammatory process suspected, consider contrast‑enhanced MRI and relevant serology (e.g., autoimmune, infectious) or CSF testing per neurology guidance.
---
Short summary
The scan shows moderate periventricular small‑vessel white matter change and diffuse brain atrophy; there is a focal T1 bright lesion in the right basal ganglia that requires correlation with prior imaging, clinical history, and possibly SWI/CT to distinguish chronic blood product or mineralization from other causes. Manage by correlating clinically and targeting investigations as above.
[2:55 pm, 13/11/2025] PPM 1: Thanks very useful 👏
@42StrokePA Will be looking forward to a medical liturgic analysis from your end for this case
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