Friday, December 27, 2024

50M With Hypokalemic Periodic Paralysis


 

23-12-2024

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.
                                
PPM 1 - @PPM3 @PPM4 we were having an afternoon journal club around your patient attached here on ticagrelor efficacy over clopidogrel in the choice of DAPT (dual antiplatelet therapy) post PTCA. I hope @PPM2 is able to join in. While we would be looking for an RCT to begin with in this meta analysis here: https://pmc.ncbi.nlm.nih.gov/articles/PMC10623206/ can any of you help us to understand what may have the authors collated as "events" and what is their idea of "total" in the figure 2 there?
PPM 1 - On reading the first individual trial mentioned in figure 2 one can figure out that those numbers are essentially of study participants who developed an event and the total number of participants.
If we go through each study we may realise none of these are differences are clinically significant.
PPM 1 - 👆@PPM4 see if you can find some similar data for beta blockers in acute myocardial infarction.
                          
PPM 1 - Afternoon session hypokalemia thesis project presentation for PI @PPM5
50M with progressive weakness and anorexia since 16/12/24 and while he could still walk around on 16-18 on the 19th he was completely bed ridden and brought to hospital. The sequence of data with the dependent variable as K+ and the intervention is attached since 19/12/24.
26-12-2024
PPM 1 - Today's update of all measured potassium values since admission @PA.
Two EMR summaries, one from the previous admission under orthopedic for his fracture where we met him for the first time for his hypokalemia assessment and another EMR summary of the current admission will be shared shortly.
EMR SUMMARY
Age/Gender: 55 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 13/08/2024 11:52 AM
Date of Operation
24/8/24- LEFT HEMIARTHROPLASTY UNDER CSE IMPLANTS USED- 47 SIZE BIPOLAR HEAD
Diagnosis
CLOSED LEFT DISPLACED INTRACAPSULAR FRACTURE OF NECK OF FEMUR WITHOUT DNVD
Case History and Clinical Findings
C/O LEFT HIP PAIN SINCE 20 DAYS
PATIENT WAS APPARENTLY ASYMPTOMATIC 20 DAY AGO THEN HE DEVELOPED PAIN OVER LEFT HIP WHICH IS SUDDEN IN ONSET RAPIDLY PROGRESSIVE AGGREVATED ON SLIGHT MOVEMENTS AND NOT RELIEVED BY TAKING REST. PATIENT ISWALKING WITH WALKER SUPPORT. PATIENTHAD RIGHT HIP PAIN WITH IC FRACTURE 6 MONTHS AGO
H/O TRAUMA ( SLIP AND FALL)
NO H/O HEAD INJURY,LOC , ENT BLEED N/K/C/O HTN, DM, ASTHAMA, TB
H/O APPENDICECTOMY DONE 20 YRS BACK O/E: PATIENT IS C/C/C
GC-FAIR
BP-130/90 MM HG PR-82 BPM
RR-18 CPM
GRBS- 276 MG/DL
NO PALLOR, ICTERUS, CYANOSIS, CLUBBING, PEDAL EDEMA, LYMPHADENOPATHY
 SYSTEMIC EXAMINATION:
CVS: S1S2+
RS: BAE+, NVBS+
P/A: SOFT, NON TENDER CNS: NFND
LOCAL EXAMINATION OF LEFT HIP :
SKIN -NORMAL
SWELLING - DIFFUSE OVER PROXIMAL ASPECT OF THE THIGH SLOCKING -PRESENT
LOCAL RISE OF TEMPERATURE- ABSENT CREPITUS- CAN'T BE ELICITED DUE TO PAIN TENDERNESS- PRESENT AT THE PROXIMAL THIGH
ROM -ANY ATTEMPT OF LEFT HIP ROM IS AGGRAVATING THE PAIN SENSATIONS- INTACT
DISTAL PULSES - PRESENT
Investigation
NameValueNameValueRFT 13-08-2024 03:00:PM UREA22 mg/dlCREATININE1.0 mg/dl URIC ACID2.5 mmol/LCALCIUM10.0 mg/dlPHOSPHOROUS2.0 mg/dlSODIUM139 mmol/LPOTASSIUM2.3 mmol/L.CHLORIDE 102 mmol/L
LIVER FUNCTION TEST (LFT) 13-08-2024 03:00:PM Total Bilurubin0.74 mg/dl Direct Bilurubin0.20 mg/dl SGOT(AST)21 IU/LSGPT(ALT)36 IU/LALKALINE PHOSPHATASE467 IU/LTOTAL PROTEINS7.4 gm/dlALBUMIN4.18 gm/dl A/G RATIO1.30COMPLETE BLOOD PICTURE (CBP) 13-08-2024 03:00:PM HAEMOGLOBIN16.0 gm/dl TOTAL COUNT20000 cells/cummNEUTROPHILS74 %LYMPHOCYTES14 %EOSINOPHILS05
%MONOCYTES07 %BASOPHILS00 %PLATELET COUNT3.65SMEARNormocytic normochromic blood picture with leucocytosis COMPLETE URINE EXAMINATION (CUE) 13-08-2024 03:00:PM COLOUR Pale yellowAPPEARANCEClearREACTIONAcidicSP.GRAVITY1.010ALBUMIN++SUGAR Trace BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS2-4EPITHELIAL CELLS2-3RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil
Treatment Given (Enter only Generic Name)
PATIENT IS CLINCORADIOLOGICALLY DIAGNOSED WITH CLOSED LEFT DISPLACED IC FRACTURE OF NECK OF FEMUR WITHOUT DNVD
PAC DONE ON 20/8/24
SURGERY PERFORMED ON 24/8/24- LEFT HEMIARTHROPLASTY
ASD DONE ON POD-2, POD-5 WOUND HEALTHY, NO DISCHARGE
1. VF- 1.NS, 1.RL @ 75ML/HR
2. INJ.MAGNEX FORTE 1.5 G IV/BD
3. INJ.AMIKACIN 500 MG IV/BD
4. INJ.METROGYL 100 ML IV/TID
5. INJ.PAN 40 MG IV/OD
6. INJ.NEOMOL 100 ML IV/TID
7. LIMB IN ABDUCTION
8. AVOID FLEXION, EXTENSION, ROTATION
GENERAL MEDICINE REFERRAL DONE ON 13/8/24 I/V/O DECREASED POTASSIUM LEVELS (2.3) AND ADVISED WITH RX
1. ADEQUATE PAIN, MANAGEMENT
2. INJ KCL 40MCG [2 AMP] WITH 1 AMP MGSO4 IN 500 ML NS OVER 4 HRS
3. SYR POTKLOR 15ML IN GLASS OF WATER PO/TID
4. POTASSIUM RICH DIET [COCONUT WATER, BANANA]
GENERAL MEDICINE REVIEW REFERRAL WAS DONE ON 15/8/24 I/V/O DECREASED POTASSIUM LEVELS (2.3) AND WAS ADVISED WITH
1.T.METFORMIN 500 MG PO/BD
2. INJ KCL 40MCG [2 AMP] WITH 1 AMP MGSO4 IN 500 ML NS OVER 4 HRS
3. SYR POTKLOR 15ML IN GLASS OF WATER PO/TID
4. POTASSIUM RICH DIET [COCONUT WATER, BANANA]
GENERAL MEDICINE REVIEW REFERRAL WAS DONE ON 17/8/24 I/V/O DECREASED POTASSIUM LEVELS (3.2) AND WAS ADVISED WITH
1. INJ KCL 40MCG [2 AMP] WITH 1 AMP MGSO4 IN 500 ML NS OVER 4 HRS
2. SYR POTKLOR 15ML IN GLASS OF WATER PO/TID
3. POTASSIUM RICH DIET [COCONUT WATER, BANANA]
4. T.AUGUMENTIN 625 MG PO/TID
GENERAL MEDICINE REVIEW REFERRAL WAS DONE ON 25/8/24 I/V/O DECREASED POTASSIUM LEVELS (2.8) AND WAS ADVISED WITH
1. ADEQUATE PAIN ,MANAGEMENT
2. INJ KCL 40MCG [2 AMP] WITH 1 AMP MGSO4 IN 500 ML NS OVER 4 HRS
3. SYR POTKLOR 15ML IN GLASS OF WATER PO/TID
4. POTASSIUM RICH DIET [COCONUT WATER, BANANA]
NEPHROLOGY REFERRAL DONE ON 16/8/24 I/V/O DERANGED RFT AND RPD CHANGES OF KIDNEYS, ADVISED WITH
1. CST
2. MONITOR INPUT-OUTPUT
Advice at Discharge
1.T.CEFTAS CL 200 MG PO/BD X 7 DAYS
2.T.PAN 40 MG PO/OD X 7 DAYS
3. T.XYKAA 1G PO/BD X 7 DAYS
4. T.LIMCEE 500 MG PO/OD X 15 DAYS
5. T.SHECAL CT PO/OD X 15 DAYS
6. SYP.POTKLOR 15 ML IN 1 GLASS OF WATER
7. POTASSIUM RICH DIET (COCONUT WATER, BANANAS)
8. .AVOID ADDUCTION,FLEXION,EXTENSION AND ROTATION X 6 WEEKS
9. KNEE IMMOBILISERS TO CONTINUE X 6 WEEKS
Follow Up
REVIEW AFTER 2 WEEKS TO ORTHOPEDICS OP DAY ON TUESDAY OR FRIDAY
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 
SIGNATURE OF PG/INTERNEE 
SIGNATURE OF ADMINISTRATOR 
SIGNATURE OF FACULTY
Drugs
Drug-Dosage Drug-Dosage Drug-Dosage
10CC SYRINGES -(BD)- 2CC SYRINGE (BD)- 3WAY STOP COCK 100CM - MEDIKIT-
3WAY STOP COCK 10CM - MEDIKIT- 5CC SYRINGES -BD- ABHAY-TOX - 0.5 ML-
ABSORBENT COTTON - 125 GMS- ABSORBENT COTTON - 400 NETT- ACEPRA - TAB(ACECLOFENAC)-
AIRACAL - D TAB(CALCIUM- D3)- AMIJECT 500 MG INJ- AMPIMOL -1000MG - TAB(PARACETAMOL)-
ANAWIN - 0.5% INJ- ANAWIN HEAVY - 4 ML- AQSOLVE - 1-0 R/B -2346-
ATROPINE SULPHATE - INJ IML- BACTIGERM -5GM OINT(MUPIROCIN )- BASI CREPE BANDAGE 6'-
BICIPHAGE - 500 MG TAB- BIOXAMIC - 5ML INJ(TRANEXAMIC)- BUPRIGESIC 0.3MG /2ML-
CEFIXM-200 MG TAB- CENTISILK - 0- R/C5037- CHYMIST FORTE TAB-
CLAVCYN - 625 MG TAB- CORTIBEST -100MG INJ(HYDROCORTISONE)- DEBRIDACE CREAM - 15 GM-
DISPOVAN SYRINGE - 50 CC- DT-ROM -2ML INJ(ONDANSETRON)- DYNOPLASTER-
ECG LEADS ( MEDICO )- EFIPRES-30MG 1ML- ENEMA 100ML-
EPIDURAL KIT - NO:18 [PORTEX]- EVEC-LC - TAB (VITAMIN - E &LEVOCARNITINE)- FOLEYS CATHETER -14SIZE -MEDIKIT-
FOLEYS CATHETER 10(ROMSONS )- GLUCOWIN - M1 - TAB(GLIMEPRIRID METFORMIN)- HIV SURGICAL KIT - BIG SIZE-
HYDROGEN PEROXIDE 100 ML- IV CANNULA - 20G - MEDIKIT- IV CANNULA -18G- MEDIKIT-
IV CANNULA -20G (MEDISUN)- IV NS - 500ML (PUNISKA)- IV NS 100ML -PUNISKA-
IV RL - 500ML - (PUNISKA)- IV SETS [POLYMED)- JETROL - CZ - TAB(CALCIUM+CALCITRIOL)-
KCL-10ML INJ (POTASSIUM)- LIDFAST 2%JELLY (LIGNOCAINE)- LIMCEE CHEW TAB-
MAGNESIUM SULPHATE - 2 ML- MALIDENS- IV 100ML(PARACETAMOL)- MAXFORMIN SR - 500MG - TAB-
METRONIDAZOLE - 100ML -PUNISKA- MRANGE KNEE SPLINT ROM - LARGE [MGRM] - OLPID -5MG TAB (ZOLPIDEM)-
OXYGEN MASK ADULT(MEDIKIT)- PANCOLY - 40MG INJPANTOPRAZOLE)- PANRAS - 40MG TAB(PANTOPRAZOLE)-
PAPER PLASTER - 1- PAQVITA - 500 -MG - TAB- PARACYN - 650MG - TAB(PARACETA)MOL-
PETCRYL - 1-0 R/C 2534- PIMET - POVIDONE IODINE SOLUTION - 100ML- POTVEN- SYRP 200ML(POTASSIUMCHLORIDE)-
QUADRIS - 7- TAB- QUMEPH - 10ML INJ(MEPHETERMIN)- ROLLER BANDAGES - 6'-
SHAVING SET -PREPARATION BLADE- SHERCEF - 1GM INJ(CEFTRIAXONE)- SHERZONE - SB -1.5GM INJ(CEFOPERAZONE&SULBACTAM)-
SKIN STAPLER (AQMEN )- SPINAL NEEDLE NO -23G(BD)- STERILE WATER - 10 ML-
SUPRIDOL - 1ml inj(tramadol_- SURGICAL BLADE - NO. 11 - SURGICAL BLADE - NO. 22-
SURGICAL BLADE - NO:20 [MEDINORM]- SURGICAL BLADE NO-15- SURGICAL GLOVE - NO - 7-5 [SURGICARE]-
SURGICAL GLOVE - NO:6-5 [SURGICARE]- SURGICAL GLOVE - NO:7-0 [SURGICARE]- SURGICAL GLOVE -7.0 -(AQMAX)-
SURGICAL SPIRIT - 100 ML- ULTRAMIC - TAB(TRAMADOL- PARACETAMOL)- URINE BAG ADULT - MEDIKIT-
VICRYL-1 R/C -2347- ZINK+WIT TAB- ZOCALM - 0.25MG TAB(ALPRAZOLAM)-
Discharge Date Date:28/8/24 Ward:MOW Unit:2

28-12-2024
PPM 1 - 
                                       
PPM 1 - Handwritten progress.
PPM 1 - Possible hypokalemia related lateral ST T changes in the same patient on 19/12 during admission.
PPM 1 - Today's possible hypokalemia related T wave changes in the medical chest leads. From 19/12 to 28/12 the serial ECGs reveal a gradual progression of the T wave changes from lateral to medical.
30-12-2024
PPM 1 - 
PPM 1 - Today's refractory hypokalemia update:
@PPM2 @PPM5 we'll need your help to take the history and figure out the cause of refractory hypokalemia in this patient. His phone number should be in the signed informed consent form.
PPM 2 - VBG/ABG and Urine K+ with Urine Ca and Na, Cl and Cr BP?
PPM 1 - @PPM6 @PPM7 @PPM8 please share the serial ABGs and Urinary potassium values.
01-01-2025
PPM 1 - We have had some time now to collate the data on this patient today for the case report as the 
OPD wasn't busy.
Attached are the series of evidences for consolidating our hypothesis on what may have happened to these patient from a casuality perspective.
The hypokalemia is still persistent albeit better since last two days and his 24 urinary potassium, sodium, calcium etc done twice since admission is attached herein for team based learning interpretation.
He developed hypotension once few days after admission and is on NORAD since then, he also had thrombocytopenia on serial hemograms to be shared by @PPM6
The other new development documented in him for the first time was hyperglycemia. His hypokalemia was first noticed during his last admission few months back with fracture femur (EMR summary in current case report link by Case reporter.
His serum ionised calcium measured in the lab daily was always on the lower side while his 24 urinary excretion of calcium appears to be on the higher side. Serum magnesium measured once was normal.
Strangely 24 hour urine was done twice but neither creatinine nor albumin was done in those samples 
inspite of the urine CUE showing albumin++? @PPM9
Will need to check if HbSAg was detected for the first time since the admission on 19/12 or was it there
 in the previous EMR summary @PA.
PPM 10 - It's done sir. This is 24 hrs UPCR report.
PPM 1- Thanks.
The mild proteinuria albeit non significant is still suggestive of a mild glomerular involvement or
 perhaps this is also related to his tubular injury due to multifactorial causes since his fracture?
Please share his serial ABGs since admission.
Was his ANA done?
PPM 10 - 
Serial ABGs sir.
PPM 1 - 👍
PPM 10 - Sir we are suspecting the case to be hypokalemic periodic paralysis secondary to type I RENAL TUBULAR ACIDOSIS - secondary to SJOGRENS syndrome.
In suspicion of sjogrens syndrome we got a ophthalmology opinion where no evidence of dry eye was found and schrimmers was also normal 
We planned to get ANA profile, but patient attenders are not affordable.
PPM 2 - Hypokalemic periodic paralysis is a myopathic disorder. Recurrent Hypokalemic paralysis (RHP) due to renal wasting of potassium is a neurological disorder.
PPM 1 - 👍
PPM 2 - What's the patient's age? Is he a glue sniffer or does he use any form of recreational drugs at all?
Where is he from? What water does he drink?
PPM 10 - Patient age is 50 yrs sir. No history of any recreational or drug usage.
He is from Telangana. And drinks mineral water.
PPM 1 - Alright. It does look like RTA doesn't it?
Which Type though. 1 or 2?
He had recurrent fractures?
Any review of literature on etiologies of RTA in 50 year old men?
PPM 10 - Yes sir it is RTA type 1
PPM 2 - How and why?
PPM 10 - Only once history of fall 3 months ago and had IT  fracture sir 
But in 50 yr old male IT fracture can be considered abnormal..
PPM 2 - In simple terms - fall from patient's own height and then having a fracture is termed a pathological fracture.
So assuming this is a low impact pathological fracture - does this mean the patient have osteoporosis?What in your assessment are common causes of Osteoporosis?
PPM 1 - I guess that was due to a recall bias as one of our previous patients (we even kept her for the final exams) was having that etiology. However in this patient there are other associations to account for.
Can you share more details as to how he sustained the fracture?
PPM 10 - Symptoms of type 1 RTA can begin in infants or as late as adulthood. Not everyone will experience the same symptoms as they can vary depending on such factors related to the specific gene change, level of acidosis (acid in the blood), age of the individual, and even how advanced the disease is. Secondary dRTA usually occurs later in life.
This patient has hypokalaemia, features of polyuria, muscle weakness, hypercalcinuria, renal calculi.
PPM 2 - Well I understand what you are saying but how do we make a definitive diagnosis? Any urine anion gap or Urine pH or Ammonium chloride stimulation test?
Such a wonderful group this is. So much conversational learning. I want to contribute to your department fund sir. Please let me know how.
PPM 1 - Contact the treasurer.
02-01-2025
Today's update
04-01-2025
Current EMR SUMMARY from his second admission discharged yesterday.
Age/Gender: 50 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 19/12/2024 06:27 PM
Diagnosis
HYPOKALEMIC PERIODIC PARALYSIS SECONDARY TO TYPE-1 RENAL TUBULAR ACIDOSIS - SJOGREN SYNDROME
B/L RENAL CALICULI SEPSIS WITH THROMBOCYTOPENIA[?SEPTIC SHOCK] K/C/O TYPE-2 DIABETES MELLITUS
HBSAG POSITIVE STATUS
LEFT FEMUR FRACTURE 3 MONTHS AGO S/P APPENDICECTOMY 10 YRS AGO
Case History and Clinical Findings
C/O WEAKNESS OF B/L LOWER LIMBS SINCE 3 DAYS HOPI:
PATIENT WAS APPARENTLY ASYMPTOMATIC 3 DAYS AGO THEN HE DEVELOPED WEAKNESS OF LOWER LIMBS, INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE N/H/O INVOLUNTARY MOVEMENTS, SEIZURE LIKE EPISODES, DEVIATION OF
MOUTH, SLURRING OF SPEECH
N/H/O FEVER, COLD, COUGH, ALLERGIES, CHEST PAIN, PALPITATIONS, SWEATING, SOB K/C/O DM II SINCE 3 MONTHS AND NOT ON ANY MEDICATION
N/K/C/O HTN, TB, EPILEPSY, ASTHMA, CVA, CAD PERSONAL HISTORY
APPETITE NORMAL
BOWEL AND BLADDER NORMAL GENERAL EXAMINATION
PT IS C/C/C TEMP.AFEBRILE PR 101BPM
BP 90/60MMHG RR 18/MIN SPO2 98%
GRBS 454 MG/DL
OPTHAL REFERRAL WAS DONE ON 26/12/24 I/V/O OPTHALMIC FEATURES OF SJOGREN'S SYNDROME
IMPRESSION-NO OPTHALMIC MANIFESTATIONS SOJGRENS SYNDROMES ADVICE -
RX 1.)E/DLUBREA 5HDAY X 1WEEK
USG ABDMONEN PELVIS WAS DONE ON 27/12/24 IMPRESSION-
B/L RENAL CALCULI MILD SPLENOMEGALY
RIGHT RENAL CORTICAL CYST
2D ECHO WAS DONE CONCLUSION-
MILD MR; TRIVIAL AR/TR, NO PAH GOOD LV SYSTOLIC FUNCTION
NO RWMA, NO AS/MS, SCLEROTIC AV NO DIASTOLIC DYSFUNCTION, NO PE /LV
Investigation
COMPLETE URINE EXAMINATION (CUE) 19-12-2024 06:48:PM COLOUR Pale yellowAPPEARANCEClearREACTIONAcidicSP.GRAVITY1.010ALBUMIN++SUGAR+++BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS2-4EPITHELIAL CELLS2-3RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil BLOOD UREA19- 12-2024 06:48:PM43 mg/dl42-12 mg/dl SERUM CREATININE19-12-2024 06:48:PM1.4 mg/dl1.3-0.9 mg/dl SERUM ELECTROLYTES (Na, K, C l) 19-12-2024 06:48:PM SODIUM135 mmol/L145-136
mmol/LPOTASSIUM1.5 mmol/L5.1-3.5 mmol/LCHLORIDE100 mmol/L98-107 mmol/LLIVER FUNCTION TEST (LFT) 19-12-2024 06:48:PM Total Bilurubin1.25 mg/dl1-0 mg/dlDirect Bilurubin0.30 mg/dl0.2-0.0 mg/dlSGOT(AST)36 IU/L35-0 IU/LSGPT(ALT)24 IU/L45-0 IU/LALKALINE PHOSPHATASE540 IU/L128-53 IU/LTOTAL PROTEINS6.6 gm/dl8.3-6.4 gm/dlALBUMIN3.8
gm/dl5.2-3.5 gm/dlA/G RATIO1.39Anti HCV Antibodies - RAPID19-12-2024 06:48:PMNon Reactive ABG 19-12-2024 09:01:PM PH7.34PCO231.7PO246.8HCO317.0St.HCO318.5BEB-7.0BEecf- 7.5TCO233.1O2 Sat80.2O2 Count18.3PHOSPHOROUS19-12-2024 10:15:PM2.0 mg/dl4.5-2.5 mg/dlSERUM ELECTROLYTES (Na, K, C l) 19-12-2024 11:41:PM SODIUM138 mmol/L145-136
mmol/LPOTASSIUM1.4 mmol/L5.1-3.5 mmol/LCHLORIDE98 mmol/L98-107 mmol/LPOST LUNCH BLOOD SUGAR19-12-2024 11:42:PM196 mg/dl140-0 mg/dlPHOSPHOROUS19-12-2024 11:42:PM1.7 mg/dl4.5-2.5 mg/dlSERUM ELECTROLYTES (Na, K, C l) 20-12-2024 07:19:AM SODIUM141 mmol/L145-136 mmol/LPOTASSIUM1.8 mmol/L5.1-3.5 mmol/LCHLORIDE103
mmol/L98-107 mmol/LT3, T4, TSH 20-12-2024 07:19:AM T30.58 ng/ml1.87-0.87 ng/mlT49.83 micro g/dl12.23-6.32 micro g/dlTSH2.57 micro Iu/ml5.36-0.34 micro Iu/mlSERUM ELECTROLYTES (Na, K, C l) 20-12-2024 10:52:PM SODIUM140 mmol/L145-136 mmol/LPOTASSIUM2.2 mmol/L5.1-3.5 mmol/LCHLORIDE101 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 21-12-2024 09:19:AM SODIUM137 mmol/L145-136 mmol/LPOTASSIUM2.7 mmol/L5.1-3.5 mmol/LCHLORIDE105 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 21-12-2024 09:20:AM SODIUM137 mmol/L145-136 mmol/LPOTASSIUM2.2 mmol/L5.1-3.5 mmol/LCHLORIDE98 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 21-12-2024 11:16:PM SODIUM140 mmol/L145-136 mmol/LPOTASSIUM3.1 mmol/L5.1-3.5mmol/L CHLORIDE105 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 22-12-2024 08:54:AM SODIUM139 mmol/L145-136 mmol/LPOTASSIUM3.3 mmol/L5.1-3.5 mmol/L CHLORIDE102 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 22-12-2024 08:55:AM SODIUM138 mmol/L145-136 mmol/LPOTASSIUM3.3 mmol/L5.1-3.5 mmol/L CHLORIDE101 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 
22-12-2024 10:45:PM SODIUM140 mmol/L145-136
mmol/LPOTASSIUM3.0 mmol/L5.1-3.5 mmol/LCHLORIDE102 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 23-12-2024 05:46:PM SODIUM139 mmol/L145-136
mmol/LPOTASSIUM2.7 mmol/L5.1-3.5 mmol/LCHLORIDE102 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 23-12-2024 11:40:PM SODIUM140 mmol/L145-136
mmol/LPOTASSIUM3.0 mmol/L5.1-3.5 mmol/LCHLORIDE104 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 24-12-2024 06:31:PM SODIUM135 mmol/L145-136
mmol/LPOTASSIUM2.9 mmol/L5.1-3.5 mmol/LCHLORIDE105 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 24-12-2024 11:22:PM SODIUM139 mmol/L145-136
mmol/LPOTASSIUM3.1 mmol/L5.1-3.5 mmol/LCHLORIDE104 mmol/L98-107 mmol/LPHOSPHOROUS2.0 mg/dl4.5-2.5 mg/dl 
25/12/2024 COMPLETE URINE EXAMINATION (CUE) 19-12-2024 06:48:PM COLOUR Pale yellowAPPEARANCEClearREACTIONAcidicSP.GRAVITY1.010ALBUMIN++SUGAR+++BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS2-4 EPITHELIAL CELLS 2-3RED BLOOD CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil BLOOD UREA
19- 12-2024 06:48:PM 43 mg/dl42-12 mg/dl SERUM CREATININE
19-12-2024 06:48:PM1.4 mg/dl1.3-0.9 mg/dl SERUM ELECTROLYTES (Na, K, C l) 
19-12-2024 06:48:PM SODIUM135 mmol/L145-136
mmol/L POTASSIUM1.5 mmol/L5.1-3.5 mmol/L CHLORIDE100 mmol/L98-107 mmol/L 
LIVER FUNCTION TEST (LFT) 19-12-2024 06:48:PM Total Bilurubin1.25 mg/dl1-0 mg/dl Direct Bilurubin0.30 mg/dl 0.2-0.0 mg/dl SGOT(AST)36 IU/L35-0 IU/LSGPT(ALT)24 IU/L45-0 IU/LALKALINE PHOSPHATASE 540 IU/L128-53 IU/LTOTAL PROTEINS 6.6 gm/dl8.3-6.4 gm/dl ALBUMIN3.8gm/dl5.2-3.5 gm/dl A/G RATIO1.39Anti HCV Antibodies - RAPID
19-12-2024 06:48:PM Non Reactive 
ABG 19-12-2024 09:01:PM PH7.34PCO231.7PO246.8HCO317.0 St.HCO318.5BEB-7.0BEecf-7.5TCO233.1O2 Sat80.2O2 Count18.3PHOSPHOROUS19-12-2024 10:15:PM2.0 mg/dl4.5-2.5 mg/dl SERUM ELECTROLYTES (Na, K, C l) 19-12-2024 11:41:PM SODIUM138 mmol/L145-136
mmol/LPOTASSIUM1.4 mmol/L5.1-3.5 mmol/LCHLORIDE98 mmol/L98-107 mmol/LPOST LUNCH BLOOD SUGAR19-12-2024 11:42:PM196 mg/dl140-0 mg/dlPHOSPHOROUS19-12-2024 11:42:PM1.7 mg/dl4.5-2.5 mg/dlSERUM ELECTROLYTES (Na, K, C l) 20-12-2024 07:19:AM SODIUM141 mmol/L145-136 mmol/LPOTASSIUM1.8 mmol/L5.1-3.5 mmol/LCHLORIDE103
mmol/L98-107 mmol/LT3, T4, TSH 20-12-2024 07:19:AM T30.58 ng/ml1.87-0.87 ng/mlT49.83 micro g/dl12.23-6.32 micro g/dlTSH2.57 micro Iu/ml5.36-0.34 micro Iu/mlSERUM ELECTROLYTES (Na, K, C l) 20-12-2024 10:52:PM SODIUM140 mmol/L145-136 mmol/LPOTASSIUM2.2 mmol/L5.1-3.5 mmol/LCHLORIDE101 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 21-12-2024 09:19:AM SODIUM137 mmol/L145-136 mmol/LPOTASSIUM2.7 mmol/L5.1-3.5 mmol/LCHLORIDE105 mmol/L98-107 mmol/L
SERUM ELECTROLYTES (Na, K, C l) 21-12-2024 09:20:AM SODIUM137 mmol/L145-136 mmol/LPOTASSIUM2.2 mmol/L5.1-3.5 mmol/CHLORIDE
98 mmol/L98-107 mmol/L
SERUM ELECTROLYTES (Na, K, C l) 21-12-2024 11:16:PM SODIUM140
mmol/L145-136 mmol/LPOTASSIUM3.1 mmol/L5.1-3.5 mmol/LCHLORIDE105 mmol/L98-107 mmol/L
SERUM ELECTROLYTES (Na, K, C l) 22-12-2024 08:54:AM SODIUM139 mmol/L145-136
mmol/LPOTASSIUM3.3 mmol/L5.1-3.5 mmol/LCHLORIDE102 mmol/L98-107 mmol/L
SERUM ELECTROLYTES (Na, K, C l) 22-12-2024 08:55:AM SODIUM138 mmol/L145-136
mmol/LPOTASSIUM3.3 mmol/L5.1-3.5 mmol/LCHLORIDE101 mmol/L98-107 mmol/L
SERUM ELECTROLYTES (Na, K, C l) 22-12-2024 10:45:PM SODIUM140 mmol/L145-136
mmol/LPOTASSIUM3.0 mmol/L5.1-3.5 mmol/LCHLORIDE102 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 23-12-2024 05:46:PM SODIUM139 mmol/L145-136
mmol/LPOTASSIUM2.7 mmol/L5.1-3.5 mmol/LCHLORIDE102 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 23-12-2024 11:40:PM SODI
UM140 mmol/L145-136 mmol/LPOTASSIUM3.0 mmol/L5.1-3.5 mmol/LCHLORIDE104 mmol/L98- 107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 24-12-2024 06:31:PM SODIUM135 mmol/L145-
136 mmol/LPOTASSIUM2.9 mmol/L5.1-3.5 mmol/LCHLORIDE105 mmol/L98-107 mmol/LSERUM ELECTROLYTES (Na, K, C l) 24-12-2024 11:22:PM SODIUM139 mmol/L145-136
mmol/LPOTASSIUM3.1 mmol/L5.1-3.5 mmol/LCHLORIDE104 mmol/L98-107 mmol/LPHOSPHOROUS25-12-2024 05:02:AM2.0 mg/dl4.5-2.5 mg/dl SERUM ELECTROLYTES 25/12/24 5:30PM
SODIUM 134
CHLORINE 99
POTASSIUM 3.0
CALCIUM IONIZED 1.25
SERUM ELECTROLYTES 26/12/24
SODIUM 133 mmol/L POTASSIUM 2.8 mmol/LCHLORIDE 101 mmol/L CALCIUM IONIZED 1.09
mmol/L
HEMOGRAM 26/12/24 HAEMOGLOBIN 12.6 gm/dl
TOTAL COUNT 14,000 cells/cumm NEUTROPHILS 85 % LYMPHOCYTES 08 % EOSINOPHILS 01% MONOCYTES 06 % BASOPHILS 00 % PCV 35.3 vol % M C V 79.9 fl M C H 28.4 pg M C H C
35.6 % RDW-CV 14.8 % RDW-SD 46.6 fl RBC COUNT 4.42 millions/cumm PLATELET COUNT 1.4
lakhs/cu.mm
SERUM ELECTROLYTES 27/12/24 5:30PM SODIUM 133
CHLORINE 99
POTASSIUM 2.6
CALCIUM IONIZED 1.12 HEMOGRAM 27/12/24 HAEMOGLOBIN 11.9 gm/dl
TOTAL COUNT 9800 cells/cumm NEUTROPHILS 91 % LYMPHOCYTES 03 % EOSINOPHILS 01 % MONOCYTES 05 % BASOPHILS 00 % PCV 33.4 vol % M C V 79.2 fl M C H 28.2 pg M C H C 35.6% RDW-CV 14.8 % RDW-SD 46.0 fl RBC COUNT 4.22 millions/cumm PLATELET COUNT 1.0
lakhs/cu.mm
SERUM ELECTROLYTES 28/12/24 SODIUM 141
CHLORINE 101
POTASSIUM 2.4
CALCIUM IONIZED 1.12
HEMOGRAM 28/12/24 HAEMOGLOBIN 11.5 gm/dl
TOTAL COUNT 12500 cells/cumm NEUTROPHILS 92 % LYMPHOCYTES 04 % EOSINOPHILS 01
% MONOCYTES 03 % BASOPHILS 00 % PCV 32.8 vol % M C V 79.5 fl M C H 27.9 pg M C H C
35.1 % RDW-CV 14.6 % RDW-SD 46.0 fl RBC COUNT 4.13 millions/cumm PLATELET COUNT
70,000lakhs/cu.mm
SERUM ELECTROLYTES 31/12/24 SODIUM 137
CHLORINE 101
POTASSIUM 2.4
CALCIUM IONIZED 1.13
BLOOD CULTURE-NO GROWTH HEMOGRAM 31/12/24 HAEMOGLOBIN 11.2 gm/dl
TOTAL COUNT 16200 cells/cumm NEUTROPHILS 82 %LYMPHOCYTES 10 %EOSINOPHILS 03%MONOCYTES 05 %BASOPHILS 00 %PCV 30.6 vol %M C V 78.3 flM C H 28.6pgM C H C 36.6
%RDW-CV 15.6 %RDW-SD 44.7 flRBC COUNT 3.91 millions/cumm
PLATELET COUNT
86,000lakhs/cu.mm NORMOCYTIC NORMOCHROMIC
STOOL FOR OCCULT BLOOD ON 30.12.24 : NEGATIVE SERUM ELECTROLYTES 1/1/25
SODIUM 135
CHLORINE 99
POTASSIUM 3.2
CALCIUM IONIZED 1.11
CRP ON 1.1.25- POSITIVE[2.4MG/DL] ON 1.1.25
BLOOD LACTATE -15MG/DL
24HR URINE PROTEIN -258MG/DL
24HR CREATININE-0.8G/DAY RATIO-0.32
URINE VOLUME-2150ML
24HR URINARY POTASIUM-23.2MMOL/DAY URINE CALCIUM-167MG/DAY
URINE CULTURE- PSEUDOMONAS SPECIES ISOLATED SENSITIVE TO
AMIKACIN, TOBRAMYCIN, NORFLAXACIN, OFLAXACIN, CEFTAZIDIME, CEFEPIME, PIPERACILLIN/TAZOBACTAM, MICROPENEM 02.01.25
COMPLETE URINE EXAMINATION (CUE)COLOUR Pale yellow APPEARANCE Clear REACTION Acidic SP.GRAVITY 1.010ALBUMIN Nil SUGAR Nil BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 2-3EPITHELIAL CELLS 2-3RED BLOOD CELLS NILCRYSTALS Nil CASTS Nil AMORPHOUSDEPOSITS Absent OTHERS Nil
 HEMOGRAM HAEMOGLOBIN 12.4 gm/dl TOTAL COUNT 11900 cells/cumm NEUTROPHILS 72
%LYMPHOCYTES 18 %EOSINOPHILS 04%MONOCYTES 06%BASOPHILS 00 %PCV 35.4vol %M C V 79 flM C H 27.7 pgM C H C 35.1 %RDW-CV 15 %RDW-SD 45.7 flRBC COUNT 4.48
millions/cummPLATELET COUNT 1.55 lakhs/cu.mm SMEAR-NORMOCYTIC NORMOCHROMIC
URINE PH-6 RFT
BLOOD UREA - 20 mg/dl SERUM CREATININE - 0.6 mg/dl URIC ACID- 2 MMOL/L CALCIUM-9.4MG/DL PHOSPHORUS-2MG/DL
SODIUM 138 mmol/L
POTASSIUM 3.4 mmol/L
CHLORIDE 102 mmol/L
PH - 7.37 PCO2 - 27.1 mmHg PO2 -101 mmHg HCO3- 15.5 mmol/LSt.HCO3- 18.0 mmol/LBEB -8.0
mmol/LBEecf -8.6 mmol/LTCO2- 31.9 VOLO2 Sat -97.9 %O2 Count- 15.6 vol % HEMOGRAM ON 3.12.24HAEMOGLOBIN 12.1 gm/dlTOTAL COUNT 10400 cells/cummNEUTROPHILS 87 %LYMPHOCYTES 25 %EOSINOPHILS 02%MONOCYTES
06%BASOPHILS 00 %PCV 36.5vol %M C V 80.7 flM C H 26.8 pgM C H C 33.2 %RDW-CV
14.8%RDW-SD 45.7 flRBC COUNT 4.52 millions/cummPLATELET COUNT 1.91 lakhs/cu.mm SMEAR-NORMOCYTIC NORMOCHROMIC
RFT on 3.1.25
BLOOD UREA - 21 mg/dl SERUM CREATININE - 0.6 mg/dl URIC ACID- 2.1 MMOL/L CALCIUM-9.7MG/DL PHOSPHORUS-2MG/DL
SODIUM 138 mmol/L
POTASSIUM 3.4 mmol/L
CHLORIDE 104 mmol/L
Treatment Given(Enter only Generic Name)
INJ.KCL 3.AMP (60ML + 1 AMP MGSO4 IN 1 UNIT NS 500ML )@75ML /HR INJ.SODA BICARBONATE 100 ML IN 500ML NS @50ML/HR TAB.DOXYCYCLINE 100MG PO/BD
IV FLUIDS - RL @50ML /HR TAB. GLIMI M1 PO/BD
TAB. NODOSIS 500MG PO/BD TAB.SHELCAL -XT PO/OD
TAB. NEUROBION FORTE BPO/OD @2PM TAB. PAN 40MG PO/OD
SYP.POTKLOR 20 ML NS IN GLASS OF WATER PO/TID POTASSIUM RICH DIET -COCUNUT WATER, BANANNA
COURSE AT THE HOSPITAL:
PATIENT WAS PRESENTED TO HOSPITAL WITH WEAKNESS IN BOTH LOWER LIMBS AND REQUIRED INVESTIGATIONS DONE SO SERUM POTASSIUM LEVELS ARE 1.4 POTASSIUM RICH DIET IS GIVEN, HE IS ALSO A K/C/O DIABETES AN ANTIDIABETIC IS ALSO GIVEN , INJ.KCL IS GIVEN ALONG WITH SYRUP POTKLOR GIVEN , VITAMIN B COMPLEX IS GIVEN, CALCIUM TABLET IS GIVEN , ANTIBIOTIC TAB IS ALSO GIVEN ALONG WITH IV FLUIDS AO THE SERUM POTASSUIM VALUE UPGRADED TO 3.4 . PATIENT IS BEING DISCHARGED IN HEMODYNAMICALLY STABLE CONDIRION
Advice at Discharge POTASSIUM RICH DIET TAB.GLIMI M1 PO/BD X 1 WEEK
TAB.NODOSIS 1 GM PO/BD X1 WEEK TAB.SHELCAL -XT PO/OD X 15 DAYS TAB.NEUROBIONFORTE PO/OD X 1 WEEK TAB.OFLOXACIN 200MG PO/BD X 7 DAYS TAB.LIMCEE 500MG PO/OD X 15 DAYS
SYRUP.POTKLOR 20ML IN 1 GLASS OF WATER PO/OD X 1 WEEK
Follow Up
REVIEW WITH SERUM ELECTROLYTES REPORT TO GENERAL MEDICINE OPD AFTER 1 WEEK
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 OF ADMINISTRATOR
SIGNATURE OF FACULTY
Discharge Date
Date:03.01.25
Ward: AMC Unit: IV
[5:09 pm, 29/01/2026] PPM 1: @PPM11 @PPM12 @PaJR Health would you like to go through this case report link of our current patient who had a fracture followed by recurrent hypokalemic paralysis and share your inputs around what is the possible etiology for his hypokalemia and how do we relate it to his fracture which appeared to have happened when he slipped and fell from his own height 👇
[5:09 pm, 29/01/2026] PaJR Health: *CASE REPORT ANALYSIS: 50M WITH HYPOKALEMIC PERIODIC PARALYSIS*
*POSSIBLE ETIOLOGY FOR HYPOKALEMIA*
💡 The patient's recurrent hypokalemic paralysis is attributed to *Type 1 Renal Tubular Acidosis (dRTA)*, as explicitly stated in the discharge diagnosis. This is supported by several clinical and laboratory findings:
📍 *Persistent Hypokalemia:* Serum potassium levels were consistently low, reaching as low as 1.4 mmol/L.
📍 *Metabolic Acidosis:* Arterial blood gas (ABG) results showed a low pH (e.g., 7.34, 7.37) and low bicarbonate (e.g., 17.0, 15.5 mmol/L), indicating systemic acidosis.
📍 *Inappropriately High Urine pH:* While not explicitly stated as "high" in the context of acidosis, a urine pH of 6.0 in the presence of systemic acidosis is considered inappropriately high for dRTA, as the kidneys are unable to acidify the urine effectively.
📍 *Hypercalciuria and Renal Calculi:* The patient exhibited elevated 24-hour urinary calcium excretion (167 mg/day) and bilateral renal calculi, which are common complications of dRTA due to increased calcium excretion and hypocitraturia.
📍 *Polyuria and Muscle Weakness:* These symptoms are consistent with the renal potassium wasting and electrolyte imbalances seen in dRTA.
The suspicion of Sjogren's Syndrome as a secondary cause for Type 1 RTA was noted, although ophthalmological evaluation did not find evidence of dry eyes, and an ANA profile was not performed due to affordability.
*RELATION TO HIS FRACTURE*
💡 The patient's left femur fracture, sustained from a slip and fall from his own height, is described as a *pathological fracture*. This suggests underlying bone fragility, which can be directly linked to the chronic metabolic acidosis caused by Type 1 RTA.
📍 *Bone Demineralization:* Chronic acidosis in dRTA leads to the buffering of excess acid by bone, resulting in the release of calcium and phosphate from the bone matrix. This process contributes to bone demineralization, increasing the risk of osteoporosis and pathological fractures.
📍 *Impaired Vitamin D Metabolism:* dRTA can also impair the renal activation of vitamin D, further contributing to bone disease and weakness.
📍 *Hypercalciuria:* The increased urinary calcium excretion, while contributing to renal calculi, also represents a loss of calcium from the body, which can negatively impact bone density over time.
Therefore, the recurrent hypokalemic paralysis and the pathological fracture are both manifestations of the systemic effects of the underlying Type 1 Renal Tubular Acidosis on electrolyte balance and bone metabolism.
[5:13 pm, 29/01/2026] PPM 1: What is in general the reason for developing type 1 distal RTA in humans?
[5:14 pm, 29/01/2026] PaJR Health: *REASON FOR DEVELOPING TYPE 1 DISTAL RENAL TUBULAR ACIDOSIS (DRTA)*
💡 Type 1 Distal Renal Tubular Acidosis (dRTA) generally arises from the impaired ability of the alpha-intercalated cells in the kidney's distal nephron to excrete hydrogen ions. This leads to a buildup of acid in the body (metabolic acidosis) and characteristic electrolyte imbalances. The reasons for developing dRTA can be broadly categorized into inherited and acquired causes.
*INHERITED CAUSES*
💡 Genetic mutations are a significant cause, often affecting the transport proteins and enzymes crucial for acid excretion in the renal tubules.
📍 *Gene Mutations:* Mutations in genes such as SLC4A4 are known to cause inherited forms of dRTA.
📍 *Hereditary Hypercalciuria:* In some hereditary cases, dRTA can be a complication of inherited conditions leading to excessive calcium in the urine.
*ACQUIRED CAUSES*
💡 Acquired dRTA can develop due to various underlying conditions, including autoimmune diseases, certain medications, and other systemic pathologies.
📍 *Autoimmune Diseases:* This is a common secondary cause.
    💡 *Sjogren's Syndrome:* Frequently associated with dRTA, often presenting with hypokalemic paralysis.
    💡 *Hashimoto's Thyroiditis:* Can also lead to dRTA.
📍 *Drugs:* Certain medications can disrupt the function of renal tubules, leading to dRTA.
📍 *Other Underlying Pathologies:*
    💡 *Plasma Cell Dyscrasias:* These conditions can be an underlying cause.
    💡 *Renal Transplantation:* Metabolic acidosis, including dRTA, can be a complication in the initial months following kidney transplantation, with factors like serum creatinine and tacrolimus levels playing a role.
    💡 *Acromegaly:* In rare instances, active acromegaly has been linked to dRTA due to altered calcium metabolism.
    💡 *Wasp Sting:* There are documented rare cases where a wasp sting has been associated with the development of dRTA.
📍 *Idiopathic:* In a notable number of cases, particularly in infants, the specific cause of dRTA remains unknown and is classified as idiopathic.
*REFERENCES*
2.  Primary Distal Renal Tubular Acidosis: Toward an Optimal Correction of Metabolic Acidosis - [https://pubmed.ncbi.nlm.nih.gov/38967973/](https://pubmed.ncbi.nlm.nih.gov/38967973/)
3.  The syndrome of distal (type 1) renal tubular acidosis. Clinical and laboratory findings in 58 cases - [https://pubmed.ncbi.nlm.nih.gov/3127650/](https://pubmed.ncbi.nlm.nih.gov/3127650/)
4.  Case Report: Recurrent hypokalemic periodic paralysis associated with distal renal tubular acidosis (type 1) and hypothyroidism secondary to Hashimoto's thyroiditis - [https://pubmed.ncbi.nlm.nih.gov/30647907/](https://pubmed.ncbi.nlm.nih.gov/30647907/)
5.  Electrolyte imbalances and nephrocalcinosis in acute phosphate poisoning on chronic type 1 renal tubular acidosis due to Sjogren's syndrome - [https://pubmed.ncbi.nlm.nih.gov/23400265/](https://pubmed.ncbi.nlm.nih.gov/23400265/)
6.  Inherited Type-1 renal tubular acidosis with short stature: a rare case report from Nepal - [https://pubmed.ncbi.nlm.nih.gov/41377247/](https://pubmed.ncbi.nlm.nih.gov/41377247/)
7.  Hypokalemic paralysis and osteomalacia secondary to renal tubular acidosis in a case with primary Sjogren's syndrome - [https://pubmed.ncbi.nlm.nih.gov/16622725/](https://pubmed.ncbi.nlm.nih.gov/16622725/)
8.  A case of active acromegaly with reduced height and type 1 renal tubular acidosis - [https://pubmed.ncbi.nlm.nih.gov/2899504/](https://pubmed.ncbi.nlm.nih.gov/2899504/)
9.  Hypernatremia Masking a Case of Primary Sjogren Syndrome-induced Distal Renal Tubular Acidosis - [https://pubmed.ncbi.nlm.nih.gov/38995305/](https://pubmed.ncbi.nlm.nih.gov/38995305/)
10. Metabolic acidosis in the initial 6 months after renal transplantation: A prospective study - [https://pubmed.ncbi.nlm.nih.gov/34302717/](https://pubmed.ncbi.nlm.nih.gov/34302717/)
11. Wasp sting associated with type 1 renal tubular acidosis - [https://pubmed.ncbi.nlm.nih.gov/18175784/](https://pubmed.ncbi.nlm.nih.gov/18175784/)
12. Hypokalemic Paralysis Revealing Primary Sjogren's Syndrome: A Case Report - [https://pubmed.ncbi.nlm.nih.gov/38289796/](https://pubmed.ncbi.nlm.nih.gov/38289796/)
13. Primary presentation with acute flaccid quadriparesis in Sjogren's syndrome sans sicca - [https://pubmed.ncbi.nlm.nih.gov/23576645/](https://pubmed.ncbi.nlm.nih.gov/23576645/)
[7:59 pm, 29/01/2026] PPM 2: Did the patient ever have Hypercalcemia?
[8:00 pm, 29/01/2026] PaJR Health: Based on the provided case report, the patient did not have hypercalcemia.
💡 His serum calcium levels were consistently within the normal range or on the lower side, particularly for ionized calcium.
📍 *First Admission (13/08/2024):*
    *   *CALCIUM:* 10.0 mg/dl (within normal limits)
📍 *Second Admission (19/12/2024 - 03/01/2025):*
    *   The report explicitly states: "His serum ionised calcium measured in the lab daily was always on the lower side while his 24 urinary excretion of calcium appears to be on the higher side."
    *   *Ionized Calcium:* Ranged from 1.09 mmol/L to 1.25 mmol/L, with several readings at the lower end of the normal range or slightly below.
    *   *Total Calcium:* 9.4 mg/dl and 9.7 mg/dl (both within normal limits).
[8:02 pm, 29/01/2026] Aditya: Based on the provided case report, the patient did not have hypercalcemia.
 His serum calcium levels were consistently within the normal range or on the lower side, particularly for ionized calcium.
 *First Admission (13/08/2024):*
    *   *CALCIUM:* 10.0 mg/dl (within normal limits)
 *Second Admission (19/12/2024 - 03/01/2025):*
    *   The report explicitly states: "His serum ionised calcium measured in the lab daily was always on the lower side while his 24 urinary excretion of calcium appears to be on the higher side."
    *   *Ionized Calcium:* Ranged from 1.09 mmol/L to 1.25 mmol/L, with several readings at the lower end of the normal range or slightly below.
    *   *Total Calcium:* 9.4 mg/dl and 9.7 mg/dl (both within normal limits).
Hmm so how do you explain those osteoporotic fractures then?
[8:02 pm, 29/01/2026] PaJR Health: Even without hypercalcemia, the osteoporotic fractures in this patient can be directly explained by the underlying *Type 1 Renal Tubular Acidosis (dRTA)*.
Here's how dRTA contributes to bone fragility:
💡 *Chronic Metabolic Acidosis:* The persistent acid buildup in the body due to dRTA forces the body to buffer this acid. A primary buffer system involves the release of calcium and phosphate from the bones. This continuous process leads to a gradual demineralization of the bone matrix.
💡 *Hypercalciuria:* As noted in the case report, the patient had elevated 24-hour urinary calcium excretion (hypercalciuria). This excessive loss of calcium through the urine, even when serum calcium levels are normal or low, depletes the body's calcium stores and contributes to negative calcium balance, further weakening the bones.
💡 *Impaired Vitamin D Metabolism:* Chronic kidney conditions, including dRTA, can impair the kidneys' ability to convert vitamin D into its active form. Active vitamin D is crucial for calcium absorption from the gut and for proper bone mineralization. A deficiency in active vitamin D can lead to osteomalacia (softening of bones) and exacerbate osteoporosis.
💡 *Hypocitraturia:* dRTA is often associated with low urinary citrate levels (hypocitraturia). Citrate normally inhibits the crystallization of calcium salts in the urine and also plays a role in bone health. Its deficiency can contribute to both kidney stone formation and bone demineralization.
These combined effects of chronic acidosis, increased urinary calcium loss, and potential vitamin D abnormalities create an environment conducive to *osteoporosis* and *pathological fractures*, even in the absence of elevated serum calcium levels. The fracture from a "slip and fall from his own height" is indeed characteristic of such bone fragility.
[10:02 am, 30/01/2026] PPM 1: Lastest EMR summary to be added to the case report link.
Interestingly the local doctors @PPM16 @PPM17 have removed the previous label of Sjogrens syn (a result of similar patient recall bias at that time) but also managed to increase the patient's age by 5 years in one year (although again this EMR aging yo yo is very common and possibly driven by intern changing EMR hands):
Age/Gender: 55 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 19/01/2026 05:25 PM
Discharge Date: 23/01/2026 10:27 AM
Diagnosis
K/C/O HYPOKALEMIC PERIODIC PARALYSIS SECONDARY TO TYPE I RTA
K/C/O T2DM
HBSAG POSITIVE STATUS
Case History and Clinical Findings
PATIENT CAME WITH C/O WEAKNESS OF BOTH LOWER LIMBS SINCE 20 DAYS
HOPI: PATIENT WAS APPARENTLY ASYMPTOMATIC 20 DAYS BACK, THEN HE NOTICED
WEAKNESS OF BOTH LOWER LIMBS INSIDIOUS IN ONSET GRADUALLY PROGRESSIVE NO AGGREVATING OR RELEVING FACTORS. NO H/O NAUSEA, VOMITING, PAIN ABDOMEN, LOOSE STOOLS. NO H/O CHEST PAIN, PALPITATIONS, PND, ORTHOPNEA, COUGH. NO H/O HEADCHE, GIDDINESS, BLURRING OF VISION, DECREASED URINE OUTPUT, HEMATURIA, BURNING MICTURITION. NO H/O INVOLUNTARY MOVEMENTS OF LIMBS, SLURRING OF SPEECH.PAST HISTORY: SIMILAR COMPLAINTS IN THE PAST.K/C/O T2DM SINCE 1 YEAR ON TAB GLIMI M1 TWICE DAILY. N/K/C/O HTN, ASTHMA, EPILEPSY, CVA, CAD, THYROID DISORDERS.SURGICAL HISTORY:? LEFT FEMUR FRACTURE ORIF,  APPENDECTOMY10YEARS AGO. PERSONAL HISTORY - MARRIED, MIXED DIET, NORMAL APPETITE, REGULAR BOWEL AND BLADDER HABITS, NO ALLERGIES, ADDICTIONS - TODDY INTAKE.
Page-2
KIMS HOSPITALS
GENERAL EXAMINATION: NO PALLOR, NO ICTERUS, NO CYANOSIS, NO CLUBBING, NO
LYMPHADENOPATHY, NO PEDAL EDEMA.VITALS: - TEMP:98F, BP: 110/70MMHG, RR: 20 CPM, PR:72BPM, SPO2: 98% AT RA.SYSTEMIC EXAMINATION- CVS- S1 S2 PRESENT, NO
MURMURS; RS-BAE+ NVBS; PER ABDOMEN-SOFT, NON TENDER; CNS: CNS-HMF INTACT, CNNORMAL,POWER: 5/5 IN RIGHT UL,5/5 IN LEFT UL,3/5 IN RIGHT LL,3/5 IN LEFT LL TONE :DECREASED IN B/L LL, NORMAL IN B/L UL.REFLEXES:BICEPS:+2 IN RIGHT,+2 IN LEFT TRICEPS :+2 IN RIGHT,+2 IN LEFT.KNEE +1 IN RIGHT, +1 IN LEFT.PLANTAR:B/L FLEXOR RESPONSE, SENSORY:INTACT.
Investigation
SEROLOGY:HBSAG-POSITIVE,HIV,HCV-NEGATIVE.ABG(19/1/26): PH 7.31, pCO2 23.50
mmHg,pO2 127 mmHg HCO3? 12mmol/L.HEMOGRAM(19/1/26): HB-13.2, PCV-39.4, TLC-18600,
RBC-4.8, PLT-2.8, CUE(19/1/26): COLOR PALE YELLOW,ALB-+30MG/DL,SUGAR-NIL ,PUS 2-
3CELLS , EPITHELIAL CELLS 2-3,URINE PH:(19/1/26):6.SERUM
MAGNESIUM(19/1/26):2.10.URINARY ELECTROLYTES(19/1/26):NA-185, K-16, CHLORIDE-
172.HS TROPONIN-I(19/1/26):8.1 RFT(19/1/26): UREA-22, CR-1.00, NA-136, K-2.8, CHLORIDE-98
LFT(19/1/26): TB-0.69, DB-0.22, SGPT -30, SGOT-20, ALP -643, TP-7.5, ALB-4.0, GLO-3.50, A/G
RATIO-1.14, HBA1C(19/1/26): 6.8.FBS(20/1/26):118,PPBS(20/1/26)-139,SERUM
ELECTROLYTES(20/1/26):NA-140, K-2.6, CHLORIDE-102.URINARY
ELECTROLYTES(20/1/26):Na-185 meq/L ,K-16.0 meq/L,CHLORIDE-172. THYROID
PROFILE(20/1/26) T3- 0.7 ng/ml T4-9.5 μg/ml TSH-2.64μIU/ml.24 Hrs URINE
POTASSIUM(21/1/26):32.2 ,24 Hrs URINE SODIUM(21/1/26): 220.0,SERUM
ELECTROLYTES(21/1/26):NA-134, K-3.0, CHLORIDE-99, USG ABDOMEN(21/1/26):B/L GRADE 1
RPD CHANGES WITH B/L RENAL CORTICAL CYSTS,LEFT RENAL CALCULI.SERUM
ELECTROLYTES(22/1/26):NA-138, K-3.7, CHLORIDE-101,SERUM ELECTROLYTES(23/1/26):NA-
136, K-3.7, CHLORIDE-101.
Treatment Given(Enter only Generic Name)
1.INJ KCL 3 AMP(60ML) +1 AMP MGSO4 IN 500ML NS @ 75ML/HR OVER 5-6 HOURS.
2.TAB.GLIMI M1 PO/BD.
3.TAB SHELCAL XT PO/OD.
4.SYP.POTCHLOR 20ML IN 1 GLASS OF WATER PO/TID.
5.TAB NODOSIS 500MG PO/BD.
6.TAB.KETOROLAC DT 10MG PO/SOS.
Advice at Discharge
1.TAB.GLIMI M1 PO/BD TO BE CONTINUED.
2.TAB NODOSIS 1GM PO/BD X 15 DAYS.
3.TAB SHELCAL XT PO/OD X 15 DAYS.
Page-3
KIMS HOSPITALS
4.SYP.POTCHLOR 20ML IN 1 GLASS OF WATER PO/TID X 15 DAYS.
5.POTASSIUM RICH DIET.
6.STRICT DIABETIC DIET.
Follow Up
REVIEW TO GM OPD WITH ABG AND SERUM ELECTROLYTES REPORTS AFTER 2 WEEKS/
SOS.
Discharge Date
Date:24/1/26 Ward: MMW Unit:I
[10:03 am, 30/01/2026] PPM 1: 👆@PPM13 @PPM14 @PPM15 I guess the HbSag wasn't addressed with either HBV dna or oral anti virals due to resource constraints and patient inability toward out of pocket expenditure oope?
[1:33 pm, 30/01/2026] PPM 2: I think there is a formula to calculate Bicarbonate requirement and dose it appropriately.




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