52M Diabetes 6 years on glim 2bd peripheral neuropathy 3 yrears WB PaJR

 

22-10-2024

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.

53M from WB with type 2 Diabetes 6 years and severe burning peripheral neuropathy pains since 3 years on tablet glimiperide 2mg twice a day. Stopped since 2 days current blood sugars 450!

Let's make glimiperide and metformin separate and let him take glimiperide 2mg before breakfast (can take it before lunch today) and before dinner and metformin 500 mg thrice after meals. Get seven point sugar profile daily for now.

Age/Gender : 53 Years/Male

Address :

Discharge Type: Relieved

Admission Date: 22/10/2024 12:49 AM

Diagnosis

PERIPHERAL NEUROPATHY (SENSORY >MOTOR) SECONDARY TO LUMBAR SPONDYLOSIS/? SCIATICA

ACID PEPTIC DISEASE RIGHT SCROTAL HERNIA K/C/O T2 DM SINCE 8 YEARS

Case History and Clinical Findings

PT CAME WITH C/O PAIN IN B/L LOWER LIMB SINCE 4 YEARS C/O SWELLING IN RIGHT SCROTAL REGION SINCE 4 YEARS C/O BURNING SENSATION OF EPIGASTRIUM SINCE 2 YEARS HOPI:

PT WAS APPARENTLY ASYMPTOMATIC 4 YEARS BACK, THEN SHE DEVELOPED PAIN IN B/L LOWER LIMBS, INSIDIOUS IN ONSET, GRADUALLY PROGRESSIVE, AGGRAVATED SINCE 2 YEARS, MORE IN SUPINE POSITION, RELIEVED ON SITTING AND MEDICATION, C/O BURNING SENSATION IN UPPER ABDOMEN (EPIGASTRIUM) SINCE 2 YEARS, AGGRAVATED ON TAKING SPICY, OILY AND SOUR FOODS A/W BELCHING. C/O SWELLING IN RIGHT SCROTAL REGION, AGGRAVATED ON EXERTION, RELIEVED ON REST, COUGH IMPULSE +.NO H/O FEVER, COUGH, COLD, BURNING MICTURITION, CONSTIPATION. NO H/O LOOSE STOOLS, CHEST PAIN, PALPITATIONS, SEIZURES.

 PAST HISTORY:

K/C/O T2DM SINCE 8 YEARS ON TAB GLIMIPERIDE 2MG+METFORMIN 500MG BD K/C/O HTN SINCE 8 YEARS ON TAB TELMISARTAN 40MG HS

K/C/O SCROTAL HERNIA SINCE 4 YEARS, (AFTER LIFTING HEAVY LOAD), NOT SURGICALLY CORRECTED.

PERSONAL HISTORY:

OCCUPATION: DRIVER

KHAINI USER SINCE 10-15 YEARS GENERAL EXAMINATION:

NO PALLOR ICTERUS CYANOSIS CLUBBING LYMPHADENOPATHY OEDEMA BP: 160/90 MMHG

PR:96 BPM RR: 17 CPM

TEMPERATURE: 98.4F SPO2: 98% AT RA GRBS:443 MG/DL

CVS: NO THRILLS, S1S2 +, NO MURMURS RS: BAE+, NVBS

PER ABDOMEN:

SOFT, NON-TENDER

LARGE SWELLING (5CM X 6CM) IN RT SCROTAL REGION CNS:

TONE: RT LT

UL NORMAL NORMAL LL NORMAL NORMAL POWER:

UL 5/5 5/5

HAND GRIP 4/5 4/5

SMALL MUSCLES OF HAND 3/5 3/5 KNEE 4/5 4/5

HIP 5/5 5/5

REFLEXES: - RT LT BICEPS: - 2+ 2+

 TRICEPS: - 2+ 2+

KNEES: - 2+ 2+

ANKLE: - +2 +2

SUPINATOR: - +2 +2 UPPERLIMBS RT LT

NECK MUSCLES GOOD; GOOD SHOULDER 5/5; 5/5

-FLEXION&EXTENSION 5/5 ; 5/5

-ABDUCTION AND ADDUCTION 5/5 ;5/5

-LATERAL AND MEDIAL ROTATION 5/5;5/5 ELBOW

-FLEXION 5/5;5/5

-EXTENSION 5/5; 5/5 WRIST

-DORSIFLEXION 5/5;5/5

-PLANTAR FLEXION 5/5; 5/5

- ADDUCTION 5/5;5/5

- ABDUCTION 5/5;5/5

-PRONATION 5/5;5/5

-SUPINATION 5/5;5/5

-HAND GRIP 4/5:4/5 LOWER LIMB RT LT HIP

- FLEXION 5/5; 5/5

-EXTENSION 5/5 5/5

-ABDUCTION 5/5 5/5

- ADDUCTION 5/5 5/5

-LATERAL ROTATION 5/5 5/5

- MEDIAL ROTATION 5/5 5/5 KNEE

FLEXION AND EXTENSION 4/5;4/5 SENSORY RT LT

- FINE TOUCH NORMAL ABSENT ON DORSUM OF LEFT FOOT

-,CRUDE TOUCH, TACTILE LOCALISATION, PAIN- NORMAL NORMAL

 - STERIOGENESIS AND ROMBERG SIGN NORMAL CEREBELLAR SIGNS

- FINGERNOSE TEST-NEGATIVE

-DYSDIADOCHOKINESIA- NEGATIVE

-KNEE HEEL TEST NORMAL

OPHTHALMOLOGY REFERRAL DONE I/V/O? DIABETIC RETINOPATHY CHANGES FUNDUS EXAMINATION DONE

IMPRESSION: NO DIABETIC RETINOPATHY CHANGES

Investigation

BLOOD UREA22-10-2024 03:03:PM36 mg/dl42-12 mg/dl SERUM CREATININE22-10-2024 03:03:PM0.9 mg/dl1.3-0.9 mg/dl SERUM ELECTROLYTES (Na, K, C l) 22-10-2024 03:03:PM SODIUM133 mmol/L145-136 mmol/LPOTASSIUM4.0 mmol/L5.1-3.5 mmol/LCHLORIDE99 mmol/L 98-107 mmol/L 

COMPLETE URINE EXAMINATION (CUE) 22-10-2024 03:03:PM COLOUR Pale yellow APPEARANCE Clear REACTION Acidic SP.GRAVITY1.010 ALBUMIN Nil SUGAR++BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS 2-3 EPITHELIAL CELLS 2-3RED BLOOD CELLS Nil CRYSTALS NilCASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil

HEMOGRAM:

HB 10.5

PCV 29.8

TLC 4800

RBC 3.92

PLATELET 1.71

Treatment Given (Enter only Generic Name)

TAB AMITRYPTILINE 10MG PO HS

TAB GLIMIPERIDE 2MG PO BD (BEFORE FOOD) TAB METFORMIN 500MG PO TID (AFTER FOOD) TAB TELMISARTAN 40MG PO OD

Advice at Discharge

TAB AMITRYPTILINE 10MG PO HS

TAB GLIMIPERIDE 2MG PO BD (BEFORE FOOD) TAB METFORMIN 500MG PO TID (AFTER FOOD) TAB TELMISARTAN 40MG PO OD

 Follow Up

REVIEW TO GM OPD SOS

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:25/10/24 Ward: MMW Unit: IV

Our patient is 52 years old male who is from West Bengal has shared his physical problem that he has type 2 Diabetes from 6 years and severe burning peripheral neuropathy pains since 3 years on tablet glimiperide 2mg twice a day. 

This problem Stopped since 2 days current blood sugars 450!

Let's make glimiperide and metformin separate and let him take glimiperide 2mg before breakfast (can take it before lunch today) and before dinner and metformin 500 mg thrice after meals. Get seven point sugar profile daily for now

[9/27, 8:49 PM] PaJR PHR Moderator: Apnader patient ra kabe aashchen ekhane? Kone date a?

[9/27, 8:55 PM] pa: 19 octobar onara train a uthbe 21 tarikh nambe apnader okhane

[9/27, 8:55 PM] +pa:  Nomoskar sir

[9/27, 8:59 PM] PaJR PHR Moderator: রোগীর অ্যাডভোকেটের জন্য প্রশ্ন;

অনুগ্রহ করে আপনার রোগীর ঘটনাগুলির ক্রম বর্ণনা করুন যা বর্তমান সমস্যার দিকে পরিচালিত করেছে। আপনার রোগীর একেবারে কোন সমস্যা না হওয়ার সময় থেকে ঘটনাগুলির ক্রম শুরু করুন। 

অনুগ্রহ করে আপনার রোগীর 24 ঘন্টা ধরে তার প্রতি ঘন্টার রুটিন বর্ণনা করুন যখন সে পুরোপুরি ঠিক ছিল 

এর পরে অনুগ্রহ করে বর্ণনা করুন যে একবার রোগটি তার জীবন ধরে নেওয়ার পরে তার প্রতি ঘন্টা 24 ঘন্টার রুটিনে কী ঘটেছিল 

রোগীর প্রতি ঘণ্টার রুটিনের কোন অংশটি ব্যাহত হয়েছে তা বিশেষভাবে উল্লেখ করুন 

আমাদের কাছ থেকে রোগীর বর্তমান প্রয়োজনীয়তাগুলি কী যেমন আমরা যদি তাকে একটি ওষুধ দিতে হয় তবে তারা কোন সমস্যাটি সমাধান করতে পছন্দ করবে?

অনুগ্রহ করে রোগীর পেট এবং বাহুর পেশীর ক্লিনিকাল ফটো পোস্ট করুন যেমনটি নীচের ছবিতে দেখানো হয়েছে:

https://userdrivenhealthcare.blogspot.com/2024/08/template-for-pajr-user-driven-history.html?m=1

এবং অন্য কোনো সমস্যাযুক্ত শারীরিক অংশের ছবি পোস্ট করুন যাতে রোগীর পরিচয় প্রকাশ না হয়

PaJR দলের জন্য কাজ:

অগ্রাধিকার অনুসারে রোগীর সমস্যা তালিকা এবং অনুভূত প্রয়োজনীয়তার তালিকা প্রস্তুত করুন 

তালিকাভুক্ত প্রতিটি সমস্যার প্রয়োজনীয়তার জন্য একটি পরিকল্পনা প্রণয়ন করুন

তারা কীভাবে একটি ডায়নামিক কেস রিপোর্ট (EHR) তৈরি করতে পারে সে সম্পর্কে আরও এখানে: 

https://sites.pitt.edu/~super1/lecture/lec53671/002.htm

[9/27, 9:16 PM] pa: Anar betha sara sorir a.onek din jabot .onek osudh khache komche na

[9/27, 9:22 PM] PaJR PHR Moderator: অনুগ্রহ করে রোগীর পেট এবং বাহুর পেশীর ক্লিনিকাল ফটো পোস্ট করুন যেমনটি নীচের ছবিতে দেখানো হয়েছে:

https://userdrivenhealthcare.blogspot.com/2024/08/template-for-pajr-user-driven-history.html?m=1

এবং অন্য কোনো সমস্যাযুক্ত শারীরিক অংশের ছবি পোস্ট করুন যাতে রোগীর পরিচয় প্রকাশ না হয়

[9/28, 9:53 AM] PaJR PHR Moderator: Need one from the side

[9/28, 9:53 AM] +pa: Ok

[10/22, 12:03 PM] +pa: Sir ani patient

[10/22, 1:16 PM] PaJR PHR Moderator: Kintu inar to onyo somoshya dekhlam

Diabetes 6 years!

[10/22, 1:17 PM]pa:   Uni amay ai somosa gulo age bolechilen?

[10/22, 7:02 PM] PaJR PHR Moderator: Share his seven point sugar values obtained till now

[10/22, 7:26 PM]pajr doc: 10am - 162 mg/dl

2pm - 347 mg/dl

4pm - 110 mg/dl

7:30 pm - 241 mg/dl - T. Glimiperide 2mg before meals, 500mg metformin after meals

[10/22, 7:28 PM] PaJR PHR Moderator: 2PM is before lunch?

[10/22, 7:28 P)pajr doc: Yes sir

[10/22, 7:37 PM] PaJR PHR Moderator: He has taken his usual glimiperide 2 mg again before dinner today?

[10/22, 7:39 PM] pajr doc: His usual one was glimiperide 2mg+ metformin 1000mg combination sir. We split it and to give glimiperide 2mg before meals, which was given now sir. And 500mg metformin will be given after meals sir

[10/22, 7:41 PM] PaJR PHR Moderator: Was he taking that combination just once a day?

[10/22, 7:43 PM] pajr doc: No sir twice daily

[10/22, 7:44 PM] PaJR PHR Moderator: So he's supposed to take it before dinner again today?

[10/22, 7:46 PM] pajr doc: Yes sir

[10/23, 8:32 AM] pajr doc: Grbs:

10pm- 260mg/dl

2am- 182mg/dl

8am-117mg/dl

Tab glimiperide dose Inc to 2.5mg bd before food

Tab metformin 500mg tid after food

[10/23, 9:18 AM] PaJR PHR Moderator: We'll need to add the first contact patient's advocate for this patient here @pajr_trained @⁨~PA⁩ so that he or she can continue to follow up on this PaJR

Only that can justify their coming all the way from 2000 kms to spend two days with us here.

[10/23, 10:36 AM] PaJR PHR

 Moderator: Why did we increase glimiperide by 0.5 mg when 2mg itself appears sufficient?

His next post breakfast blood sugars needs to be done by 12:30PM today

[10/23, 1:48 PM] +pajr doc: Grbs at 1 was 406mg/dl

[10/23, 1:49 PM] pajr doc:  He did not eat anything between 10:30 and 1.

[10/23, 1:53 PM] PaJR PHR Moderator: That means even 2.5mg was inadequate for him in the morning and the dose needs to be increased further!

[10/23, 2:11 PM] pajr doc: Yes sir, was planning to make it 3mg from tomorrow morning

PA: 

[10/23, 2:53 PM] PaJR PHR Moderator: Ok

Etar ashol naam holo metformin

[10/23, 3:43 PM] pajr doc: Grbs at 3:40 PM - 582mg/dL

[10/23, 4:13 PM] PaJR PHR Moderator: 👆He appeared to be much better yesterday with a lesser dose of glimiperide!

What happened to him today!😳

[10/23, 4:22 PM] +PA: Sir Bengali Language Type

[10/23, 4:23 PM] PaJR PHR Moderator: You can ask @⁨Meta AI⁩ here to translate all text for you into Bengali

@⁨Meta AI⁩ please translate the text above and below to Bengali

👆He appeared to be much better yesterday with a lesser dose of glimiperide!

What happened to him today!😳

[10/23, 4:23 PM] Meta AI: I don’t understand Bengali yet, but I’m working on it. I will send you a message when we can talk in Bengali.

[10/23, 4:24 PM] PaJR PHR Moderator: @⁨PAJR_TRAINEE⁩ please teach him how to copy paste all English text into Google translate and convert English to Bengali

[10/23, 4:32 PM] pajr member: 10 am: chatur (it's a paste like thing they make by grinding rice and chickpeas) 

Morning dose of glimiperide and Metformin taken

 lunch at 2: 3 chapatis, one plate of rice, sambar, 1banana, 1 egg, 1 cup curd

Metformin after lunch taken.

[10/23, 4:39 PM] pajr member: Is it likely sir, that him eating rice (which I'm not sure if he's used to), could have caused spikes in his blood sugars

[10/23, 4:39 PM] PaJR PHR Moderator: Is that Chhatu (pronounced sattu in Hindi) the reason for his meteoric blood sugar rise today? Was it sweet?

[10/23, 4:40 PM] PaJR PHR Moderator: He didn't have rice for breakfast. Lunch rice and chapatis do look quite substantial though without any fruits and vegetables to buffer

[10/23, 4:41 PM] pajr trainee: https://24fpatientblog.blogspot.com/2024/10/52m-diabetes-6-years-on-glim-2-bd.html

[10/23, 4:42 PM] pajr_doc : There's ground rice in the paste like thing that he ate in the morning right sir

[10/23, 4:43 PM] pajr_member: No sir sattu is like powder rt? Gram flour powder. And sugar content is next to nil for that I believe. Its like a substitute for protein powder in some households

[10/23, 4:53 PM] PaJR PHR Moderator: Yes but sweet can always be added to it. Only tasting his breakfast would have confirmed our suspicions

[10/23, 8:03 PM] PAJR_DOC: Grbs @7:30 - 406 mg/dl

[10/23, 8:11 PM] PaJR PHR Moderator: Pre dinner?

Give only 2mg

PA: 

[10/23, 8:20 PM] pajr_member: Does he have any insulin reserve at all?

[10/23, 8:25 PM] PaJR PHR Moderator: Keep vigilance in the ward in case he goes into hypoglycemia (keeping in mind his sugar values with lower dose yesterday)

[10/23, 8:26 PM] PaJR PHR Moderator: 👆

[10/23, 8:27 PM] PaJR PHR Moderator: Oh he had taken 2.5 yesterday as well this time? @⁨pajr_dov

[10/23, 8:28 PM] PaJR PHR Moderator: We'll know once we keep up titrating slowly as per his sugar values

[10/23, 8:29 PM] +pajr member: Perhaps the easiest way would be to get a C peptide level?

[10/23, 8:29 PM] pajr member: And any insights into his peripheral neuropathy sir?

[10/23, 8:29 PM] PAJR DOC: Okay sir

[10/23, 8:29 PM] PAJR DOC : Yes sir, but he took 2mg yesterday. Today we increased his dose.

[10/23, 8:50 PM] PaJR PHR Moderator: @⁨~Dr.N V⁩ please share the clinical findings of CNS exams including detailed sensory examination of touch, pain, joint position and vibration sense along with motor power and reflex testing.

Collect our 16,000 department fund from Bharat and transfer to your or any PGY2 account and procure these monofilaments through Amazon 👇

https://www.amazon.in/Neuropathy-Monofilaments-Diabetes-Screening-Diabetic/dp/B0CB8RCPGT/ref=mp_s_a_1_2?dib=eyJ2IjoiMSJ9.alRmWNBHoYsit9VL9tDQuK1XgiJSOUlqFkX2lzHzmdY-Tz-bDe2wUpjupssK0K0HMDrFOHx09RdUmUq-RL_2CeQezfPnBUnVLu4j-ypIAaDPD23OqMyAht5cxPG3Kmy6YUzDFMrSG6u5t2FV_2DvaLzEAlwNZnj-moAKvB8_GorCwu9BqMjgZ0rEcW7dWq-NLRwgCiO0dk34TayrrvEWpQ.bFH_AEgmrFN9wjFwYAa0Av15RIyO-177Gcp7cK0GAHE&dib_tag=se&keywords=monofilament&qid=1729696764&sr=8-2

[10/23, 8:51 PM] pajr member: How much would a C peptide cost?

[10/23, 8:54 PM] PaJR PHR Moderator: They are two different goals

Neuropathy evaluation

Vs

Diabetes cause evaluation

C peptide in a diabetic for 6 years would be less reliable than the insulin secretagogue driven pancreatic beta cell challenge test we are currently doing?

[10/23, 8:58 PM] pajr member: I disagree sir.

If the peripheral neuropathy is being attributed to the Diabetes here, then secondary complications have onset and it is concerningly too early for Type 2 DM.

He also does not have the metabolic phenotype for Type 2 DM and a C peptide would tell us if he has any insulin reserve at all. If no then insulin is the only way forward. If yes, then how long?

Ideally this has to be discussed with the patient on whether he would consider getting a C peptide to check for insulin reserve or for this sulphonyl urea trial being attempted.

An even simpler test could be using a ketometer to check for subtle Ketones. Unfortunately urine Ketones may be unreliable as they tend to show up in overt ketoacidosis

[10/23, 8:59 PM] +pajr member: Even Chronic Pancreatitis can be a worthy consideration. Any historical events or features suggestive of CP at all?

[10/23, 9:00 PM] pajr member: Perhaps this fund could be useful to get ketone strips?

[10/23, 9:03 PM] PaJR PHR Moderator: It's not for this patient but for the PGs to learn to use these tools on all diabetic patients. Ideally each PG should buy and keep his own

[10/23, 9:04 PM] PaJR PHR Moderator: How is C peptide going to change his management?

If he fails the insulin secretagogue test he will need to be instituted on insulin. As simple as that?

[10/23, 9:06 PM] pajr member:  Let's go back for a bit.

What is your diagnosis of his diabetes? Is it type 2 sir?

[10/23, 9:09 PM] pajr member: If type 2? Does he have any features of insulin resistance? There is sarcopenia yes, but there are no other features such as abdominal obesity, acanthosis, skin changes etc.

Is the sarcopenia from subtle vitamin and mineral and macronutrient deficiencies? If yes, then is he having malabsorption (likely due to chronic pancreatitis). If no, then why does he have sarcopenia? What are his daily activities like? Do they explain the muscle wasting?

If this diabetic amyotrophy, then it becomes concerning as it is far too early in his diabetes natural history to be affected so soon.

Plenty of questions here! Apologies

[10/23, 9:10 PM] PaJR PHR Moderator: Which type would LADA or FCPD be?

And what's the big deal about deciding how to manage them other than deciding if when to start insulin?

[10/23, 9:11 PM] pajr member: That body habitus appears to have more wasting in the Proximal muscles (particularly Deltoids and quadriceps) with increased skin fold thickening in the triceps - perhaps suggesting equal loss of fat and muscle with elevated BMR - consistent with a diagnosis or cahcexia. This definitely warrants a full input (calorie intake) and output (stool and urine) evaluation.

[10/23, 9:12 PM] pajr member: LADA is type 1. Just late onset Type 1.

[10/23, 9:13 PM] PaJR PHR Moderator: Keep them coming

The current medicine knowledge base is just a few grains of sand compared to the vast unknown ocean!

It's been a fascinating personal journey for me seeing these patients and so many newer insights that add on every day

One of the untested recent insights was the relationship between sarcopenia and visceral fat driving diabetes (or i should just say metabolic syn) outcomes where even very lean sarcopenics like this patient show hyperglycemia with minimal visceral fat

[10/23, 9:14 PM] PaJR PHR Moderator: Yes to put it simply whichever gets depleted of all insulin reserves is type and needs insulin. No further amount of biochemical testing would add value

[10/23, 9:14 PM] pajr member: The deal is that he has already had complications of diabetes far too early for what is expected - hence the expedited need to decide whether he needs insulin.

[10/23, 9:15 PM] pajr member: Retinal screening done?

[10/23, 9:16 PM] PaJR PHR Moderator: Well if you look at all the evidence till now there's not much that says that one can achieve any benefits with better control once microvasculopathy has set in

[10/23, 9:16 PM] pajr member: Perhaps the same line of thought was applied earlier and a C peptide was never done? And he ended up with neuropathy?

It's never too late if you ask me.

[10/23, 9:17 PM] PaJR PHR Moderator: @⁨~Dr.N V⁩ please get his fundoscopy tomorrow and share the fundus images here.

Ask them to use the indirect Ophthal lens fitted into their mobile phone

[10/23, 9:17 PM] pajr member:  Chat with Meta AI on WhatsApp: https://wa.me/13135550002?s=5

[10/23, 9:17 PM] PPM 2: That evidence is overwhelmingly in Type 1 Diabetes. And we still are unsure of what type of diabetes this is.

[10/23, 9:18 PM] PaJR PHR Moderator: I don't think there is much evidence to suggest strict control helps to even prevent neuropathy. DCCT was a disaster for hypoglycemia and UKPDS was a damp squib

[10/23, 9:18 PM] pajr member: Okay sir

[10/23, 9:18 PM] +pajr member Can also do with checking for microalbuminuria? Is he losing protein?

[10/23, 9:19 PM] PaJR PHR Moderator: Please share that overwhelming evidence in a PICO format

[10/23, 9:19 PM] pajr member: You said it with DCCT.

But should we pause for a bit and actually make a diagnosis first and then pivot our literature search on that diagnosis?

[10/23, 9:20 PM] PaJR PHR Moderator: @⁨PPM4 what's the urine cue suggesting?

Just like the other 40M long distance diabetic patient in the same ward is collecting his 24 hour protein and creatinine from 8:00 tomorrow please start collecting this patient's as well

[10/23, 9:21 PM] PaJR PHR Moderator: As said earlier, how would it change the management?

[10/23, 9:21 PM] pajrmember: I will be looking forward to some of these. Interested in FCPD as a possibility. IgG4 is notorious in East India, as you will perfectly recall.

[10/23, 9:23 PM] pajr_member: Insulin and a completely different diet pattern?

If type 1, then he can pretty much enjoy what he wants and titrate insulin doses accordingly.

If type 2, then the natural history is vastly different and needs stricter diet control?

[10/23, 9:30 PM] PaJR PHR Moderator: Insulin we shall find out once we see the secretagogue challenge outcomes

Diabetic diet for every human diabetic on this planet as well as every normal human on this planet is simply a normal diet of 50% fruits, vegetables and 50% whole grains and legumes.

[10/23, 9:31 PM] +pajr_member: Too idealistic with the second statement and bereft of patient affordability and choices?

[10/23, 9:32 PM] PaJR PHR Moderator: Well ideals drive our ability to achieve them!😅

[10/23, 9:33 PM]  pajr _member: The very bedrock of PaJR is precision and individual centric. Let's see what he enjoys and dislikes!

[10/23, 9:37 PM] PaJR PHR Moderator: The biggest challenge here is to be able to hear the patient's voice here

The other group of the 40M diabetic it's still more assertive

[10/23, 9:38 PM] pajr doc:  Cue shows nil - albumin, and glucosuria (+2 glucose)

[10/23, 9:39 PM] pajr member: Thanks doc. Probably will still need quantified albumin levels in urine. I remember we have urine microalbuminuria at Kamineni

[10/23, 9:40 PM] pajr _member: Can we add Dr x here?

[10/23, 9:41 PM] PaJR PHR Moderator: Sure but I'm not sure if he would really find any of our interaction useful

[10/23, 9:41 PM] pajr_member: I will never say no to a curious learner. He will. I'm sure.

[10/23, 9:42 PM] PaJR PHR Moderator: Can add him to the collective group and let him decide where he wants to join among the 1000 PaJRs

[10/23, 9:42 PM] paJr_doc: Yes sir, will get it done.

[10/23, 9:42 PM] pajr_member: Thank you everyone. Such a joy learning and working remotely :)

[10/23, 9:42 PM] PaJR PHR Moderator: 👆@⁨pajr_member start both their 24 hour collection from 8:00 sharp tomorrow

[10/23, 9:43 PM] pajr_member: It's an incredible privilege. Though I don't contribute much. Thank you so much really :)

[10/23, 9:43 PM] pajr_member: To also be sure that the first urine in the morning is discarded as it counts towards the previous day

[10/23, 9:45 PM] pajr_doc: Okay sir

[10/23, 9:45 PM] +PAJR_doc Yes sir

[10/23, 10:52 PM] PA:  Sugar test 10:51 clock - 362

[10/24, 8:28 AM] +91 73862 32097: *23/10*

8am - 117 mg/dl

10am - 210 mg/dl

1pm - 406 mg/dl

4pm - 505 mg/dl

8pm - 406 mg/dl

10pm - 342 mg/dl

*24/10*

2am - 200 mg/dl

7am - 264 mg/dl

[10/24, 2:44 PM] PaJR PHR Moderator: Urine for 24 hour protein and creatinine collection started from 8:00 AM?

[10/24, 2:47 PM] PaJR PHR Moderator: @⁨Meta AI⁩ in a 24 hour urine collection for albumin estimation, what would be regarded as microalbuminuria and what would be regarded as macroalbuminuria?

[10/24, 2:47 PM] Meta AI: In a 24-hour urine collection for albumin estimation, the results are classified into three categories based on the amount of albumin present:

*Normoalbuminuria*: Less than 30 mg/24 hours (normal)

*Microalbuminuria*: 30-300 mg/24 hours (moderate increase, indicative of early kidney damage or diabetic nephropathy)

*Macroalbuminuria*: More than 300 mg/24 hours (severe increase, indicative of advanced kidney damage or nephrotic syndrome)

These thresholds help clinicians diagnose and monitor kidney-related issues, particularly in patients with diabetes or hypertension.

[10/24, 3:47 PM] pajr member: Opthal opinion: no fundal changes.

[10/24, 4:07 PM] pajr member: Yes sir

[10/24, 4:42 PM] pajr member: Then it is quite unlikely that the neuropathy is secondary to diabetes here.

Often, the neuropathy starts with small fiber and then goes to large fiber. How is it like in this gentleman?

[10/24, 9:05 PM] pajr member: Any update on CNS findings?

[10/24, 9:25 PM] PaJR PHR Moderator: @⁨~pajr doc can you share the CNS findings of this patient?

[10/24, 9:29 PM] +pajremember: Sorry sir, today's my duty day. Couldn't get time to do detailed examination. I'll definitely do it as soon as I possibly can sirs.

Sorry about the delay

[10/24, 9:58 PM] pajr member: Yes sir... In casualty right now. Will update.

[10/24, 11:42 PM] pajr member: Abnormal findings:

1. Dorsum of left foot fine touch absent. 

2. Dorsum of left foot 2 point discrimination after more than 5cm distance. 

3. B/l palmar interossei power reduced on paper test. (3/5? Pulled by minimal force) 

4. Tandem walking: unable to maintain balance.

[10/25, 12:00 AM] pajr member: I must congratulate you guys for giving so much of your valuable time and effort to see this patient - something practically impossible here in UK. Thoroughly appreciate it.

[10/25, 12:03 AM] member: Just a few points I'd like to highlight - Romberg's is a sign of sensory ataxia and not cerebellar ataxia; From his clinical images - it appears he has muscle wasting and perhaps his muscle bulk is symmetrically reduced and may not be normal. For Autonomic Nervous system - Postural hypotension is a much later manifestation of ANS involvement - the earliest sign in men is erectile dysfunction and loss of early morning penile tumescence and subtle bowel and bladder disturbances - and perhaps examination of the anal sphincter reflex (the internal anal sphincter and not the external anal sphincter) could have helped. I understand this can happen but in so much precise and thorough examination - examination of tone was missed!

[10/25, 12:04 AM] pajr member:  The left lower limb neurological lesion is likely a CPN impingement ? However quite a few findings are bilaterally symmetrical and with intact reflexes and assuming normal tone, favour a myopathy

[10/25, 12:06 AM] pajr member: Tone is normal sir. I mentioned under motor system examination.

[10/25, 12:07 AM] pajr member: Oh yes I see that now! Apologies! so this would then be a myopathy ?

[10/25, 12:09 AM] pajr member : And why was ankle struck off ? Did you notice any subtle foot drop ? Was he able to weight bear on toes ?

[10/25, 12:09 AM] pajr member Yes sir bulk I did not exactly know what to judge as normal. I failed to mention that patient has noticed reduced bulk of both upper and lower limbs as compared to before(nothing specific mentioned..vaguely said as compared to 2 yrs before)

[10/25, 12:10 AM] +pajr member: As mentioned previously - he does appear to have features of cachexia

[10/25, 12:10 AM] pajr member: No foot drop, wrist drop or trophic ulcers.

[10/25, 12:10 AM] +pajr member:  What is your neurological diagnosis ? Anatomical, pathological and etiological

[10/25, 12:13 AM] pajr member:  The abnormal findings do not seem to be due to any cns lesions. I think peripheral neuropathy(more sensory symptoms than motor) or myopathy 

I attribute unable to maintain balance in tandem walking also to defecits in sensation.. As no other cerebellar signs are positive

[10/25, 12:15 AM] pajr member: If there are no signs of a lower motor neuron involvement - such as loss of reflexes, hypotonia etc. why do you think this is a peripheral motor neuropathy at all ?

[10/25, 12:19 AM] pajr member: Okay. I would say peripheral sensory neuropathy then. Wasn't sure whether to attribute inability to maintain balance to purely sensory neuropathy and that palmar interossei weakness to myopathy Or motor neuropathy also to some extent sir..

[10/25, 12:23 AM] pajr member :  You see 2 point discrimination is a higher cortical function as the sensation is decoded at the post-central gyrus ? And there are no other objective findings of a peripheral sensory neuropathy of large fiber - such as loss of vibration, loss of joint position and movement etc. or small fiber - loss of pain and temperature and trophic changes? How would you interpret this?

[10/25, 12:25 AM] +pajr member: Worth reading this wonderful paper here - https://www.emjreviews.com/wp-content/uploads/2020/03/Diabetic-Amyotrophy.pdf

[10/25, 12:44 AM] pahr member: The patient does complain of pain but it's not severe.. He had mentioned that he gets pain in b/l lower limbs, back, hip occasionally.. Not all at once..neither localized to one side.. Definitely Could be due to muscle weakness

Muscle bulk is definitely reduced. 

I now feel like the patient better fits into diabetic amyotrophy than peripheral neuropathy.. But there's still that absence of fine touch on dorsum of left foot.

[10/25, 12:48 AM] pajr member :  Alright. Very coherently presented. 👍🏼

In that case, would our next question be what are the predictors of diabetic amyotrophy and why did this man get it and not others?

[10/25, 12:49 AM] pajr member:  So this also brings the question of myositis vs myopathy?

[10/25, 12:49 AM] pajr member: Sir 2 point discrimination also requires his crude touch to be intact.. Which it was.. And fine touch wasn't which is carried by both small and large fibres... Possibly that's why its altered.. Maybe there is involvement of both small and large fibres..

[10/25, 12:50 AM] +pajr member: I think the entity of crude touch has been discarded if I recall correctly. May check.

However the more objective vibration and joint position and movement are intact?

[10/25, 12:51 AM]pajr member: 2 point in its very definition is fine touch isn't it?

[10/25, 12:51 AM] pajr member: Sure sir I'll recheck. 

Vibration and joint position is intact

[10/25, 12:52 AM] pajr member: This probably makes us home in on a myo-pathology? Myositis vs Myopathy is the next question?

[10/25, 12:52 AM] pajr member: Yes sir sorry. So then I feel it's because of the diminished fine touch itself.

[10/25, 12:53 AM] pajr member: Wait, let's go back, he was able to sense it >5 cm apart wasn't he?

[10/25, 12:56 AM] pajr member: He did. But i want to repeat it in the morning. It's possible that maybe I applied more pressure on accident and it was no longer purely fine touch

[10/25, 1:21 AM] pajr member: Hmmm great point. Fine touch is so reliant on technique whereas Vibration and joint position are much more objective

[10/25, 7:56 AM] pajr member:  Today sugar test - 230

[10/25, 8:55 AM] +pajr_member: *24/10*

10am - 283 mg/dl - T. Glimiperide 3mg + Metformin 500mg

1pm - 199 mg/dl - Metformin 500mg

4pm - 124 mg/dl 

8pm - 143 mg/dl - T. Glimiperide 3mg + metformin 500mg

*25/10*

2am - 170 mg/dl

7am - 230 mg/dl - Glimiperide 3mg + Metformin 500mg

[10/25, 9:58 AM] PaJR PHR Moderator: @⁨pajr_trainee can you insert all his blood sugar values to chatGPT and ask it to provide you a line graph with the timeline in x axis and sugar values in y axis? Added @⁨~pajrmember to help you with it. Check out her graphs in her portfolio

[10/25, 9:59 AM] PaJR PHR Moderator: Kudos to @⁨~pajrmember @⁨pajr member⁩ for this amazing illustration of a real patient centred CBME! 👏👏

[10/25, 10:21 AM] pajr member: Where to check

[10/25, 10:25 AM] PaJR PHR Moderator: Scroll up and gather all the blood sugar values of the patient shared here in the timeline and then copy paste them in a manner to prompt chatGPT to generate a graphical timeline as illustrated here 👇

https://userdrivenhealthcare.blogspot.com/2024/10/tutorial-for-our-case-reporter-patient.html?m=1

[10/25, 10:41 AM] pajr member: Rechecked sir. 

So fine touch I tested with cotton. While 2 point discrimination was tested with a caliper. The fine touch was absent. The finding remains the same that 2 point discrimination is sensed at >5cm. I'm guessing it's 2 points of pressure rather than fine touch..and the pressure sensation is intact.

[10/25, 10:46 AM] pajr trainee : Okay ..from which day the line graph should be made...??

[10/25, 10:49 AM] PaJR PHR Moderator: We would also need to redo the joint position test because I find most people veer off much more than 15 degree here. Please send him down to OPD ASAP

[10/25, 10:49 AM] PaJR PHR Moderator: From the day of admission here since his blood sugar values started getting recorded here

[10/25, 10:51 AM]pajr trainee:  Okay

[10/25, 11:01 AM] pajr trainee: I've tried it for the first time and Chat gpt shows this ... Seems like needs to verify by the professionals

[10/25, 12:26 PM] +pajr member: Correction after examination in opd:

 1.Dorsum of left foot fine touch impaired not absent. 

2. Joint position sense in left foot also impaired. 

3. Areflexia.?

PA: 

[10/25, 1:40 PM] pajr_doc:  That's a lot of rice😅

[10/26, 9:49 AM] PaJR PHR Moderator: Shudhu ekbar khawar por

[10/25, 2:49 PM] PaJR PHR Moderator: Areflexia yes

Overall classic polyneuropathy

What about his motor power?

[10/25, 2:54 PM] PaJR PHR Moderator: The points could have been joined this way I guess? Wonder what ChatGPT will do if given the prompt again

[10/25, 4:46 PM] member: Precision 👍🏼

[10/25, 4:47 PM] member: Oh boy! Areflexia where?

[10/25, 4:48 PM] PaJR PHR Moderator: @⁨~pajr_member lower limbs were absent. Upper limbs too?

[10/25, 4:49 PM] member:  Makes me wonder CIDP as a possibility

[10/25, 4:51 PM] member: Absent sir.

[10/25, 6:01 PM] member: What's your unifying diagnosis?

[10/25, 7:36 PMmember: Back to Peripheral neuropathy (areflexia, impaired joint position sense and sense of fine touch) with..Possibly myopathy..due to the other complaints of weakness and pain which is gradual, progressive according to the patient. CIDP..I'm not sure how to rule out any autoimmune pathology purely on clinical examination... We did not run any more labs on the patient.

[10/25, 7:53 PM] PaJR PHR Moderator: CIDP as many other autoimmune etiologies, is generally a diagnosis of exclusion

[10/25, 7:54 PM] pajr member: Agreed. If this involves the upper limbs too (with areflexia and muscle wasting) clearly this chronic and unrelated to diabetes.

NCS may help. Just by clinical judgment though this seems like CIDP

[10/25, 8:32 PM]pa: স্যার এই মেডিসিন গুলো কত দিনের জন্য দিয়েছেন

[10/25, 8:43 PM] PaJR PHR Moderator: Oshudh sob somoi ek pata (10 ta kore) kinben ebong shei packet er chobi ta dekhle confirm kora jabe oshudh guno shothik khacchen kina.

Baki ekhane joto din joga jog rakhben toto din roj jante parben koto din khete habe

[10/25, 10:12 PM] PaJR PHR Moderator: Glimiperide ta deene kota khacchen?

[10/25, 10:15 PM] PA: দিনে দুটা করে খাচ্ছি

[10/25, 10:20 PM] PaJR PHR Moderator: Sokale ekta raate ekta?

[10/25, 10:21 PM] PaJR PHR Moderator: Unar aajke Khali peter ebong protyek ta khawar du ghonta baade blood sugar koto chilo. Time somet share korun

[10/25, 10:56 PM] PA:  স্যার এই মেডিসিন দিনে কত বার খাবার আগে না পারে

[10/26, 9:49 AM] PaJR PHR Moderator: Shudhu ekbar khawar por

[10/29, 10:53 PM] PA: স্যার বাবার তো পুরো শরীল ব্যথা করতেছে

[10/30, 7:46 AM] PA: পুরো শরীল ব্যাথা আর জ্বর এসেছে কাল থেকে

[10/30, 10:15 AM] PaJR PHR Moderator: Proti char char ghontai temperature ta ekhane janaben ebong proti 6 ghontai ekta kore paracetamol 500 mg dine char bar khete paren

[10/30, 10:19 AM] PaJR PHR Moderator: Are baki oshudh guno?

Tablet glimiperide 2mg khacchilen je dine dubar kore?

Unar blood sugar aekhon dine char bar share korben:

Fasting

Breakfast ebong glimiperide er 2 ghonta bade (glimiperide ta khawar aage khawar kotha are metformin ta khawar por)

Lunch ebong metformin er du ghonta bade 

Dinner ebong du ghonta bade 

 

 

Hyponatremia ProJR

Medicine department project on resolving diagnostic and therapeutic uncertainty in patients with hyponatremia

Project OUTCOMES from 2018-2021 documented by Dr Manasa, MD medicine Resident from 2018

For more Medicine department projects please click here:

https://medicinedepartment.blogspot.com/2021/02/medicine-department-projects.html?m=0

_DISTRIBUTION OF HYPONATREMIA CASES IN DIFFERENT AGE GROUPS

Age group (in years)	No. of cases (n=60)	Percentage
13 -39	4	7
40 – 59	28	46
60 -79	24	40
80 – 99	4	7
Total	60	100

DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEL

Serum Sodium (in meq/l)	No. of cases n=60	Percentage
100 – 109	2	3
110 – 119	19	32
120  - 129	39	65
TOTAL	60	100

FIGURE 9 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEL

FIGURE 10 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON SERUM SODIUM LEVEL

Out of the 60 hyponatremia patients studied, only 2 patients have severe

Hyponatremia, majority of patients have mild asymptomatic hyponatremia.

Most of the cases of mild hyponatremia are secondary to chronic kidney 

Disease.

TABLE 4 – ETIOLOGY OF HYPONATREMIA

ETIOLOGY  OF HYPONATREMIA	NO.OF CASES (n=60)	percentage
Vomitings + loose stools	4	6
Dehydration secondary to vomitings	7	12
Diarrhoea	1	2
Chronic liver disease	1	2
Cerebral salt wasting syndrome	4	6
Chronic kidney disease	13	22
Hyperglycemia	2	3
Dehydration	3	5
Dialated cardiomyopathy	2	3
Diuretics	6	10
Post TURP hyponatremia	1	2
SIADH	9	15
Anti psychotic drugs	1	2
Mixed causes	6	10
TOTAL	60	100

FIGURE 11 – ETIOLOGY OF HYPONATREMIA

TABLE 5 – MIXED CAUSES OF HYPONATREMIA

Mixed causes of hyponatremia	No.of cases
CCF + CLD + CKD	1
Hypothyroidism +thiazides	2
Hypothyroidism + vomitings	1
Vomitings+ thiazides+ hypothyroidism	1
CKD + thiazides	1
Total	6

FIGURE 12 – FREQUENCY DISTRIBUTION OF MIXED CAUSES OF HYPONATREMIA

Most common cause of hyponatremia in present study is 

Hypervolumic hyponatremia secondary to chronic kidney 

Disease. Second most common cause being SIADH followed by 

Hypovolemia which is secondary to vomitings, loose stools and 

Dehydration. 

Hypothyroidism alone rarely causes hyponatremia. Hypothyroidism

Need to be severe (myxedema coma) to cause hyponatremia.

 Most of the mixed Causes of hyponatremia are associated 

with hypothyroidism. In most of the mixed causes of hyponatremia 

which one actually lead to hyponatremia remains Unclear.

TABLE 6 – PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA

Primary diseases associated with hyponatremia	No. of cases	Percentage (%)
1. Acute gastroenteritis	5	8
2.Chronic kidney disease	9	15
3. Cerebro vascular accident	4	7
4. surgical causes of vomitings	4	12
5.food poisoning	4	12
5. Hypertention on thiazide diuretics	6	10
6. Pulmonary tuberculosis	3	5
7. Meningitis	4	7
8. Uncontrolled diabetes	2	3
9. AKI with hyponatremia	2	3
10. Heart failure	3	5
11. CCF + CKD + CLD	1	2
12. Hypothyroidism	2	3
13. Miscellaneous	11	18s
14. TOTAL	60	100

FIGURE 13 – PERCENTAGE DISTRIBUTION OF PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA

Primary cause of hyponatremia in most of the cases chronic kidney 

Disease followed by SIADH. Dehydration Secondary to vomitings, loose 

stools and sepsis also contributed to large number of hyponatremia 

cases. Surgical causes like Renal colic, appendicitis, intestinal  

obstruction and pyloric stenosis are the causes of vomiting which lead to 

hyponatremia in the study group

TABLE 7 – MISCELLANEOUS PRIMARY DISEASES ASSOCIATED WITH HYPONATREMIA

Primary diseases associated with hyponatremia	No. of cases ( n = 12 )
1. Septic arthritis with dehydration	1
2. Dengue shock syndrome	1
3. Acute subarchnoid hemorrage	1
4. Encephalitis	1
5. Necrotising fasciitis with pyogenic brain abscess	1
6. CLD with hepatorenal syndrome	1
7. Schzophrenia	1
8. SIADH secondary to antidepressants	1
9. Post TURP hyponatremia	1
11. CVA with hypertention and hypothyroidism	1
12. CVA causing SIADH	1
TOTAL	12

TABLE 8 – DISTRIBUTION OF CASES BASED ON TONICITY OF    HYPONATREMIA

Most of the cases of hyponatremia are hypotonic which includes 

Hypovolemic, euvolemic and hypervolemic causes of hyponatremia. 

Isotonic hyponatremia is considered as pseudohyponatremia. Hypertonic 

Causes of hyponatremia are secondary to hyperglycemia.

FIGURE 14 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON TONICITY

FIGURE 15 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON TONICITY

TABLE 9 – DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS

Volume Status	No. Of  Cases( n=60)	percentage
Hypervolemic	22	37
Euvolemic	9	15
Hypovolemic	26	43
Hypertonic Hyponatremia	3	5
TOTAL	60	100

FIGURE 16– PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS

FIGURE 17 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON VOLUME STATUS

Hypovolumic and hypervolumic hyponatremia cases are much higher 

Compared to euvolemic cases

TABLE 10– DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY

Chronicity of hyponatremia	No. of cases n=60	percentage
Acute Hyponatremia	20	33
Chronic Hyponatremia	40	67
TOTAL	60	100

FIGURE 18 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY

FIGURE 19 – FREQUENCY DISTRIBUTION OF HYPONATREMIA CASES BASED ON CHRONICITY

Out of the 60 hyponatremia patients studied, 40 are chronic hyponatremia 

Patients and 20 are acute hyponatremia cases.

TABLE 11 – TREATMENT OF HYPONATREMIA

TREATMENT  GIVEN	NO.OF CASES(n=60)	percentage
0.9% NaCl	8	13
0.9% NaCl  and 3% NaCl	11	18
Fluid restriction + diuretics	11	18
Fluid restriction  + Tolvaptan	5	8
Fluid restriction +  increase dialysis ultrafiltrate	6	10
I.V  insulin	2	3
Stop thiazides	11	18
3% NaCl + T.Tolvaptan + fluid restriction	3	6
T.THYROXINE + i.v fluids/diuretics	3	6
TOTAL	60	100

FIGURE 20 – TREATMENT OF HYPONATREMIA

Fluids like 0.9% NaCl were given to patients with hypovolumic 

Hyponatremia who have signs of dehydration. 3% NaCl was given to 

Patients with severe  hypovolemic hyponatremia who have neurological 

Symptoms. Diuretics were given to patients with hypervolumic 

Hyponatremia. Fluid restriction and vaptans were used in SIADH.

Insulin and thyroxine supplementation were used in hyperglycaemia and

Hypothyroidism respectively

TABLE 12 – DISTRIBUTION OF HYPONATREMIA CASES BASED ON OUTCOME

Outcome	No. of cases n=60	Percentage
Symptomatically better	36	60
Same status	8	13
Asymptomatic	15	25
Died	1	2
TOTAL	60	100

FIGURE 21 – PERCENTAGE DISTRIBUTION OF HYPONATREMIA CASES BASED ON OUTCOME

DISCUSSION

The present study included patients with serum sodium less than 

130meq/l. there were 42 males and 18 females with ratio of 2.3 : 1 .

In general, more number of males were admitted in KIMS, Narketpally 

When compared to females . so no conclusion was made on this 

Difference in incidence.

In present study, hyponatremia was seen more commomly in patients

 above 45 years of age than in younger patients. youngest patient with 

hyponatremia in our study is of 25 years age. Eldest patient is of 87 years 

age. Incidence of hyponatremia is higher in elderly patients similar 

trend was also observed by Hochman (9) and Vurgese (10) in their study

The hydration status in the present study was noted based on clinical 

Examination like capillary refilling time, jugular venous pulse, blood 

Pressure, pressure or absence of pedal edema and IVC (inferior vena 

Cava diameter) .Hydration status was divided into euvolumic, 

Hypovolemic and hypervolemic states. In the present study 26 patients 

Were hypovolemic, 22 patients were hypervolemic and 9 patients were

Euvolumic representing 43%, 37% and 15% respectively.

TABLE : 13

Hyponatremia	Hochman( %)	Anderson (%)	Present study(%)
Euvolumia	50	34	15
Hypovolumia	30.5	35	43
Hypervolumia	19.5	31	37

In the present study hypervolumic cases are more compared to Hochman 

Study. Most of them are secondary to chronic kidney disease as in our 

Hospital locality (Nalgonda district) renal failure is commonly which was 

Thought to be due to fluorosis. Hypovolemia cases slightly higher than 

Both the studies. Most of the hypovolemic cases are due to vomitings, 

Loose stools and dehydration. Study also includes surgical causes of 

Vomiting which leads to hyponatremia.

Euvolumic cases are less compared to Hochman and Anderson studies

In the present study may due to underdiagnosis of adrenal insufficiency 

In our hospital setting and also relatively more cases of ESRD (end stage

Renal disease) which contribute to hypervolumic hyponatremia. 

The mean age was 58.4 years. The commonest age group affected was

40 to 79 years. The commonest cause of hyponatremia was chronic 

Kidney disease and vomitings,loose stools and dehydration. Next 

Common cause was SIADH which was secondary to pneumonia,

Pulmonary tuberculosis and sub arachnoid hemorrhage.

In study done by vurgese, the incidence of hyponatremia was 3.6%

With the defnation of hyponatremia as serum sodium levels less than

Or equal to 130meq/l. the study population consisted of 66 patients with

56% 

males and 44 % females. The mean age was 57.07 years. The 

Commonest age group affected was 45 to 64 years (72.8 %) and the least

Affected group was 12 to 25 years.

TABLE 14 

	Vurgese	Present study
Study population
Male	56%	70 %
Female	44%	30 %
Mean age	57.95 years	58.4 years
>45 years with hyponatremia	72.8 %	83 %
Common causes	SIADH	Chronic kidney disease
Other causes	Renal failure CCF	SIADH

Hyponatremia cases in the present study were also distributed based on 

serum sodium level. Most of the cases of hyponatremia are with the 

serum sodium level between the range of 120 to 129 meq/l (39 patients 

out 60). most of the cases with mild hyponatremia are hypervolemic 

secndary to chronic kidney disease

In tpresent study, In patients with euvolumic hyponatremia, 9 patients 

satisfied the criteria to diagnose SIADH. They had low serum osmolality, 

high urine osmolality and high urine sodium. However, in brain injury

cases like cerebral sinus venous thrombosis (CSVT) if patient presents 

with hyponatremia probable diagnosis of hyponatremia can be kept as 

SIADH or cerebral salt wasting syndrome. Clear cut differentiation

Between SIADH and cerebral salt wasting syndrome will be very difficult 

In the first 24 hours as important differentiating feature between SIADH 

And cerebral salt wasting syndrome is urine output.

Hypovolemic cases of hyponatremia are secondary to acute 

Gastroenteritis mostly due to Ecoli, salmonella and staph aureus.

Surgical causes of vomiting like intestional obstruction, pyloric stenosis,

Appendicitis and renal colic also contributed to hypovolemic causes of 

Hyponatremia. Thiazide diuretics usuage in patients with hypertention 

And chronic renal disease also contributed to hypovolemic 

hyponatremia.

Hyponatremia secondary to anti psychotic drugs presented with 

increased thirst, patient drank 6 to 7 litres of water for 2 days and 

passed only 1 to 2 litres of urine each day for 2 days.

Thyroid function tests and adrenal function

Thyroid function tests and random serum cortisol test was done in all

this patients. There are 2 cases of hypothyroidism, in both the patients

 cause of hypothyroidism is mixed. In one patient cause of hyponatremia 

 is both hypothyroidism and thiazide diuretics volume status in this

patient is hypovolemic. In another case cause of cause of hyponatremia 

is both hypothyroidism and vomitings secondary to acute illness like 

dengue. 

Patients with hypovolemic hyponatremia are 26 patients (43 %) among 

60 Patients of hyponatremia. Cause of hypovolemic hyponatremia is 

Mostly dehydration. Other cause of hypovolemic hyponatremia is 

Cerebral salt wasting syndrome. In present study there are 4 cases of

Hypovolemic hyponatremia are cerebral salt wasting syndrome.

Majority of cases in  present study are of hypervolumic hyponatremia

Chronic kidney disease is the major cause of hypervolumic 

Hyponatremia. Other causes are dilated cardiomyopathy, chronic liver 

Disease and mixed causes like CCF + CLD +CKD. Patients with mild 

hyponatremia are almost always asymptomatic. Severe hyponatremia is 

usually associated with central nervous system symptoms and can be 

life-threatening. Diagnostic evaluation of patients with hyponatremia is

 directed toward identifying the extracellular fluid volume status, the 

neurological symptoms and signs, the severity and duration of 

hyponatremia, the rate at which hyponatremia developed. The first step

 to determine the probable cause of hyponatremia is the differentiation of 

the hypervasopressinemic and non-hypervasopressinemic 

hyponatremias with measurement of plasma osmolality, glucose, lipids 

and proteins. For further differential diagnosis of hyponatremia, the

 determination of urine osmolality, the clinical assessment of 

extracellular fluid volume status and the measurement of urine sodium 

concentration provide important information. The most important

 representative of euvolemic hyponatremias is SIADH. The diagnosis of 

SIADH is based on the exclusion of other hyponatremic conditions; low 

plasma osmolality (<275 mosmol/kg) and inappropriate urine 

concentration (urine osmolality >100 mosmol/kg) are of pathognomic 

value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates 

emergency care with rapid restoration of normal osmotic milieu

 (1 mmol/l/hr increase rate of serum sodium). Patients with chronic 

symptomatic hyponatremia have a high risk of osmotic demyelination 

syndrome in brain if rapid correction of the plasma sodium occurs 

(maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or

 less). The conventional treatments for chronic asymptomatic 

hyponatremia (except hypovolemic patients) include water restriction 

and/or the use of demeclocycline or lithium or furosemide and salt 

supplementation. Vasopressin receptor antagonists have opened a new

 forthcoming therapeutic era. V2 receptor antagonists, such as 

lixivaptan, tolvaptan, satavaptan and the V2+V1A receptor antagonist 

conivaptan promote the electrolyte-sparing excretion of free water and 

lead to increased serum sodium

TREATMENT AND MONITORING

Monitoring of sodium was done on a 6 hourly to12 hourly basis in most 

Of the patients with symptomatic and severe hyponatremia. 

Fluid correction depended on the type, cause and presence of 

symptoms.

The mean rate of correction was adequate and comparable with most of 

The international studies. Normal saline alone, 3% saline, fluid 

restriction, + duration, dialysis, steroids alone and in combination were 

used to treat symptomatic and severe hyponatremia.

 Excessive antidiuretic hormone and continued fluid intake are the 

pathogenetic causes of these hyponatremias. Whereas hypovolemic 

hyponatremia is best corrected by isotonic saline, conventional 

proposals for euvolemic and hypervolemic hyponatremia consist of the 

following: fluid restriction, lithium carbonate, demeclocycline, urea and 

loop diuretic. None of these nonspecific treatments is entirely 

satisfactory. Recently a new class of pharmacological agents -orally 

available vasopressin antagonists, collectively called vaptans- have 

been described. A number of clinical trials using vaptans have been 

performed already. They showed vaptans to be effective, specific and 

safe in the treatment of euvolemic and hypervolemic hyponatremia.  

vaptans generally had favorable effects on fluid balance

 also. To date two vaptans, ie, conivaptan and tolvaptan, have been 

marketed in the United States for the treatment of euvolemic and 

hypervolemic hyponatremia, whereas tolvaptan has been marketed in 

Europe with the limitation of euvolemic hyponatremia. Although these 

drugs have a good safety profile, caution should be used, and treatment 

should be initiated in a hospital setting in order to closely monitor

 patients and avoid overly rapid correction or overcorrection. Vaptans 

can be considered a new effective tool for the treatment of euvolemic 

and hypervolemic hyponatremia. Nevertheless, more comparative 

research of vaptans vs other therapies on clinical grounds is needed to 

more accurately assess the value of these drugs in the treatment of 

hyponatremia. Acute hyponatremia causes serious brain swelling that 

can lead to permanent disability or death. A 4-6 mEq/l increase in serum

 sodium is sufficient to reverse impending herniation. Brain swelling is 

minimal in chronic hyponatremia, and to avoid osmotic demyelination,

 correction should not exceed 8 mEq/l/day. In high-risk patients, 

correction should not exceed 4-6 mEq/l/day. Inadvertent overcorrection

 of hyponatremia is common and preventable by controlling unwanted 

urinary water losses with desmopressin. Even mild chronic 

hyponatremia is associated with increased mortality, attention deficit, 

gait instability, osteoporosis, and fractures, but it is not known if the 

correction of mild hyponatremia improves outcomes.

 Controlled trials are needed to identify affordable treatments for 

hyponatremia that reduce the need for hospitalization, decrease hospital

 length of stay, and decrease morbidity. Such trials could also help

 answer the question of whether hyponatremia causes excess mortality

 or whether it is simply a marker for severe, lethal, underlying disease

CONCLUSIONS

1. Asymptomatic hyponatremia is more common than symptomatic 

         Hyponatremia

2. Renal failure,dehydration and SIADH formed the largest subgroup in the study

3. Drugs, especially thiazide diuretics are common cause of 

Hyponatremia

4. Incidence of hyponatremia is higher in patients aged above 

45years 

5. Symptoms of hyponatremia increased with severity of 

Hyponatremia

6. Neurological symptoms like headache, seizures and altered 

Sensorium are commonly seen in severe hyponatremia patients

7. To distinguish between SIADH and cerebral salt wasting syndrome

In patients of hyponatremia with head injury is difficult  

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43.    PROFORMA

44. S.no                   sex Ipno.                 DOA

    Age                                                                    DOD

    Weight

    Primary diagnosis

    H/o present illness

SNO.	SYMPTOMS	STETUS		DURATION
1	Nausea	Y	N
2	Vomiting	Y	N
3	Headache	Y	N
4	Altered mineral status	Y	N
5	Hiccups	Y	N
6	Seizures	Y	N
7	Others	y	N

If others please specify

Diet habits:

         Fluid intake

         Decreased intake

SNO.s	comorbid conditions	status		duration	specify
1	Diabetis mellitus	Y	N
2	Hypertension	Y	N
3	cardiovascular	Y	N
4	Renal problems	Y	N
5	Endocrine	Y	N
6	respiratory	Y	N
7	neurological
8	gastrointestinal
9	Others	y	N

CURRENT  MEDICATIONS

s.no	Drug name	duration	Dosage/day	Causes  hypontremia
1				Y	N
2				Y	N
3				Y	N
4				Y	N
5				Y	N
6				y	N

CLINICAL FINDINGS

Pulse rate

Blood pressure 

Volume status at the time of admission;  hypo/hyper/euvolumic   

Oedema      y/n

Dehydration                 y/n

Ascitis /paedal edema

Others

BIOCHEMICAL PARAMETERS(AT THE TIME OF ADMISSION)

Serum sodium level

Urine spot sodium

Serum osmolarity

Serum urea

Grbs

Random serum cortisol      done/not done

Tft:   done/not done

Tsh :   free t4 

TREATMENT GIVEN

Infusion plan

Diuretics       y/n

Fluid restriction       y/n

Specific  drugs if given

Other treatment

OUTCOME

Asymptomatic/symptomatically better/same status

Discharged/discharged at request/lama/reffered to higher centre

 hyponatremia cause:

  possible secondary cause

                             CONSENT FORM

Thesis title ; Etiology, management and outcome in patients with hyponatremia in ICU KIMS, Narketpally

I/We, relative of patient have read and understood the information provided in the “ patient information sheet “ and have been informed and explained the purpose and nature of the study in the language I understand.

Iam aware of the fact that I may not derive any benefit from the study and that I reserve the right to opt out of the study at any point of time

I willingly agree to participate in this study.

Patient’s sign / thumb impression                witness’s sign

Name;                                                          Name;

Date;                                                            Date;

Resident’s sign;

Resident’s name;

Date