If you have a patient with cerebral edema from acute hyponatremia you need to 3% Saline first and ask questions later.
3/ If patients have hyponatremia and have severe symptoms it is 150 ml of 3% then recheck the sodium and give another 150 ml of 3% (I'm using the European guidelines) eje.bioscientifica.com/view/journals/…
3b/ Be careful with vomiting there 👆🏻
This means if the hyponatremia is causing the vomiting, then you have severe symptoms and it is 3% time. But if the vomiting is causing the hyponatremia, that doesn't automatically indicate severe symptoms and you will need to dig deeper.
4/ The goal of acute mgmt is to raise the Na by 5 or stop the symptoms, which ever is quicker. If you have raised the Na by 5 and they are still seizing, then it is probably not the low Na causing the seizure and you need to 👀 deeper. Algorithm from eje.bioscientifica.com/view/journals/…
5/ But when @tonlajr asked about the approach to sodium he wanted to know abot dx, not acute mgmt so...onward to diagnosis!
6/ I am goin to be walking you through this algorithm:
Step one check the serum osmolarity (and get a repeat sodium, just to make sure it wasn't a lab error)
7/ Since we are looking at a low sodium we expect a low osmolarity (don't worry about the difference between osmolality and osmolarity, anyone who is a stickler about that is being a dick)
If we don't find a low osmolality something weird is going on:
7b/ Low sodium with a normal osmolarity: Lab error from too much protein (IVIG, multiple myeloma) or too much fat (High lipids or triglys) in the blood. This throws off some lab machines.
(Specifically but not point of care iStats or ABG laboratories)
7c/ Low sodium with a high osmolality: this is usually due to hyperglycemia (but can be seen with mannitol, glycine and other edge cases). The hyponatremia is real, but due to another osmotically active particle (glucose in most cases) the are no consequences to the hyponatremia
8/ So that leaves the true hyponatremia. Low sodium and low osmolarity. The branch point here is:
What is the urine osmolarity?
The urine osmolarity tells us if the kidney is causing the hyponatremia or just unable to correct the hyponatremia (despite the best intentions)
9/ The urine osmolarity is less than 100 (maybe up to 150 or 200 if the patient has CKD). This indicates a lack of ADH and a kidney that is doing its best to correct the hyponatremia. The problem is not the character of the urine but the amount. Right urine, not enough.
9b/ The differential for low sodium, low serum and urine osmolarity is short:
9c/ In low Na, low serum and urine osmolarity the urine is getting rid of excess water but the kidney cannot make enough urine because:
• Kidney failure (low GFR)
• T & T / Beer drinkers (lack of solute)
• Psychogen polydipsia (you are drinking faster than you are peeing)
10 Low sodium, low serum osm, high urine osm. This is ADH dependant hyponatremia. The kidney, stimulated by ADH, is causing the hyponatremia by generating free water. Making more urine here, just makes the Na fall further.
10b/ ADH can be 𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝗶𝗰 due to low volume or a perceived low volume state:
Low volume states: GI losses like diarrhea or vomiting; renal losses like diuretics
High volume/low perceived volume: heart failure, liver failure, nephrotic syndrome
Next session started by Rovin to talk about IGAN pathophysiology and the selection of therapeutics
4-hit model 1. formation of IGA galactose deficient 2. formation of autoantibodies against these IgA 3. Formation of circulating IgG-IgA1 immune complexes 4. Deposition of the immune complexes in the kidney
#RKDSummit
1st case
Hematuria on U/A
Gross hematuria after covid vaccine
10 RBC/HPF, no casts
Scar 0.9 mg/dl, 24-hr urine 750 mg of protein
#RKDSummit
A bit “Juicy”
Mesangial expansion (arrows, fig 1)
Mesangial hypercellularity (circle, fig 2)
Biopsy has no chronicity (fig 3)
Lights up with C3 and IgA (fig 4)
When we published our study <> of ODS and hyponatremia we were pummeled for including people at low risk of ODS because we included Na levels between 120 and 130. They said it is well known "that ODS is incredibly rare/non-existent at those levels." 1/4evidence.nejm.org/doi/10.1056/EV…
Of course one of the reasons it was thought to be incredibly rare was that no one looked for CPM in patients with Na from 120-130. We found a fair number (≤5 of 12). 2/4
Our findings are replicated in a study from Australia. The authors took a different approach to investigating ODS. Instead of starting w/ hyponatremia and working forward to ODS, they started with a dx of ODS and worked backwards
3/4ncbi.nlm.nih.gov/pubmed/35717664
Gadolinium in dialysis patients.
What's up with that?
#Tweetorial
1/11
Nephrogenic systemic fibrosis (NSF) is an iatrogenic disease that presents with hardening of the skin and other organs. It is often lethal. I treated 5 people with this condition (including one with AKI). Terrible.
2/11
The etiology of NSF was unknown and there were many theories. In 2006, Thomas Grobner published a small case series showing 5 patients developing NSF within weeks of receiving gadolinium contrast for MRI.
3/11pubmed.ncbi.nlm.nih.gov/16431890/
I just recently recommended the Renal Physiology book by Bruce Koeppen and Bruce Stanton. I thought it was a good medical student level text book: pbfluids.com/2023/08/ouwb-s…
But I came across this question in Chapter 8 Regulation of Acid Base. It is a straight forward question asking the learner to interpret simple acid-base cases.
But the question falls apart when you look at the answer...