Is it hard to convince docs to give IV saline?

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Would you mind explaining in a little bit more detail what you meant by "The important ones" ? What would distinguish these from other antibodies?
The important ones are the high affinity antibodies, generally IgG, that confer long term protection, being produced by long lived plasma cells and binding tightly to antigen. IgM and low affinity IgG appear earlier but tend not to be made long term so may serve largely a 'prototype' function that facilitates the development of high affinity IgG through somatic hypermutation and class switching. Useful IgG may well be produced within a week or so but the classic peak is at 20 days.
 

Hip

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IV infusions have a reputation for strong placebo effects. In trials of TNF inhibitors for rheumatoid arthritis I have been studying recently as part of my work as an expert witness I noted that about 20% of people given a placebo infusion they thought might be a TNF inhibitor achieved a clear benefit for one to two weeks. However, none showed benefit at a month. In the Norwegian rituximab study I think 15% of patients given placebo reported a response, even at 6 months.
Has there been any placebo-controlled trials to determine whether the benefits that these rheumatoid arthritis patients (and other patients) report after receiving IV infusions might actually be due to real physical effects, rather than the assumed placebo effect?

I am thinking of a trial setup where one group of patients gets a real IV infusion of saline, and the other group has a sham infusion (eg, saline drip needle inserted into their vein, but the drip is not turned on, so no actual saline flows into their bloodstream).

It seems that if IV infusions do have the reputation for an (assumed) strong placebo effect as you say, somebody ought to test whether it actually is placebo as assumed, or whether it might be a real effect. Especially because I would guess that many studies on infusion-administered drugs might use a pure saline infusion for the control group, so if saline IV had active effects, it would not make a good inert control substance.



Just another thought: could some sort of antibody and autoantibody protein denaturation occur as a result of IV saline infusion, rendering these autoantibodies non-functional, and thereby providing temporary relief from autoimmune symptoms for some days or weeks?

Perhaps an osmotic shock effect from the saline infusion? I read that IV saline is typically 0.9% sodium chloride, whereas the blood is 0.6% sodium chloride, so there is a difference in salt concentration, and perhaps there might be some osmotic effects that damage the autoantibodies, and thereby temporarily reduce autoimmune symptoms.


EDIT: there is an error: the blood is close to 0.9% sodium chloride, not 0.6% as I stated. I read somewhere it was 0.6%, but I think that is a mistake.
 
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Jesse2233

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I really think the benefits form saline have to do with blood volume being boosted. There's only so much the stomach can absorb orally, and with low ADH most of it gets dumped immediately to the bladder.

Futhermore in Dr Bell's work, he found that daily IV saline put some patients into remission and cured two teenage patients who he caught early. If memory serves, 75% of his patients saw a benefit from IV saline.
 
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I really think the benefits form saline have to do with blood volume being boosted. There's only so much the stomach can absorb orally, and with low ADH most of it gets dumped immediately to the bladder.

Futhermore in Dr Bell's work, he found that daily IV saline put some patients into remission and cured two teenage patients who he caught early. If memory serves, 75% of his patients saw a benefit from IV saline.
I think you are confusing the physiology here. Fluid taken orally certainly gets dumped in the bladder, but so does fluid taken IV and both have to go via the blood because the bladder only gets fluid from the kidneys and they only get fluid from the blood. So the situation is exactly the same. Moreover, people who drink several pints of beer in an hour (not unusual) will be absorbing fluid from the gut into the blood at least as fast as a 20 minute IV saline infusion.

This is the problem with all the theories Hip is trying to raise - they apply just as well to drinking a bowl of salty soup.

If this Dr Bell's treatment really made a big difference why did he not establish the optimal dose and publish proper trials? We are back to the PACE issue of unblinded studies with subjective outcomes.
 

Hip

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This is the problem with all the theories Hip is trying to raise - they apply just as well to drinking a bowl of salty soup.
I do appreciate what you are saying about oral consumption of salty water ending up in the bloodstream just as IV drip does. And I agree that this makes the benefits that patients report after IV saline seem like they could be the placebo effect.

At the same time, given the strong benefits reported by patients, it's perhaps worth entertaining a few theories about possible real physical effects that IV saline may have which may not arise from consumption of salty water.

I just found the following paper, which indicates that there are more complexities and biological effects occurring during saline infusions that one might first think:

The history of 0.9% saline (full paper here).

Here is an extract from that paper:
Rudolph Matas, regarded as the originator of modern fluid therapy, introduced the concept of "the continued intravenous drip", but also warned of the potential dangers of saline infusions. He referred to work by Roessle who showed organic changes in human heart muscle after saline infusions, by Hoeszli who noted degenerative changes in the heart and kidneys of guinea-pigs 6 - 7 h after massive saline infusions, and by Thiess who in 1910 pointed out "that a healthy man needs 17 gm of salt per day, but receives 27 gm when given 3 litres of 0.9 per cent salt solution ... part of the salt is eliminated by the kidneys, but some is retained in tissues, where it attracts liquids and causes oedema". Matas concluded for the above reasons that his preferred solution was 5% glucose rather than saline.

In 1936 Coller et al studied three groups of postoperative patients who received 5% dextrose in either a "solution of sodium chloride, in Ringer’s solution or in distilled water". Although they used a "physiologic solution of sodium chloride" containing 8.5 g NaCl/l, they again found fluid retention, when saline solutions were given intravenously to sick surgical patients, in contrast to 5% dextrose which was excreted more rapidly.

Fluid retention in postoperative patients, receiving crystalloid infusions, is exacerbated by their diminished ability to excrete an excess sodium and water load. This classical feature of the metabolic response to injury is unfortunately sometimes forgotten. That such fluid retention is not innocuous is shown by the work of several authors who have described an increase in postoperative complications and adverse outcomes associated with excess sodium and water administration in the perioperative period.

Even healthy volunteers have difficulty with saline. When 2-l infusions administered over 1 h of either 0.9% saline or Hartmann’s solution were compared, at 6h 56% of the infused saline was retained in contrast to only 30% of the Hartmann’s solution. A marked and sustained hyperchloraemia was also seen following saline infusion. Infusion of large volumes of saline in healthy volunteers have also been shown to produce abdominal discomfort and pain, nausea, drowsiness and decreased mental capacity to perform complex tasks.

The persistent hyperchloraemia after saline infusions reflects the lower [Na+]:[Cl-] ratio in saline (1:1) than inHartmann’s solution (1.18:1) or plasma (1.38:1). While infusions of 0.9% saline produce a significant hyperchloraemic acidosis, infusions of Hartmann’s solution do not significantly alter bicarbonate and chloride concentrations or pH. The decrease in the anion gap is more pronounced with saline than with Hartmann’s solution and reflects the differential fall in serum albumin concentration. As the negatively charged albumin molecule accounts for about 75% of the anion gap, the acute dilutional hypoalbuminaemia produced by crystalloid infusions can reduce the anion gap by 2.5 mmol/l for every 10 g/l fall in serum albumin concentration in critically ill patients.

Stewart has described a mathematical approach to acid base balance in which the strong ion difference ([Na+] + [K+] – [Cl-]) is the major determinant of the H+ ion concentration. A decrease in the strong ion difference is associated with a metabolic acidosis and an increase with a metabolic alkalosis. Chloride concentration is the major anionic contributor to H+ homeostasis and hyperchloraemia decreases the strong ion difference, resulting in a metabolic acidosis.

Veech has emphasized that the kidney is slow to excrete an excess chloride load after the infusion of large amounts of saline. Wilcox found, in animal studies, that sustained renal vasoconstriction was related to hyperchloraemia, which was potentiated by previous salt depletion and related to the tubular reabsorption of chloride which appeared to be initiated by an intrarenal mechanism and was accompanied by a reduction in glomerular filtration rate.

Wilcox also established that, although changes in renal blood flow and glomerular filtration rate were independent of changes in the fractional reabsorption of sodium, they correlated well with changes in the fractional reabsorption of chloride, suggesting that renal vascular resistance was related to the delivery of chloride, but not sodium, to the loop of Henle. Chloride-induced vasoconstriction appeared to be specific for the renal vessels, so that the regulation of renal blood flow and glomerular filtration rate by chloride could override the effects of hyperosmolality on the renal circulation.

Further studies on young adult men have shown that plasma renin activity is suppressed 30 and 60min after infusion of sodium chloride, but not after infusion of sodium bicarbonate, suggesting that both the renin and blood pressure responses to sodium chloride are dependent on chloride. Hyperchloraemic acidosis, as a result of saline infusions has also been shown to reduce gastric blood flow and decrease gastric intramucosal pH in elderly surgical patients, and both respiratory and metabolic acidosis have been associated with impaired gastric motility in pigs. In patients undergoing colonic surgery, salt and water overload delayed recovery of gastrointestinal function, increased complications and prolonged hospital stay. Acidosis also impairs cardiac contractility and may decrease the response to inotropes.

At the cellular level, salt and water overload can result in cytosolic acidification, membrane hyperpolarisation, inactivation of protein kinases and disruption of phosphorylation, leading to cellular dysfunction. In addition, there is increasing evidence that 0.9% sodium chloride solution has adverse effects on immune cells. Although in vitro studies have demonstrated that 0.9% sodium chloride solution causes activation of human neutrophils, an effect on neutrophil function was not demonstrated in a study in which healthy human volunteers were infused with 2 l of 0.9% saline. Recent animal models of haemorrhagic shock that employed 0.9% sodium chloride as a resuscitation fluid found this led to significant pulmonary inflammatory infiltrates and decreased oxygenation. It has been suggested that the use of 0.9% sodium chloride may exacerbate injury-related neutrophil activation, thus predisposing the host to infectious complications.
 
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I do appreciate what you are saying about oral consumption of salty water ending up in the bloodstream just as IV drip does. And I agree that this makes the benefits that patients report after IV saline seem like they could be the placebo effect.

At the same time, it given the strong benefits reported by patients, it's perhaps worth entertaining a few theories about possible real physical effects that IV saline may have which may not arise from consumption of salty water.

I just found the following paper, which indicates that there are more complexities and biological effects occurring during saline infusions that one might first think:

The history of 0.9% saline (full paper here).

Here is an extract from that paper:
Hip, this is a rather poorly written review produced by a trainee in Nottingham and the last sentence of the abstract shows that he had no real idea what he wanted to say anyway. All the effects mentioned would occur exactly the same with real sodium chloride - that is the point I have repeatedly tried to make. Saline is dangerous if renal homeostasis is impaired as after surgery but every medical registrar should know that. The point the author is probably trying to make is that saline is not necessarily the best fluid for rehydration post-operatively, with dextrose or Hartmann's solution having advantages in some situations. Every medic of my generation knew that. Recent trainees may not have been exposed to the sort of detailed physiological teaching we had forty years ago - everything is now dumbed down. So he is really just talking to the ignorant of his own generation.

And it makes no difference whatever to what we are talking about !!!
 

sharks

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I've got a GP appointment tomorrow and I'd like to ask about trying IV saline, even just once. I've been having GI problems so she told me to use osmolax, but I've started feeling pretty bad. Looked up how it works, which is by holding water in the intestines so it's excreted, making the stool softer. So I think that I probably have hypovolemia and the osmolax has exacerbated things. I've also had a cold, which is further confusing things and making it hard to attribute the cause of various symptoms :(

I've missed my first two weeks of college because my cold + CFS + POTS + GI issues has just been too hard to handle. I'm getting a little behind in study, and I have a few things coming up over next few weeks (engagement party, exam, interstate friends visiting, dad's bday). I was hoping to be able to convince my GP that trying IV saline might give me a boost to get through this difficult stage. I haven't tried POTS meds yet though, mainly because I'm scared it will make me worse. I tried salt tablets last year and even when tapering the dose and eating before taking it, it gave me terrible constipation and postural hypotension (don't usually have).

Does anyone have any advice on how to approach it with her despite not trying any POTS meds yet? I'm just struggling so much and I'm scared that they will make me worse, which would just break me right now. I'm already at the point where I often wish I just didn't exist, because existing is so difficult. Not in a suicidal way - definitely not thinking like that, in a 'life is just too hard and I don't know how to handle it' way.
I'm late to this. But there are services that will go to your house and give you if solutions also some urgent cares will do it too. Some urgent cares take insurance.

They are mostly marketed towards people with hangovers, but they do the same thing.
 
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Saying IV fluids are a placebo effect is ignorant. I have CFS, Fibro, POTS and a few other things and IV fluids are the only thing that have helped me. Until you suffer with this or truly deal with patients who do, I think you should refrain from being so disrespectful.
 

barbc56

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Saying IV fluids are a placebo effect is ignorant. I have CFS, Fibro, POTS and a few other things and IV fluids are the only thing that have helped me. Until you suffer with this or truly deal with patients who do, I think you should refrain from being so disrespectful.
Ha ha, welcome to Phoenix Rising. Congratulations, you stayed right on script! ;)
 
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Gosh the debate...
From what i know saline can help people with low bp, low electrolyte, low blood volume, etc. (which pots patients have).
(Ex: treatment for diarrhea)

And if it does help pots patients whats the problem? It does more good than bad?

Theres also still a possibility that something missed about the mechanism. Were not God who knows it all. Were human and human makes mistakes/has flaws.
 

pibee

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I have no idea where to ask, so to avoid opening new thread i'll ask here:

In July I got IV saline (think it was 500 mL) because of dehydration -in ER - i had 40 C temp. it was about 4am. Later I got IV rocephine.
then next day i came for IV rocephine around 10 am.

felt big impovement that afternoon, about 3pm, and next day whole day. Maybe best I ever felt, with some symptoms at least.

So could this be IV saline? delay was 35 hrs. Take into consideration that i was not my usual dehydrated, but more, because of 40 C fever
(that went away on its own beause it was not infection, but drug induced fever, i think.. it happened few times before, as aquired allergy to rifampicin, within 3 hrs of taking it, i get 40 C fever which goes away within 12 hrs with ibuprofen, by the time i got to ER i had 37 C, but i went to have them check my basic functions because i was afraid i'm having sepsis)
 
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Hip

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Revisiting the question of whether the improvement POTS patients feel from IV saline infusions are real or just placebo:

One possible way to answer this question might be to do an active standing test (the "poor man's tilt table test") soon after receiving IV saline, and seeing if the increase in your heart rate on standing is the same as it usually is, or whether the heart rate increase is less than normal.
 

pibee

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Revisiting the question of whether the improvement POTS patients feel from IV saline infusions are real or just placebo:

One possible way to answer this question might be to do an active standing test (the "poor man's tilt table test") soon after receiving IV saline, and seeing if the increase in your heart rate on standing is the same as it usually is, or whether the heart rate increase is less than normal.
cant they simply do very cheap double blind placebo study? patients dont get to see what's being injected... and the one administering the treatment is not researcher?

So placebo would be simply putting port/needle into hand and not injecting anything.


It would be cheapest study in history. And maybe worth something.
 
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I have been on Saline IVs for a few months and they have made the difference between being a non person to low functioning. I hope to improve but it is definitely slow going. I don't believe it is a placebo effect, so for anyone who wishes to try it, I say do so and find a dr who is willing to prescribe it. If you're like me and nothing else helped and it improves your quality of life, well, that's the goal isn't it?
 

JES

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I have been on Saline IVs for a few months and they have made the difference between being a non person to low functioning. I hope to improve but it is definitely slow going. I don't believe it is a placebo effect, so for anyone who wishes to try it, I say do so and find a dr who is willing to prescribe it. If you're like me and nothing else helped and it improves your quality of life, well, that's the goal isn't it?
Have you tried drinking large amounts of salt water (as in 1-2 liters of water mixed with 1-2 teaspoons of salt, preferably sea salt). This is a popular POTS home treatment and has helped quite a few CFS/ME patients as well.
 

Sushi

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unicorn7

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I don’t think it’s placebo. Research has shown a lot of people with ME have low blood volume, of course iv saline would help.

I see no reason why taking ors orally wouldn’t help though?
 

JES

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I don’t think it’s placebo. Research has shown a lot of people with ME have low blood volume, of course iv saline would help.

I see no reason why taking ors orally wouldn’t help though?
I agree. The point that I think that was implied previously in this thread and commented by Prof. Edwards was whether IV saline or fluids would have some extra special benefit for CFS/ME over oral. It would be the "simplest" treatment ever if it worked, but first the mechanism of it would need to be understood, i.e. why it would be dramatically different than intake of fluids via drinking.