X-Message-Number: 33223
Date: Thu, 13 Jan 2011 06:17:00 EST
Subject: Hypertonic saline for brain edema 

Doug asks about hypertonic saline for cerebral edema in cryopatients. The  
most succinct answer is that we don't know the answer. However, I think I 
can do  a little better than that.
As the papers Doug cites indicate, hypertonic sodium chloride (typically  
23% sodium chloride (NaCl): saline) is far superior to anything else for  
controlling cerebral edema from a variety of causes, including traumatic and  
post-ischemic brain injury. It is more effective than mannitol, urea, 

glycerol,  or even, very interestingly, other simple salts of sodium. The same 
true when  the chloride anion is combined with cations other than sodium. 
There are a  couple of credible theories as to why this strange state of 

affairs should  pertain, but there is very little doubt that hypertonic saline 
the most  effective acute treatment for cerebral edema - in critically ill 
patients who  are noromothermic, or only very slightly hypothermic. 
And the latter is a very important qualification. In cryonics patients, any 
 sodium chloride given will stay in the patient. This is in sharp contrast 
to  what happens in a living, actively metabolizing patient where the excess 
NaCl  will be fairly rapidly excreted via the kidneys. This will not happen 
in  cryonics patients because the induction of profound/ultraprofound 
hypothermia  will abolish active ion transport in the renal tubules. Even if 
blood continues  to flow under adequate pressure, all that will issue from the 
kidneys is an  non-concentrated plasma ultrafiltrate. Thus, most of sodium 
(and chloride) will  remain 'on-board' in the patient.
Unfortunately, two of the principal drivers of cellular edema in both  
ongoing cerebral ischemia, and in profound or ultraprofound hypothermia, are  
sodium and chloride. The molecular weight of NaCl is only 58.44, roughly half  
that of glycerol. Both of the ions that comprise sodium chloride transit 
across  the cell membrane with comparative ease. Under normal conditions, 
these ions are  actively pumped out of cells at a considerable cost in energy 
expenditure -  in fact, about 30% of the cell's resting energy requirement is 
spent just on  regulating ion homeostasis (and thus, in large measure, water 
balance). In  theory (and in the laboratory) adding large amounts of 

additional sodium  chloride IN THE ABSENCE OF ACTIVE ION PUMPING results in much
increased cellular  edema under conditions of deep hypothermia or continuing 
hypoxia or ischemia. 
In the event that cryonics stabilization technology evolves to the point  
that extracorporeal support can be virtually guaranteed as a RAPID (30-60 
min)  follow-on to closed chest cardiopulmonary support, hypertonic saline may 
prove  invaluable. Under such conditions, blood washout could be initiated, 
or  hemodilution with concurrent extended moderate hypothermic perfusion 
might be  used. Under such conditions it is possible to 'dial in' any 

electrolyte  concentration deemed desirable by adding a hemofiltration device to
extracorporeal circuit.
Having said that, under no circumstances would I suggest hypertonic saline  
be used in cryopatients until it has been thoroughly validated in a 
RELEVANT  animal model(s).
I hope that provides some perspective on this question. And BTW, Aschwin  
deWolf and I have agonized over just this issue for onto 3 years now - and 
maybe  more. Well over a decade ago, I had the privilege of attending one of 
the first  comprehensive presentations on the clinical use of hypertonic salin
e by Rocha e  Silva - leader in the field. Since that time, I have been 

intrigued, if not  mesmerized by its potential for improving cerebral perfusion
following ischemia.  If I ever get into the laboratory again, that would be 
one of the many things  I'd like to investigate.
Mike Darwin

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