Steroids for Spinal Cord Injury (again)

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> ALL readers of this list server must remember that virtually all of the 
> studies on MAP in head injured patients have been in patients that were 
> flooded with LR prior to the neurosurgeon every seeing the patient.  I 
> know of no studies on MAP in head injuried patients where the 
> intravascular and interstital volume had not been expanded by fluids 
> prior to the study beginning in any particular patient.    Remember if 
> you fill up a sponge (?brain, lungs, etc) with water, its size 
> increases tremendously, as well as its weight.  The water must be 
> squeezed out before it can get small again.    If one puts that sponge 
> inside a closed box (?Cranium), then the pressure to push more water 
> into the now supersaturated sponge is much greater, thus the 
> theoriticcal basis for the neurosurgeons mandating a higher MAP.    
> 
> A study is long overdue to study the head injured patients that have 
> NOT been fluid overloaded and the clinician accepts a lower MAP than 95 
> or higher.    AND where the MAP is maintained by vasopressors, not 
> fluids.  

Sometimes I read this list and shake my head in despair. I paraphrase, but I contend accurately: 
"The brain is a sponge that soaks up water"."All patients get flooded with LR" (whatever that 
is). "The basis for a raised MAP is as a result of the brain being a helpless, supersaturated 
sponge."

There are so many elementary errors of physiology in the statements quoted that I cannot stay 
quiet. Let me make one statement that I have made many times on this list before and (naturally) 
have never had challenged.

There is no (none, nix, nada, ne rien, nul, zero) type 1 evidence in man or other species that fluid 
restriction is of benefit in blunt trauma. There is evidence that there is benefit of fluid restriction 
in penetrating trauma in certain health care systems and acute blood loss states such as a 
ruptured aortic aneurysm or experimental aortic tear.

Having got that important message out of the way once more, let me turn to head injury. At its 
simplest, head injury leads to brain injury by two mechanisms. Mechanism one is as a result of 
a bleed within the rigid box that is the skull, leading to volume expansion and secondary 
pressure rise, and I shall not dwell on that further. 

Mechanism two is blunt head trauma. The body has only a limited number of responses to 
trauma, and if enough energy is imparted there will be tissue tearing and disruption, leading to 
vascular fluid loss into the tissues, kinin activation and cell autolysis. All these lead to the 
clinical picture we see as a bruise, with swelling and discolouration. 

Bruise your finger and apart from the swelling and discolouration and a transient loss of 
function, tissue repair mechanisms ensure recovery in a few days. This is because a finger is 
like a lollipop on a stick ,and can expand freely around a central core of bone.

The brain bruises too. The normal processes of autoregulation break down, and the same injury 
processes start. However, the brain is enclosed in a rigid box with only one exit hole. As the 
swelling starts, the brain increases in volume. Initially, cerebrospinal fluid and venous blood is 
displaced, but a point is reached where the displacement of fluid can proceed no further, and so 
pressure starts to rise within the skull, as the bone does not give way. This is not good, as 
blood needs to get in to nourish and oxygenate the brain. The perfusion of the brain is 
dependent on the cerebral perfusion pressure (CPP), which is the difference between the mean 
arterial pressure (MAP) and the intracranial pressure (ICP).  So to provide continued perfusion, 
the arterial pressure has to rise (and, incidentally, if misguidedly brought down again leads to 
an abrupt close of play) to maintain an adequate perfusion pressure, as the autoregulation is 
such a powerful driver to the medulla and hence the control systems for the cardiovascular 
system. As the blood pressure rises, so compensatory mechanisms (CO=HR x SV, for those still 
awake) lead to a bradycardia, producing the effect known as Cushing's reflex; hypertension and 
bradycardia.  Unfortunately, in many cases this is not sufficient, and the increasing pressure 
places the damaged structures under greater stress so that they lose more fluid and there is 
only one outcome - the brain gets squeezed physically out of the skull like toothpaste from a 
tube. This is called coning. This is fatal.

Now I have told this story in a little detail, and it will be one well known to many. What is does 
NOT depend on is fluid administration to the patient for these adverse effects. The problem is 
the bruise. That is a function of tissue damage. However, what will kill or create severe 
secondary damage is hypotension leading to cerebral hypoperfusion or hypoxia as the attempts 
to raise blood pressure at the behest of the autoregulatory mechanisms are impaired. Fluid 
restriction does both these, and for this reason is to be condemned in head injury. What we 
badly, badly need is a drug, operation or manoeuvre that will stop bruising in its tracks, or at 
the very least ameliorate it. Fluid administration is a minor sideshow, and in the fullness of time 
will be shown to be irrelevant. The doctor who will do the most good to the most patients is the 
doctor who can fix the bruise.

Best wishes,


Rowley Cottingham

rowley at cix.co.uk
http://www.emergencyunit.com

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