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Physiology and Monitoring
of Intravascular Volume
Status in the Neurosurgical
David J. Stone MD
Patient
I. Introduction and General Issues
The focal point in the care of neurosurgical patients is the
control of intracranial pressure (ICP) and systemic
hemodynarnics in a manner that maximizes cerebral
perfusion and surgical brain exposure while avoiding brain
edema, hemorrhage, and ischemia Attention must also be
devoted to preventing injury to other systems. A keyelement
in providing such care is an understanding of the physiology
and monitoring of systemic fluid volume status to allow
effective manipulation of intracranial mechanics and
hemodynamics.
This review will address two specific clinical situations:
Clipping of a ruptured cerebral aneurysm and surgery for a
supratentorial tumor with elevated ICP. It is important to
apply the underlying physiological principlei to each
scenario rather than arote approach to "fluid management in
neuroanesthesia". Of necessity, the fundamental issues of
cerebral blood flow, intracranial pressure, and cerebral
ischemia will not be reviewed in detail since excellent
sources on these subjects are available.
11. Fluids, Osmolarity and Intracranial Pressure
Systemic dehydration, while a seemingly simple and
obvious measure, is a very inefficient and dangerous way to
decrease ICP because renal and coronary perfusion may be
impaired before ICP is effectively reduced. Furthermore,
anesthetically-modulatedblood pressure control, especially
important in neurovascular procedures, is very difficult in
the hypovolemic patient. It is important to specify exactly
why ICP is of such concern. First, increases may cause brain
herniation when the cranium is intact or exposure difficulties
during craniotomy. Secondly, ICP is essentially the
downstream pressure for cerebral perfusion such that any
marked elevation in conjunction with or even wiihout a
concomitant decrease in systemic mean arterial blood
pressure may cause cerebral ischemia and infarction.
Fortunately, there is sufticient reserve in cerebral perfusion
that the normal cerebral perfusion pressure (CPP) can
actually be reduced markedly during anesthesia without the
onset of irreversible ischemia However, the patient with
cerebral vasospasm, occlusive cerebral atherosclerotic
disease, pressure from a neurosurgical retractor, or
significant anemia may not possess the same degree of
reserve and these patients may also have occult or known
coronary or renovascular disease that results in serious
ischemic problems elsewhere.
When the blood brain barrier (BBB) is reasonably intact,
it appears that serum osmolarity rather than oncotic pressure
controls water movement in and out of the brain.' This is so
because the tight junctions between the endothelial cells that
make up the BBB are so narrow that the movement even of
sodium ions is limited. Therefore, manipulation of
osmolarity is employed to decrease ICP and provide
improved operating conditions when there is amass effect or
simply to improve operating conditions as in aneurysm
clipping. When the blood brain barrier is seriously disrupted,
oncotic pressure may become more important in the
determination of ICP as small molecules such as sodium and
simple sugars are no longer anatomically excluded from the
brain. Such disruption may occur during head trauma,
significant ischemia, and when blood pressure exceeds the
upper limit of flow autoregulation. It should be noted that the
distinction between osmolarity (solute concentration per
liter of solution) and osmolality (solute concentration per
kilogram of solvent) is not clinically critical. In practice,
molar concentrations are reported but the osmometer that
employs freezing point depression as an indicator of the
number of molecules in solution actually measures
osmolality. In any case, osmolarity is determined only by the
number of molecules in solution regardless of size. A
sodium ion counts for as much as a huge protein molecule in
this chemical democracy.
Currently, the osmotic agent most widely employed for
ICP reduction is mannitol in 20% solution which has an
osmolarity of 1098 mOsm-L-!. In contrast, the osmoiarities
for lactated Ringer's and normal saline are 273 and 308
m0sm.L-l, while normal ... serum osmolarity is 286k4
mOsm- L-'.2 Osmolality can also be calculated from the
molar concentrations of the three major solutes- sodium,
glucose and urea [2 x Na + (glu in mg-dl-' - 18) + (BUN in
mg-dl-' + 2.8)]. A gap of greater than 10 m0srn.L-' between
measured and calculakd osmolarities indicates that the