Hypertonic Saline

Saline in concentrations of 323% achieves a state of hyperosmolarity by

adding solute to the circulation directly rather than by a causing diuresis. It
follows that the main difference from mannitol is that the vascular
compartment is expanded with saline, instead of contracted, as it is with
continued use of mannitol. The net effect of saline infusions is reflected in
elevated serum sodium or osmolarity, as it is for mannitol. Either a bolus of
high concentration hypertonic saline (723%) or a continuous infusion of a 3%
solution can be used to sustain the level of hypernatraemia adequate to
shrink the brain but the bolus method is more rapid for initial treatment.
Lactated Ringer's solution may appear to be a suitable alternative for
hyperosmolar therapy based on its calculated osmolarity above 310 mOsm/L
but lactate and citrate associate with sodium ions and make the effective
osmolarity only 289 mOsm/L.
The concentrations of hypertonic saline used in the USA are typically 3
23.4% as shown in Table 1 but 7% and other concentrations are used
elsewhere with similar effect. I begin with 3% sodium chloride in boluses of
150 mL or 23% in 30 mL boluses. After the initial treatment with either saline
or mannitol, I initiate a constant infusion of 3% to maintain serum
hyperosmolarity, checking sodium concentrations every 68 h to maintain a
level of 145149 mEq/L. It may also be suitable to follow the first bolus of
hypertonic saline with an infusion of normal (0.9%) saline as this solution
contains 154 mEq/L of sodium and an effective osmolarity of 285 mOsm/L
(although the calculated value is 309 mOsm/L). However, homoeostatic fluid
mechanisms reverse the attained hypertonicity and a 3% concentration is
usually required to maintain a high serum osmolarity.
A central venous catheter is needed to accommodate 3% sodium chloride if it
is used for more than a day or two, or if higher concentrations are needed at
any time. Sodium and fluid overload from these infusions may cause
congestive heart failure in patients with poor cardiac output, especially if there
is diastolic heart failure.
One report, now quite dated, suggested that continuous hypertonic saline
infusion did not reduce cerebral swelling and was associated with higher

mortality, although the reasons for these findings were not clear.[8] In part
based on this retrospective finding, many centres use hypertonic saline in
boluses, similar to mannitol, rather than in continuous infusions. Continuous
hypertonic saline does not appear to lead to more complicationssuch as
venous thrombosis, renal failure or infectionthan does normal saline. [9] Most
studies comparing various modes of administering hypertonic saline are
selective or retrospective and pertain only to patients with traumatic brain
injury, making generalisation difficult
Lactate increases blood viscosity, mimics stress, causes inflammation, and contributes to shock. Lactated
Ringers solution contributes to the tissue damage caused by shock, when its used to resuscitate shock
victims (Deree, et al., 2007, 2008): it contributes to the inflammatory processes associated with shock, unlike
the use of hypertonic saline and other solutions. Lactate contributes to diabetes, inhibiting the ability to
oxidize glucose. It promotes endothelial cell migration and leakiness, with increased vascular permeability
factor (VPF or vascular endothelial growth factor, VEGF) (Nagy, et al. 1985): this can lead to breakdown of
the blood-brain barrier. -Ray Peat, PhD
Lactated Ringers solution: A salt solution that has been used to increase blood volume in treating shock; the
lactate was apparently chosen as a buffer in place of bicarbonate as a matter of convenience rather than
physiology. This solution is toxic, partly because it contains the form of lactate produced by bacteria, but our
own lactate, at higher concentrations, produces the same sorts of toxic effect, damaging mitochondria.
Estrogenic phytotoxins damage mitochondria, kill brain cells; tofu is associated with dementia. -Ray Peat,
PhD
When a person has an accident, or surgery, and goes into shock, the degree of lactic acidema is recognized
as an indicator of the severity of the problem. Lactated Ringers solution has been commonly used to treat
these people, to restore their blood pressure. But when prompt treatment with lactated Ringers solution has
been compared with no early treatment at all, the patients who are not rescuscitated do better than those
who got the early treatment. And when Ringers lactate has been compared with various other solutions,
synthetic starch solutions, synthetic hemoglobin polymer solution, or simply a concentrated solution of
sodium chloride, those who received the lactate solution did least well. For example, of 8 animals treated
with another solution, 8 survived, while among 8 treated with Ringers lactate, 6 died. -Ray Peat, PhD

Pathophysiology
Maintaining alertness requires intact function of the cerebral
hemispheres and preservation of arousal mechanisms in the reticular
activating system (RASalso known as the ascending arousal system)
an extensive network of nuclei and interconnecting fibers in the upper
pons, midbrain, and posterior diencephalon. Therefore, the mechanism

of impaired consciousness must involve both cerebral hemispheres or

dysfunction of the RAS.
To impair consciousness, cerebral dysfunction must be bilateral;
unilateral cerebral hemisphere disorders are not sufficient, although they
may cause severe neurologic deficits. However, rarely, a unilateral
massive hemispheric focal lesion (eg, left middle cerebral artery stroke)
impairs consciousness if the contralateral hemisphere is already
compromised or if it results in compression of the contralateral
hemisphere (eg, by causing edema).
Usually, RAS dysfunction results from a condition that has diffuse
effects, such as toxic or metabolicdisturbances (eg, hypoglycemia,
hypoxia, uremia, drug overdose). RAS dysfunction can also be caused
by focal ischemia (eg, certain upper brain stem infarcts), hemorrhage, or
direct, mechanical disruption.
Any condition that increases intracranial pressure (ICP) may decrease
cerebral perfusion pressure, resulting in secondary brain ischemia.
Secondary brain ischemia may affect the RAS or both cerebral
hemispheres, impairing consciousness.
When brain damage is extensive, brain herniation (see Figure: Brain
herniation. and Effects of Brain Herniation) contributes to neurologic
deterioration because it directly compresses brain tissue, increases ICP,
may lead to hydrocephalus, and results in neuronal and vascular cell
dysfunction. In addition to the direct effects of increased ICP on
neuronal and vascular cells, cellular pathways of apoptosis and
autophagy (which are forms of programmed cell death or destruction)
can become activated.
Impaired consciousness may progress to coma and ultimately to brain
death