[neuro0000]

Hi, I was just wondering if someone could explain to me better the use of 3% saline, and 1/4NS, etc. and how it affects sodium levels. Also just a review of how they work in the body. Thanks I appreciate it.

[NeuroICURN]

Ok, I got this from the article: Administering Hypertonic Saline to Patients With Severe TBI - on Medscape. If I could figure out how to insert a link to the article, I would. But, if you go to www.medscape.com and type in "hypertonic saline" in the search area, it will bring up the full article.


Osmotic Effect
HTS exerts an osmotic effect. It draws fluid out of edematous cerebral tissues because it has a higher concentration of sodium and a lower concentration of water than blood. When HTS is administered intravenously, plasma osmolarity increases. The higher sodium concentration causes blood to be hypertonic compared to cerebral tissue, which has a lower sodium concentration. These concentration differences set up an osmotic gradient that promotes the flow of excess water from cerebral tissue to the blood via osmosis. Osmosis occurs because water moves passively along the concentration gradient. Water moves from areas of lower concentration to areas of higher concentration (Feig & McCurdy, 1977).

This osmotic effect can be used to combat cerebral edema. By reducing the water content of the injured brain, HTS can reduce mass effect. HTS can also control ICP, leading to a decrease in secondary brain injury (Qureshi & Suarez, 2000; Qureshi et al., 1998; Qureshi, Suarez, Castro, & Bhardwaj, 1999).

Hemodynamic Effect
The hemodynamic effect of HTS occurs because it is an effective plasma volume expander. Volume expansion improves blood pressure and cerebral perfusion pressure. Improved perfusion yields better oxygenation to areas of the brain that are at risk for secondary damage (Doyle et al., 2001; Kramer, 2003).

Vasoregulatory Effect
The use of HTS may also have beneficial effects on cerebrovascular regulation in the brain's microcirculation. Decreasing edema in the vascular endothelium of injured tissues lowers vascular resistance, allowing more blood to flow through the vessels. Thus, HTS modulates the hypoperfusion often seen in secondary brain injury. The effective increase in microvessel diameter can also help the injured brain combat hyperemia by allowing blood to flow out of the region (Doyle et al., 2001; Kramer, 2003; Pascual, Khwaja, Chaudhury, & Christou, 2003).

Immunomodulatory Effects
HTS can play a role in enhancing the immune modulation of brain cells. Head trauma can activate the inflammatory cascade, causing leukocytes to migrate and adhere to injured neurons. This inflammatory process can ultimately cause the injured cells to die. HTS, by a mechanism that is not yet fully established, can prevent leukocytes from becoming activated and adhering to brain cells, minimizing secondary pathologic events (Hartl et al., 1997).

Neurochemical Effects
HTS has neurochemical properties. After TBI, neuronal membranes may become destabilized, and the neurochemical environment can be disrupted. As a result, detrimental excitatory amino acids accumulate, leading to eventual cell death. HTS may modulate this process by normalizing neuronal cell membranes, by restoring normal electrolyte and neurotransmitter levels in brain cells, and by restoring normal cell volumes. Thus, HTS can limit secondary injury from neurochemical changes (Suarez, 2004).

Hypernatremic Effect
HTS has an important role in countering hyponatremia in the brain. Low serum sodium levels following TBI can lead to extracellular volume depletion, cerebral ischemia, and cerebral edema. These can all result in dangerous increases in ICP. HTS can help avoid the negative effects of hyponatremia by increasing serum sodium levels in the acute phase of head trauma care (Johnson & Criddle, 2004; Suarez, 2004).



Ok, well hope this gives you the info. you need!

Take care,
NeuroICURN

[kindaquazie]

OK - 3% is usually administered to TBI patients to decrease the likelihood of seizures. When sodium is low, neurons fire at a lower threshold. If you compare this to the effects of potassium on the cardiac conduction system, it may make more sense. Low K+ = depressed cardiac conduction and bradycardia. High K+ = irritible cardiac conduction or ventricular tachycardia. Very rarely is 3% sodium used as an osmotic diuretic. 27% saline may be used this way, but more likely manitol is used for hypertonic diuresis to decrease cerebral edema. This is also why brain injured patients should not be on TPN if at all possible. (It is extremely hypertonic)

3% sodium should not be run at high rates (>30-100ml/hr) nor should sodium be corrected too quickly as Central Pontine Demyelination may result. Also, any hypotonic solution or even free water taken orally or via feeding tube can decrease serum sodium levels.

If you are working in a neuro ICU you really need to be familiar with these concepts. The AANN is a great source of information. Also, there are several very well writen texts specific to neuro nursing. Please visit www.aann.org for more information.

[neurogeek]

all I can say is be careful, take it VERY seriously, and go slow with your infusion. The big risk is pontine myelinolysis. You don't want your patient to end up a quad.