Administering Hypertonic Saline to Patients With Severe Traumatic Brain Injury

Diane Schretzman Mortimer; Jon Jancik


J Neurosci Nurs. 2006;38(3):142-146. 

In This Article

Clinical Effects of HTS

Hypertonic saline refers to any saline solution with a concentration of sodium chloride (NaCl) higher than physiologic (0.9%). Commonly used preparations include 2%, 3%, 5%, 7%, and 23% NaCl. HTS may have an important role in preventing and treating the effects of secondary brain injury. It works primarily by an osmotic effect but also has other effects (Doyle et al., 2001). The clinical effects of HTS are outlined in Table 1 .

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).

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).

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).

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).

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).

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).


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