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

Secondary Brain Injury

The pathological cascade of secondary brain injury that may occur in the hours and days after a primary traumatic injury can have devastating consequences. Secondary injury may be attributable to factors associated with cerebral ischemia. Cerebral ischemia can be caused by hypoxia, systemic hypotension, or relative hypoperfusion produced by intracranial hypertension (Bayir et al., 2003).

Secondary injury can cause both cerebral edema and worsened cerebral ischemia. It can also lead to intractable increased intracranial pressure (ICP), which contributes to development of secondary brain damage and subsequent morbidity and mortality. In addition, TBI itself may lead to an inflammatory response that can promote and aggravate secondary brain damage (Bayir et al., 2003).

The prevention and treatment of secondary brain injury involves a multifaceted strategy. Critical care monitoring includes ICP assessment, cerebral perfusion pressure, and, if available, cerebral oxygenation. Patients are positioned with appropriate head elevation and body alignment and sedated with medications such as narcotics, analgesics, anesthetics, and barbiturates. Hemodynamics are stabilized using fluids and pressors. Oxygenation is optimized with careful airway and ventilator management. Cerebral edema can be treated with surgery or medications or both. Osmotic agents (e.g., mannitol, HTS) are also a part of this effort (Fields, Blackshear, Mortimer, & Wallace, 2004).


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