Total body water (TBW) separates into intracellular and extracellular compartments, comprising approximately two-thirds and one-third of TBW, respectively. According to Starling’s hypothesis, capillary and tissue hydrostatic pressure, along with tissue oncotic pressure, acts to move water from the vascular to the extravascular compartment. In contrast, plasma oncotic pressure promotes water reabsorption back into capillaries.
In peripheral tissues, the capillary endothelium is loosely connected, allowing water and dissolved particles, such as ions and glucose, to pass freely between compartments. However, large molecules cannot pass through endothelial pores. Therefore, water movement in peripheral tissue largely depends on transcapillary hydrostatic pressure gradients and the concentration gradient of large macromolecules. Total osmotic pressure does not play a significant role in peripheral tissues.
The brain is unique because water movement is dictated by the blood–brain barrier (BBB). The BBB is made up of specialized capillary endothelial cells connected via tight junctions. As a result, the pore size in the BBB is 1/10 of those in the periphery. Therefore, this specialized barrier is impermeable to most ions (i.e., Na+, Cl–, K+) in addition to the large macromolecules. Despite the tight junctions of the BBB, water, oxygen, and carbon dioxide remain freely permeable. Accordingly, ions contribute to the osmotic gradient, making ion contribution to water movement across the BBB much larger than oncotic gradient contribution. The osmolar gradient is determined by the relative concentrations of all osmotically active particles, including electrolytes. Therefore, water movement in the brain is uniquely driven by the osmotic gradient between plasma and extracellular fluids.
Because the skull is an incompressible compartment with a fixed volume, intracranial pressure (ICP) can be altered by any disruption in the equilibrium between the skull’s contents. This is demonstrated by Monroe–Kellie’s hypothesis (intracranial volume = V brain + V CSF + V blood) whereby an increase in any one component must be met with a decrease in another in order to maintain ICP. Accordingly, the goals for fluid management in neurosurgical patients are listed in Table 39-1.
TABLE 39-1Goals of Fluid Management in the Neurosurgical Patient |Favorite Table|Download (.pdf) TABLE 39-1 Goals of Fluid Management in the Neurosurgical Patient
|Minimize cerebral edema while preventing intravascular volume depletion |
|Preserve adequate Cerebral perfusion pressure |
|Maintain glucose and electrolyte homeostasis |
|Reduce brain size |
The type of fluid being administered plays a large role in maintaining adequate cerebral perfusion pressure (CPP) and blood volume. Inappropriate fluid administration could prove detrimental to the neurosurgical patient.
Hypoosmolar crystalloids have an osmolality less than plasma (< 285 mOsm/kg). Administration of these fluids should not be used in the management of a patient during neurosurgery due to concern for increased ICP and subsequent cerebral edema. Water from hypoosmolar solutions will follow the osmotic gradient and freely cross the BBB into the brain. For the same reason, all glucose-containing solutions are avoided in these patients. An exception to the use of hypoosmolar crystalloids during neurosurgery is in a patient being treated for diabetes insipidus.
Isoosmolar crystalloids such as normal saline (NaCl 0.9%) and lactated ringers have an osmolality approximately equivalent to plasma. Such similarity prevents osmotic gradients and ...