The Patient with Cerebral Edema
Fluid management of patients with cerebral edema (see Chapter
53
) is directed at maintaining cerebral perfusion pressure, avoiding elevations
of cerebral venous pressure and hypertension, preventing large changes in plasma
osmolality (particularly depression of plasma osmolality), and avoiding hyperglycemia.
Cerebral perfusion pressure (CPP) should be maintained in the normal range (80 to
90 mm Hg) because autoregulation is impaired in the damaged brain, with a baseline
increase in cerebrovascular resistance. Avoidance of intracranial hypertension,
the other determinant of CPP, is crucial to preserve blood flow to compromised but
viable brain tissue. Cerebral edema formation is related to capillary pressure,
COP, and permeability. The capillary pressure is between the arterial and venous
pressures. Systemic arterial or venous hypertension should be prevented. The normal
brain capillary bed is essentially impermeable to sodium, mannitol, and protein,
although water crosses freely. The damaged capillary bed becomes excessively permeable,
with conductivity being greatest for the smallest molecules but less for colloids.
A degree of water dehydration without hypovolemia is desired to
maintain the plasma sodium level between 142 and 148 mEq/L. It is common to provide
75% to 90% of maintenance fluids with 0.9% NaCl or lactated Ringer's solution and
to minimize water volume required for other medications. Isotonic crystalloids or
colloids do not cause edema in normal brain and can be used to sustain intravascular
volume.[133]
Hyponatremia is often caused by hypovolemia
with inappropriate sodium loss[134]
and subsequent
water retention. This should be
treated with intravascular volume expansion with isotonic or hypertonic sodium chloride.
Parenteral nutrition can be prepared with 15% amino acid solutions, 20% lipid, and
70% dextrose to give full protein and caloric support in a minimal volume. Similarly,
tube-feeding formulations with 2 cal/mL should be prescribed. Hypovolemia must be
carefully avoided. Colloid infusion to sustain intravascular volume, guided by hemodynamic
monitoring, tends to provide better long-term control of the intravascular volume
than crystalloid. If diuretics or diabetes insipidus cause loss of more than 2 mL/kg/hour
for more than 2 to 4 hours, a pulmonary artery catheter may be indicated for closer
monitoring. Blood glucose should be maintained at 80 to 175 mg/dL by close monitoring,
initially hourly, with decreasing frequency as stability is demonstrated. During
acute resuscitation, dextrose administration is limited to no more than 2 mg/kg/min.
Fortunately, indications for steroid use have become fewer in recent years, lessening
the problems of hyperglycemia.
