Severe cerebral contusion is often associated with nonhemorrhagic mass effect that progresses rapidly within 12 to 48 hours posttrauma. The mechanisms underlying such a rapid progression of mass effect cannot be fully explained by classic concepts of vasogenic and cytotoxic brain edema. Data from previous clinical trials, including diffusion-weighted magnetic resonance imaging studies, have indicated that cells in the central (core) area of the contusion undergo shrinkage, disintegration, and homogenization, whereas cellular swelling is located predominately in the peripheral (rim) area during this period. The authors hypothesized that high osmolality within the contused brain tissue generates an osmotic potential across the central and peripheral areas or causes blood to accumulate a large amount of water. To elucidate the role of tissue osmolality in contusion edema, they investigated changes in tissue osmolality, specific gravity, and ion concentration in contused brain in both experimental and clinical settings. Their results demonstrated that cerebral contusion induced a rapid increase in tissue osmolality from a baseline level of 311.4 ± 11.3 to 402.8 ± 15.1 mOsm at 12 hours posttrauma (p < 0.0001). Specific gravity in tissue significantly decreased from 1.0425 ± 0.0026 to 1.0308 ± 0.0028 (p < 0.01), reflecting water accumulation in contused tissue. The total ionic concentration [Na+] + [K+] + [Cl−] did not change significantly at any time point. Inorganic ions do not primarily contribute to this elevation in osmolality, suggesting that the increase in colloid osmotic pressure through the metabolic production of osmoles or the release of idiogenic osmoles can be a main cause of contusion edema.
Tatsuro Kawamata, Tatsuro Mori, Shoshi Sato and Yoichi Katayama
Tatsuro Mori, Yoichi Katayama, Tatsuro Kawamata and Teruyasu Hirayama
Object. To reduce the risk of ischemic complications in patients with subarachnoid hemorrhage (SAH), hypervolemic therapy is generally advocated. However, such conventional treatment cannot always ensure the maintenance of an effective intravascular volume expansion, because excessive natriuresis and osmotic diuresis occur after SAH. In this prospective study the authors examined the effects of inhibition of natriuresis with fludrocortisone acetate on intravascular volume expansion during hypervolemic therapy.
Methods. Thirty patients with SAH were randomized and divided into two groups: controls (Group 1, 15 patients) and patients treated with 0.3 mg/day of fludrocortisone (Group 2, 15 patients). In all patients sodium and fluid intake levels were in excess of maintenance requirements in an attempt to maintain a positive water balance and a central venous pressure (CVP) of 8 to 12 cm H2O. The mean sodium and water intake levels for 14 days after SAH were significantly reduced by fludrocortisone in Group 2 (487 ± 34.52 mEq/day and 5159.2 ± 249.29 ml/day, respectively; p < 0.01) compared with Group 1 (634.2 ± 42.86 mEq/day and 6611.7 ± 365.67 ml/day). Fludrocortisone significantly reduced the urinary sodium excretion (p < 0.01) and urine volume (p < 0.01) in parallel, and effectively prevented a negative shift in the sodium as well as water balance (p < 0.01). The serum sodium level tended to decrease in Group 1, reaching 135 mEq/L on average, but not in Group 2 (p < 0.01). Hyponatremia in Group 1 was always observed at the optimal range of CVP values. A decrease in serum potassium level within the range of 2.8 to 3.5 mEq/L was transiently noted in 11 patients (73.3%) of Group 2, but was easily corrected. Possible side effects of fludrocortisone, such as pulmonary edema, were not encountered.
Conclusions. Intravascular volume expansion in the presence of excessive natriuresis requires a large sodium and water intake and is often associated with hyponatremia. Inhibition of natriuresis with fludrocortisone can effectively reduce the sodium and water intake required for hypervolemia and prevent hyponatremia at the same time.