title: 0.45% saline and 5% dextrose in water, but not 0.9% saline or 5% dextrose in 0.9% saline, worsen brain edema two hours after closed head trauma in rats.
abstract: In this study, we examined the effect of four i.v. fluids (250 mL/kg) on blood glucose and osmolality and brain tissue specific gravity after closed head trauma (CHT) in rats. CHT was delivered at Time 0; blood was sampled at 60 min; fluid infusion began at 75 min and ended at 105 min. Blood was again sampled at 105 and 120 min, and brain tissue specific gravity was determined at 120 min. Five groups (one control and four fluid-treated groups) received CHT, and five other groups (one control and four fluid-treated) did not (n = 9 in each group). 0.45% saline (1/2 NS) and 5% dextrose in water (D5W) accentuated the decrease of brain tissue specific gravity (1.0366 +/- 0.0025 and 1.0368 +/- 0.0028, respectively; mean +/- SD) caused by CHT (1.0395 +/- 0.0036), but 5% dextrose in 0.9% saline (D5NS) and 0.9% saline (NS) did not (1.0431 +/- 0.0042 and 1.0389 +/- 0.0049, respectively). In addition, 1/2 NS decreased blood osmolality (248 +/- 6 mOsm/L), D5W increased blood glucose (1095 +/- 173 mg/dL), D5NS increased blood osmolality (350 +/- 5 mOsm/L) and glucose (1695 +/- 76 mg/dL), and NS caused no significant change. We conclude that administering hypoosmolar i.v. fluids after CHT causes a significant worsening of cerebral edema 2 h after CHT.
  
  
  CONCLUSIONS
  We previously reported worse neurological outcome and/or mortality after closed head trauma in rats when 5% dextrose in water or 0.45% saline was given i.v. compared with 0.9% saline or 5% dextrose in 0.9% saline. The present results and our previous findings indicate that worsening of outcome after closed head trauma in rats may be caused more by edema formation than by hyperglycemia.
authors.affiliation: Division of Anesthesiology, Soroka Medical Center and the Faculty of Health Science, Beer-Sheva, Israel.
authors.forename: D
authors.initials: D
authors.lastname: Talmor
authors.forename: Y
authors.initials: Y
authors.lastname: Shapira
authors.forename: A A
authors.initials: AA
authors.lastname: Artru
authors.forename: B
authors.initials: B
authors.lastname: Gurevich
authors.forename: V
authors.initials: V
authors.lastname: Merkind
authors.forename: L
authors.initials: L
authors.lastname: Katchko
authors.forename: E
authors.initials: E
authors.lastname: Reichenthal
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D001812:Blood-Brain Barrier; D001921:Brain / Q000187:drug effects / Q000473:pathology; D001929:Brain Edema / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D018450:Disease Progression; D005500:Follow-Up Studies; D005947:Glucose / Q000008:administration & dosage / Q000009:adverse effects*; D016489:Head Injuries, Closed / Q000097:blood / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology*; D006863:Hydrogen-Ion Concentration; D007262:Infusions, Intravenous; D009460:Neurologic Examination; D009994:Osmolar Concentration; D011188:Potassium / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride / Q000008:administration & dosage / Q000009:adverse effects*; D013046:Specific Gravity
chemical_list: D001786:Blood Glucose; D012965:Sodium Chloride; D012964:Sodium; D005947:Glucose; D011188:Potassium